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 Medical Hypotheses  takes a deliberately different approach to review: the editor sees his role as a 'chooser', not a 'changer', 
choosing to publish what are judged to be the best papers from those submitted. The Editor sometimes uses external referees to inform 
his opinion on a paper, but their role is as an information source and the Editor's choice is final. The papers chosen may contain radical 
ideas, but may be judged acceptable so long as they are coherent and clearly expressed. The authors' responsibility for the integrity, 
precision and accuracy of their work is paramount.
  
 
From Charlton BG. Peer usage versus peer review BMJ 2007; 335: 451 :- "Traditionally, 
editorial review is the main alternative to peer review. A scientist editor or editorial team applies a sieve, with varying degrees of 
selectivity, to research submissions. Strictly, this process should not attempt to predict whether ideas and facts are "true," because 
truth can be established only in retrospect. Instead, editorial selection works within constraints of subject matter on the basis of 
factors such as potential importance and interest, clarity and appropriateness of expression, and broad criteria of scientific plausibility. 
Even probably untrue papers may be judged worth publishing if they contain aspects (ideas, perspectives, data) that are potentially stimulating 
to the development of future science." 
 
Papers in  Medical Hypotheses  take a standard scientific form in terms of style, 
structure and referencing. The journal therefore constitutes a bridge between cutting-edge theory and the mainstream of medical and scientific 
communication, which ideas must eventually enter if they are to be critiqued and tested against observations. 
 
 Abstracting/indexing 
 

 Medical Hypotheses  is indexed and abstracted in: Science Citation Index, Index Medicus/Medline, Adonis, BIOSIS, Chemical Abstracts, 
Elsevier BIOBASE/Current Awareness in Biological Sciences, Current Contents/Clinical Medicine, Current Contents/Life Sciences, EMBASE/Excerpta 
Medica, Medical Documentation Service, Reference Update, Research Alert, SciSearch, UMI (Microfilm), Russian Academy of Science</description><link>http://www.medical-hypotheses.com//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc.  </dc:rights><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:issn>0306-9877</prism:issn><prism:publicationDate>2010-03-15</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc.  </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000782/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000861/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000903/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000915/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000927/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000939/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000721/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000800/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000848/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS030698771000085X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000824/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000836/abstract?rss=yes"/><rdf:li 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rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000708/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000174/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000307/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000332/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS030698771000037X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000502/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS030698771000054X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000551/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000563/abstract?rss=yes"/><rdf:li 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rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000356/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medical-hypotheses.com/article/PIIS0306987710000277/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000782/abstract?rss=yes"><title>Eating when empty is good for your health - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000782/abstract?rss=yes</link><description>Summary: It is hypothesised that eating is regulated when eating pleasure fulfills (and thus extinguishes) the desire to eat and that eating pleasure is maximised when eating is prompted by an Empty Hollow Sensation (EHS). Absent, unrecognised, misinterpreted or false hunger sensations may account for non-regulated eating in many so-called normal eaters, not only in anorexic or obese people. As a regime in which the EHS is present before most meals, the EHS Meal Pattern (EHSMP) is suggested. Existing evidence to support its efficacy is reviewed. Obesity, diabetes and heart disease are among a range of conditions associated with excessive caloric intake owing to poorly regulated eating. If upheld, the EHSMP could assist people to maintain their own well being and could help to prevent and treat some of the major scourges of Western society.</description><dc:title>Eating when empty is good for your health - Corrected Proof</dc:title><dc:creator>David Lovell-Smith, Timothy Kenealy, Stephen Buetow</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.013</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-15</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-15</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000861/abstract?rss=yes"><title>Would increased interstitial fluid flow through in situ mechanical stimulation enhance bone remodeling? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000861/abstract?rss=yes</link><description>Summary: Bone accommodates to changes in its functional environment ensuring that sufficient skeletal mass is appropriately positioned to withstand the mechanical loads that result from functional activities. Increasing physical activity will result in increased bone mass, while the removal of functional loading would result in bone loss. Bone is a composite material made up of a collagen–hydroxyapatite matrix and a complex network of lacunae–canaliculi channels occupied by osteocyte and osteoblast processes, immersed in interstitial fluid. There are strong indications that changes in interstitial fluid flow velocity or pressure are the means by which an external load signal is communicated to the cell. In vitro studies indicate that shear stress, induced by interstitial fluid flow, is a potent bone cell behavior regulator. One of the forms of altering interstitial fluid flow is through the mechanical deformation of skeletal tissue in response to applied loads. Other methods include increased intramedullary pressure, negative-pressure tissue regeneration, or external mechanical stimulation. Analysis of these methods poses the question of process effectiveness. The efficacy of each method theoretically will depend on the mechanical efficiency of transmitting an external load and converting it into changes in interstitial fluid flow. In this paper, we combine recent knowledge on the effect of the bone’s interstitial fluid flow, different fluid patterns, the role of gap junctions, and the concept of mechanical effectiveness of different methods that influence interstitial fluid flow within bone, and we hypothesize that the efficiency of bone remodeling can be improved if a small mechanical percussion device could be placed directly in contact with the bone, thus inducing local interstitial fluid flow variations. Enhancement of bone repair and remodeling through controlled interstitial fluid flow possesses many clinical applications. Further investigations and in vivo experiments are required. Practical methods and clinical apparatuses need to be conceived and developed to validate and facilitate the clinical use of this technique.</description><dc:title>Would increased interstitial fluid flow through in situ mechanical stimulation enhance bone remodeling? - Corrected Proof</dc:title><dc:creator>J.E. Letechipia, A. Alessi, G. Rodriguez, J. Asbun</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.021</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-15</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-15</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000903/abstract?rss=yes"><title>From alpha to gamma: Electrophysiological correlates of meditation-related states of consciousness - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000903/abstract?rss=yes</link><description>Summary: Meditation practice is difficult to access because of its countless forms of appearances originating from the complexity of cultures it has to serve. This makes a suitable categorization for scientific use almost impossible. However, empirical data suggest that different forms of meditation show similar steps of development in terms of their neurophysiological correlates. Some electrophysiological alterations can be observed on the beginner/student level, which are closely related to non-meditative processes. Others seem to correspond to an advanced/expert level, and seem to be unique for meditation-related states of consciousness. Meditation is one possibility to specialize brain/mind functions using the brain’s immanent neural plasticity. This plasticity is probably recruited by certain EEG patterns observed during or as a result of meditation, for instance, synchronized gamma oscillations. While meditation formerly has been understood to comprise mainly passive relaxation states, recent EEG findings suggest that meditation is associated with active states which involve cognitive restructuring and learning.</description><dc:title>From alpha to gamma: Electrophysiological correlates of meditation-related states of consciousness - Corrected Proof</dc:title><dc:creator>Juergen Fell, Nikolai Axmacher, Sven Haupt</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.025</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-15</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-15</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000915/abstract?rss=yes"><title>Why we need semisolid decalcification system in bone tissue engineering? A story begins with honeycomb - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000915/abstract?rss=yes</link><description>Summary: The repair of large segmental bone defects remains a tough problem disturbing surgeons and researchers. Bone tissue engineering brings some new sight in this field. However, it has not been effectively applied in clinics, for the reason that the involved mechanism is not well understood. Thus, we need to know the osteogenesis process of the tissue-engineered bone including distribution, proliferation and interaction among seed cells pre-inoculated in biomaterials as well as the function of surrounding tissues. As a matter of fact, the tissue-engineered bone or the biomaterials are solid and opaque, which makes the study difficult. Here, inspired by the structure of honeycomb and amber, we hypothesize a semisolid decalcification protocol to solve this problem.</description><dc:title>Why we need semisolid decalcification system in bone tissue engineering? A story begins with honeycomb - Corrected Proof</dc:title><dc:creator>Shan Jiang, Qian-li Jiang, Yang Zhang, Le Li, Pei-ran Zhao, Yan-fei Pan, Wei Chang, Luan-jia Liu, Guo-xian Pei</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.026</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-15</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-15</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000927/abstract?rss=yes"><title>Speciation in Anopheles gambiae is consistent with the predictions of the Master Development Program - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000927/abstract?rss=yes</link><description>I have suggested that various developmental diseases may be related to mutations within pericentromeric regions of chromosomes, which cause erroneous expression of non-coding RNAs that regulate differentiation of cell clones . In fact, I proposed  that the pericentromeric regions are the essential seats of speciation within organisms. Specifically, I hypothesized a Master Development Program (MDP) that facilitates evolution of species by natural selection acting on new phenotypes produced by punctuated terminal addition of DNA sequences in pericentromeric regions that give rise to non-coding RNAs that regulate clone differentiation. Although individual steps in this process are supported by experimental evidence , I continue to look for examples that will demonstrate control of cell clone differentiation and the processes of evolution and speciation as predicted by the proposed MDP.</description><dc:title>Speciation in Anopheles gambiae is consistent with the predictions of the Master Development Program - Corrected Proof</dc:title><dc:creator>George E. Parris</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.027</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-15</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-15</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000939/abstract?rss=yes"><title>Influence of neurosteroids on the pathogenesis of multiple sclerosis - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000939/abstract?rss=yes</link><description>Summary: This paper summarizes neuroendocrine effects on myelination and their possible relevance for the pathogenesis of multiple sclerosis (MS).Steroid hormones known as neurosteroids are synthesized in the human central nervous system (CNS) and exert local effects on glial and neuronal tissue. Progesterone derivatives seem to act as promyelinating factors in the slow but continuous process of myelin maintenance in the adult human brain. Diminished production of these myelin-promoting factors may lead to the formation of structurally altered and less stable myelin, resulting in the observed pathology of the normal-appearing white matter (NAWM) in MS. Dysmyelination, characterized by an altered myelin protein composition, reduced myelin content and increased vulnerability of the myelin sheath, precedes the formation of inflammatory lesions and the clinical onset of disease. Defects in the myelin sheath first occur in mechanically strained areas of the brain, where myelin turnover is physiologically increased. The continuous exposure of myelin proteins, normally sheltered from immunosurveillance, will lead to microglia activation and phagocytosis of myelin. Phagocytic cells from the brain and myelin material may drain to cervical lymph nodes with subsequent priming of T-cells. Finally, heterogenous focal auto-inflammatory reactions contribute to the clinical symptoms of the disease.Neurosteroids influence the biochemical composition of myelin proteins and promote myelin renewal. These promyelinating neurosteroidal functions seem to be impaired in the MS brain. Contrary to the view of auto-inflammatory demyelination being a causative factor in MS pathogenesis, it is argued here that widespread dysmyelination in the adult human brain precedes and induces a focal immune response to various myelin compounds.</description><dc:title>Influence of neurosteroids on the pathogenesis of multiple sclerosis - Corrected Proof</dc:title><dc:creator>Helmut Leitner</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.028</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-15</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-15</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000721/abstract?rss=yes"><title>Possible influence of nicotine on osteoporosis - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000721/abstract?rss=yes</link><description>An article recently published in this journal hypothesizes about a possible use of nicotine against osteoporosis , despite the unquestionable correlation, admitted in the article itself, between active smoking and osteoporosis. After careful consideration, it has seemed to me that there is an important risk of misinterpretation of this proposal, resulting from some heterogeneity and confusion among the different papers cited in the main article. Most especially, the article should not be misinterpreted as suggesting, let alone proving, that “light to moderate” smoking could be beneficial for osteoporosis.</description><dc:title>Possible influence of nicotine on osteoporosis - Corrected Proof</dc:title><dc:creator>M.C. Gracia</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.007</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-11</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-11</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000800/abstract?rss=yes"><title>Covert drug dependence should be the null hypothesis for explaining drug-withdrawal-induced clinical deterioration: The necessity for placebo versus drug withdrawal trials on normal control subjects - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000800/abstract?rss=yes</link><description>Summary: Just as a placebo can mimic an immediately effective drug so chronic drug dependence may mimic an effective long-term or preventive treatment. The discovery of the placebo had a profound result upon medical practice, since it became recognized that it was much harder to determine the therapeutic value of an intervention than was previously assumed. Placebo is now the null hypothesis for therapeutic improvement. As David Healy describes in the accompanying editorial on treatment induced stress syndromes , an analogous recognition of the effect of drug dependence is now overdue. Drug dependence and withdrawal effects should in future become the null hypothesis when there is clinical deterioration following cessation of treatment. The ideal methodology for detecting drug dependence and withdrawal is a double-blind placebo controlled and randomized trial using disease-free normal control subjects. Normal controls are necessary to ensure that the possibility of underlying chronic disease is eliminated: so long as subjects begin the trial as ‘normal controls’ it is reasonable to infer that any clinical or psychological problems (above placebo levels) which they experience following drug withdrawal can reasonably be attributed to the effects of the drug. This is important because the consequences of failing to detect the risk of covert drug dependence may be considerably worse than failing to detect a placebo effect. Drug dependent patients not only fail to receive benefit and suffer continued of inconvenience, expense and side effects; but the drug has actually created and sustained a covert chronic pathology. However, the current situation for drug evaluation is so irrational that it would allow chronic alcohol treatment to be regarded as a cure for alcoholism on the basis that delirium tremens follows alcohol withdrawal and alcohol can be used to treat delirium tremens! Therefore, just as placebo controlled trials of drugs are necessary to detect ineffective drugs, so drug withdrawal trials on normal control subjects should be regarded as necessary to detect dependence-producing drugs.</description><dc:title>Covert drug dependence should be the null hypothesis for explaining drug-withdrawal-induced clinical deterioration: The necessity for placebo versus drug withdrawal trials on normal control subjects - Corrected Proof</dc:title><dc:creator>Bruce G. Charlton</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.015</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-11</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-11</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000848/abstract?rss=yes"><title>Are microvascular complications of diabetes mellitus really associated with prostate cancer? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000848/abstract?rss=yes</link><description>We read with great interest the paper by Weiwei and his colleague in the January issue of Medical Hypotheses . The authors state that capillary basement membrane thickening and capillary occlusion and degeneration, which are typical histological changes of microvascular lesions in diabetes mellitus (DM), cause capillary dysfunction and organ ischemia leading to local microvascular dysfunction and prostate ischemia, which prevent initiation and development of prostate cancer (PCa). The authors hypothesize that microvascular complications of diabetes mellitus (DM) might play a possible role against the development of PCa.</description><dc:title>Are microvascular complications of diabetes mellitus really associated with prostate cancer? - Corrected Proof</dc:title><dc:creator>Yavuz Beyazit, Murat Kekilli, Tugrul Purnak</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.019</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-11</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-11</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS030698771000085X/abstract?rss=yes"><title>Should resistance exercise be recommended during breast cancer treatment? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS030698771000085X/abstract?rss=yes</link><description>Summary: Epidemiological evidence has pointed to the benefits of physical activity in reducing breast cancer risk, which in turn has prompted the American Cancer Society (ACS) to make specific recommendations for adopting a life style of physical activity as a guideline for cancer protection. There is also evidence for benefits of physical activity during and after cancer treatments of chemotherapy and radiation therapy. The ACS recommendations for exercise as prevention and for exercise during/after cancer treatment are the same: “that adults engage in at least 30min of moderate to vigorous physical activity, above usual activities, on 5 or more days of the week; 45–60min of intentional physical activity are preferable.” These recommendations suggest participation in aerobic types of physical activity (e.g. brisk walking, biking). Effects of resistance exercise were not addressed specifically by the ACS but have been found to increase lean body mass in patients undergoing cancer treatment. Also, many women preferred resistance exercise over aerobic exercise during breast cancer treatment. In response to strenuous resistance exercise, however, muscle satellite (progenitor) cells are activated to reenter the cell cycle and proliferate. Satellite cells can then contribute their nuclear material into the fiber to facilitate muscle repair, regeneration, and hypertrophy. Cancer therapy damages rapidly dividing cells and thus has the potential to target satellite cells that enter into the cell cycle. Although satellite cells are self-renewing, they are not completely replenished over the lifespan so losses in this progenitor population via resistance exercise and cancer therapy may impair the maintenance of muscle mass with aging. Before recommending resistance training during breast cancer treatment, we must have more information about cancer treatment effects on activated satellite cells in human studies.</description><dc:title>Should resistance exercise be recommended during breast cancer treatment? - Corrected Proof</dc:title><dc:creator>Priscilla M. Clarkson, Seth A. Kaufman</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.020</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-11</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-11</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000824/abstract?rss=yes"><title>The question of ethnic variability and the Darwinian significance of physiological neonatal jaundice in East Asian populations - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000824/abstract?rss=yes</link><description>Summary: Recent work in Darwinian medicine has suggested that physiological neonatal jaundice (PNJ) might serve an adaptive function in scavenging reactive oxygen species that in later life are removed by the mature antioxidant enzyme system in the liver. This treatise examines this hypothesis in light of novel epidemiological and genetic findings which suggest that the incidence of PNJ is significantly increased in East Asian populations. Though found across all ethnic groups, it has been established that neonates of East Asian origin are at a significantly greater risk of developing PNJ, with more than one studying finding the incidence to be near double. For any Darwinian explanation of physiological neonatal jaundice to be considered in clinical circles, it is essential that the elevated incidence of PNJ in this population be explained both mechanistically and in terms of adaptation. Recent work has linked PNJ to a specific enzyme polymorphism, a variation of the UGT1A1 gene, in the glucoronidation pathway which is essential for bilirubin metabolism and is strongly correlated with ethnic origin. In this paper it is hypothesized that the elevated incidence of PNJ in East Asian populations is not random or due to a flaw in the system but rather due to an evolved mechanism. Two potential pressures which might have selected for an elevated neonatal bilirubin in East Asian populations versus other ethnic groups are a diminished ability to reduce harmful oxidant radicals due to variations the P450 liver metabolic pathway and the endemic nature of Hepatitis B in the Asia–Pacific region. This is the first work to attempt to explain PNJ through a Darwinian yet clinically relevant lens while suggesting a specific proximate mechanism that is correlated with a pre-existing evolutionary environment and can be associated with differential reproductive success.</description><dc:title>The question of ethnic variability and the Darwinian significance of physiological neonatal jaundice in East Asian populations - Corrected Proof</dc:title><dc:creator>Daniel E. Wasser, Israel Hershkovitz</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.017</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-08</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-08</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000836/abstract?rss=yes"><title>Exploring the reasons why melatonin can improve tinnitus - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000836/abstract?rss=yes</link><description>Summary: Melatonin has been proposed as a treatment for tinnitus, especially on the basis of its favourable effects on sleep and its vasoactive and antioxidant properties. However, to our knowledge no attempts of interpretation have been advanced through a detailed analysis of the various specific properties of melatonin possibly cooperating in a coincidental way to relieve tinnitus: among these, its modulatory effect on central nervous system resulting in a protective mechanism against an exaggerated sympathetic drive; its capacity to induce a more steady hemodynamic condition, through a multifactorial and multi-organ activity, resulting in a more regular labyrinthine perfusion; a possible action on the skeletal muscle tending to a reduction of the muscular tone, which could relieve tinnitus of muscular origin deriving from tensor tympani tonic contractions; its possible reported antidepressive effect, which could indirectly act on tinnitus; a direct regulation of inner ear immunity as proposed in literature when melatonin was reported to be present in the inner ear. All these observations seem to indicate melatonin as a tool deserving a greater attention than other antioxidants in the attempt of relieving tinnitus, justifying its application from a more precise rationale based on a series of physio-pathological aspects.</description><dc:title>Exploring the reasons why melatonin can improve tinnitus - Corrected Proof</dc:title><dc:creator>Antonio Pirodda, Maria Chiara Raimondi, Gian Gaetano Ferri</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.018</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-08</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-08</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987709005015/abstract?rss=yes"><title>Do 5-alpha reductase inhibitors influence the severity of brain injury in men after a stroke? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987709005015/abstract?rss=yes</link><description>Strokes are a major cause of disability in men and are associated with a higher death rate than in women. The incidence of stroke increases significantly after age 55, as does coronary heart disease and carotid atherosclerosis. Likewise, the incidence of symptomatic benign prostatic hyperplasia (BPH) increases after age 55 and is often treated with 5-alpha-reductase inhibitors.</description><dc:title>Do 5-alpha reductase inhibitors influence the severity of brain injury in men after a stroke? - Corrected Proof</dc:title><dc:creator>Paul Cohen</dc:creator><dc:identifier>10.1016/j.mehy.2009.07.010</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-04</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-04</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000666/abstract?rss=yes"><title>Self-injury in autism as an alternate sign of catatonia: Implications for electroconvulsive therapy - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000666/abstract?rss=yes</link><description>Summary: Multiple reports show the efficacious usage of ECT for catatonia in individuals with autism. There are also a few reports showing that ECT improves self-injury in people with and without autism. In this hypothesis, self-injury in autism and other developmental disorders may be an alternate sign of catatonia, and as such an indication for electroconvulsive therapy. The issue is important because self-injury occurs at an increased rate in autistic and intellectually disabled individuals, but is poorly understood and often difficult to treat with psychological and pharmacological means. Self-injury may be considered a type of stereotypy, a classic symptom of catatonia that is exquisitely responsive to electroconvulsive therapy (ECT). Historical and modern reports further support the association of self-injury, tics and catatonia. Central gamma-aminobutyric acid (GABA) dysfunction may provide an important explanatory link between autism, catatonia and self-injury. Therefore, people with autism and other developmental disorders who develop severe self-injury (with or without concomitant tics) should be assessed for catatonia, and ECT should be considered as a treatment option. Further studies of the utility of ECT as an accepted treatment for catatonia are warranted in the study of self-injury in autism.</description><dc:title>Self-injury in autism as an alternate sign of catatonia: Implications for electroconvulsive therapy - Corrected Proof</dc:title><dc:creator>Lee E. Wachtel, Dirk M. Dhossche</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.001</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-04</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-04</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000496/abstract?rss=yes"><title>Amyotrophic lateral sclerosis (Lou Gehrig’s disease) is caused by electric currents applied to or induced in the body: It is an iatrogenic disease of athletes caused by use of electrotherapy devices - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000496/abstract?rss=yes</link><description>Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease after the famous New York Yankee baseball player, is a rare condition, characterized by deterioration of both upper and lower motor neurons. It has in incidence of about 2.4 per 100,000 population per year with peak onset between 55 and 75years of age and an average survivorship of 3years after onset . Over 90% of ALS cases are sporadic, with familial cases making up the balance. An ALS variant which is clinically different from sporadic ALS is present in the Western Pacific and is associated with symptoms and pathological characteristics of both Parkinson’s disease and Alzheimer’s disease.</description><dc:title>Amyotrophic lateral sclerosis (Lou Gehrig’s disease) is caused by electric currents applied to or induced in the body: It is an iatrogenic disease of athletes caused by use of electrotherapy devices - Corrected Proof</dc:title><dc:creator>Samuel Milham</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.033</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000538/abstract?rss=yes"><title>Are the ingredients extracted from fruits and vegetables superior to fruits and vegetables in cancer prevention? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000538/abstract?rss=yes</link><description>Summary: A diet high in fruits and vegetables decreases the risk of various cancers. And recently, several ingredients extracted from fruits and vegetables are observed to have a protective effect against different cancers as well. Many of them have been allowed to enter clinical trial. Due to the fact that these ingredients possess not only a comparatively high purity and quantity, but also a potential economic value, it seems that they are superior to and could replace fresh vegetables and fruits in cancer prevention in the future. Herein, we proposed the hypothesis: the ingredients cannot take the place of fresh fruits and vegetables in cancer prevention.</description><dc:title>Are the ingredients extracted from fruits and vegetables superior to fruits and vegetables in cancer prevention? - Corrected Proof</dc:title><dc:creator>Yuhua Li, Chen Li, Yang Sun, Yinbo Niu, Li Liu, Qibing Mei</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.037</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000575/abstract?rss=yes"><title>Beads but no collar; the significance of an asymptomatic rib bone healing pattern in infants - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000575/abstract?rss=yes</link><description>Summary: When a long bone, such as a rib, is broken, the position of the break can be seen in the following weeks by a temporary collar of a collagen based material (callus) which holds the broken ends together during the repair process. However in infants a different pattern is sometimes found at autopsy, in which the repair material occurs as widely spaced “beads” along the shaft of the rib. The consistency of the bead material corresponds to the progress of repair in the normal way, but there is no focal region as would be expected in a clean break or greenstick fracture. It is proposed that this results from micro-fractures in the compact bone forming the outer aspect of the rib when it is bent excessively, during thoracic compression such as required in Cardiopulmonary Resuscitation, (CPR), or when the infant is “grabbed” when about to slip from the hands of a carer. The compact bone surface is covered by a relatively very elastic layer, the periosteum, which carries nerves sensitive to stretch or tearing of this periosteum. It is proposed that the local stretch induced in the periosteum bridging these micro-fractures is insufficient to cause these nerves to signal pain and so the condition is asymptomatic, and may be quite common in infancy. It should not be confused with imposed trauma.</description><dc:title>Beads but no collar; the significance of an asymptomatic rib bone healing pattern in infants - Corrected Proof</dc:title><dc:creator>David Talbert</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.041</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS030698771000071X/abstract?rss=yes"><title>High selenium may be a risk factor of adolescent idiopathic scoliosis - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS030698771000071X/abstract?rss=yes</link><description>Summary: The pathogenesis of adolescent idiopathic scoliosis (AIS) remains little understood. Previous work has shown that guppy fish is an ideal animal model of idiopathic scoliosis which has similar epidemiological and morphological characteristic with AIS. However, some research speculated that the high-selenium environment could also induce idiopathic-type scoliosis of fish. We believe that the high-selenium related deformity of spine and guppy curveback syndrome may have the same pathogenesis. And high selenium may be a risk factor of AIS.</description><dc:title>High selenium may be a risk factor of adolescent idiopathic scoliosis - Corrected Proof</dc:title><dc:creator>Zongde Yang, Yang Xie, Jiayu Chen, Diqing Zhang, Changwei Yang, Ming Li</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.006</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000733/abstract?rss=yes"><title>Transient ischemic attack may present a target for normobaric hyperoxia treatment - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000733/abstract?rss=yes</link><description>Abstract: According to the new revised tissue-based definition, transient ischemic attack is a transient episode of neurological dysfunction caused by a focal brain, spinal cord, or retinal ischemia without acute infarction. This review addresses the pathophysiology of transient ischemic attack and the impact of normobaric hyperoxia on the penumbral tissue. Neuroimaging in transient ischemic attack patients and advances in penumbra imaging allow the transient ischemic attack, from pathophysiological viewpoint, to be defined as an ischemic penumbra of varied duration, which could proceed to a cerebral infarction or reduce to a benign oligemia. Persisting perfusion abnormalities are observed, despite resolution of the neurological symptoms. Preclinical and clinical studies have shown that the normobaric hyperoxia treatment is associated with improvement of hemodynamic and metabolic disturbances, particularly in the penumbral tissue. Transient ischemic attack, considered an ischemic penumbra, may present an ideal target for early normobaric hyperoxia therapy, administered as soon as possible after the onset of the neurological deficit. Follow-up perfusion imaging could guide and individualize the treatment.</description><dc:title>Transient ischemic attack may present a target for normobaric hyperoxia treatment - Corrected Proof</dc:title><dc:creator>Dimiter I. Hadjiev, Petya P. Mineva</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.008</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000745/abstract?rss=yes"><title>Can time-related patterns in diagnosis for hospital admission help identify common root causes for disease expression? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000745/abstract?rss=yes</link><description>Summary: For many years medical admissions to acute hospitals have been increasing at a rate far higher than expected from demographic change. Analysis shows that the admissions tend to increase in a step-like manner at an interval of 3–6years. This study characterises the specific diagnoses associated with the step-changes and uses the resulting pattern in admissions over time to identify further diagnoses with a far lower incidence which may also conform to this pattern. All of the diagnoses located using this method have a common immune function linkage in the expression of the chronic form of the condition. It is proposed that the wider use of data mining techniques may enable association between diagnoses associated with the need for inpatient care arising from unexpected common causes.</description><dc:title>Can time-related patterns in diagnosis for hospital admission help identify common root causes for disease expression? - Corrected Proof</dc:title><dc:creator>Rodney P. Jones</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.009</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000757/abstract?rss=yes"><title>Drinking air and manoeuvering it to the pyloric region of the stomach for the treatment for Helicobacter pylori infection - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000757/abstract?rss=yes</link><description>Summary: Helicobacter pylori is a flagellate, gram-negative bacterium which lives in the pyloric region of the human stomach and is a major cause of a large proportion of peptic ulcers, some non-ulcer dyspepsias and rarely, gastric cancers. It is a microaerophilic (anaerobic) organism. In place of the several drugs currently in use for treating H. pylori infection, plain simple atmospheric air swallowed or sucked into the stomach, or drunk by any of the various techniques described here and then posturally manoeuvered to the pyloric region by inverting the trunk for a few minutes on a daily basis could be used as a preventive as well as a therapeutic measure for established H. pylori infection. Air is always present in the fundus of stomach, which is the reason why H. pylori does not colonise in the fundal region.</description><dc:title>Drinking air and manoeuvering it to the pyloric region of the stomach for the treatment for Helicobacter pylori infection - Corrected Proof</dc:title><dc:creator>P.C. Malshe</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.010</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000769/abstract?rss=yes"><title>Multifunctional Merkel cells: Their roles in electromagnetic reception, finger-print formation, Reiki, epigenetic inheritance and hair form - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000769/abstract?rss=yes</link><description>Summary: Merkel cells are located in glabrous and hairy skin and in some mucosa. They are characterized by dense-core secretory granules and cytoskeletal filaments. They are attached to neighboring keratinocytes by desmosomes and contain melanosomes similar to keratinocytes. They are excitable cells in close contact with sensory nerve endings but their function is still unclear. In this review, following roles are attributed for the first time to the Merkel cells: (1) melanosomes in Merkel cells may be involved in mammalian magnetoreception. In this model melanosome as a biological magnetite is connected by cytoskeletal filaments to mechanically gated ion channels embedded in the Merkel cell membrane. The movement of melanosome with the changing electromagnetic field may open ion channels directly producing a receptor potential that can be transmitted to brain via sensory neurons. (2) Merkel cells may be involved in finger-print formation: Merkel cells in glabrous skin are located at the base of the epidermal ridges the type of which defines the finger-print pattern. Finger-print formation starts at the 10th week of pregnancy after the arrival of Merkel cells. Keratinocyte proliferation and the buckling process observed in the basal layer of epidermis resulting in the epidermal ridges may be controlled and formed by Merkel cells. (3) Brain–Merkel cell connection is bi-directional and Merkel cells not only absorb but also radiate the electromagnetic frequencies. Hence, efferent aspects of the palmar and plantar Merkel nerve endings may form the basis of the biofield modalities such as Reiki, therapeutic touch and telekinesis. (4) Adaptive geographic variations such as skin color, craniofacial morphology and hair form result from interactions between environmental factors and epigenetic inheritance system. While environmental factors produce modifications in the body, they simultaneously induce epigenetic modifications in the oocytes and in this way adaptive changes could be passed onto the next generations. Merkel cells are multisensorial cells that can receive almost all environmental stimuli including electromagnetic and ultraviolet radiations, temperature, humidity and food type and they seem to transfer the environmental information to oocytes by affecting nuclear receptors in oocytes. (5) Hair form is categorized as straight, wavy and spiral. Merkel cells found at the bulge region of hair follicles may determine the hair form with their different paracrine secretions related to hair cycle producing variations between populations. In conclusion, Merkel cells are multifunctional cells which may close the gap between orthodox medicine and complementary medicine such as acupuncture and Reiki.</description><dc:title>Multifunctional Merkel cells: Their roles in electromagnetic reception, finger-print formation, Reiki, epigenetic inheritance and hair form - Corrected Proof</dc:title><dc:creator>M. Kemal Irmak</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.011</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000630/abstract?rss=yes"><title>Cleft lip and palate: An adverse pregnancy outcome due to undiagnosed maternal and paternal coeliac disease - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000630/abstract?rss=yes</link><description>Summary: Development of orofacial component involves a complex series of events. The main categories are isolated cleft palate and cleft lip with or without cleft palate. There have been many factors implicated in the development of the anomaly. The environmental factors which contribute and the genes which predispose to the condition remain obscure despite decades of research. Though it is generally agreed that folic acid deficiency is a contributory factor for non-syndromic cleft lip and palate, fewer concerns are directed towards the role for maternal/paternal nutrition in orofacial cleft origin. However, previously undescribed, here we consider the potential influence of maternal and paternal coeliac disease on the etiology of non-syndromic cleft lip and palate as an unfavorable pregnancy outcome. We postulated this relationship based on our observation, study and an empirical survey, and could be due either to (I) folic acid mal absorption (II) a genetically mediated genomic imprinting system.</description><dc:title>Cleft lip and palate: An adverse pregnancy outcome due to undiagnosed maternal and paternal coeliac disease - Corrected Proof</dc:title><dc:creator>Gururaj Arakeri, Veena Arali, Peter A. Brennan</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.047</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-26</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-26</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000162/abstract?rss=yes"><title>The most sensitive sign of meningeal irritation: Heel-drop jarring test for meningitis - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000162/abstract?rss=yes</link><description>Meningeal irritation by meningitis may cause abnormal contraction of various spinal extensor muscle groups. Irritation of craniocervical dura produces nuchal rigidity, and irritation of lumbosacral dura elicits Brudzinski’s or Kernig’s sign. Since dural afferents consist of A-delta and C-fibers, inflamed dura has properties of chemosensitivity and sensitization like other tissues under potentially harmful or pathological conditions . Thus, inflamed dura shows an enhanced responsiveness to mechanical stimuli that is relevant to signs of meningeal irritation. Although nuchal rigidity, Kernig’s and Brudzinski’s signs all use mechanosensitivity of inflamed dura, it is hard to judge whether or not meningitis is present because these diagnostic tools have very low sensitivity (each 30%, 5% and 5%) . So, better diagnostic methods are needed. To improve sensitivity for detecting meningeal irritation, jolt accentuation of headache was invented . This test is positive if patient’s headache worsens when he turns his head horizontally at a rate of two to three rotations per second. This useful sign of meningitis exhibits high sensitivity of 97% for cerebrospinal fluid pleocytosis .</description><dc:title>The most sensitive sign of meningeal irritation: Heel-drop jarring test for meningitis - Corrected Proof</dc:title><dc:creator>Dong-Gyun Han, Mi-Kyung Jeon, Hwa-Ja Kim</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.012</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-25</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-25</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000691/abstract?rss=yes"><title>Migraine and enuresis in children: An unusual correlation? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000691/abstract?rss=yes</link><description>Summary: Several reports in the medical literature suggest the existence of a correlation and/or comorbidity between sleep disorders and headache, linked to probably common pathophysiological substrates.Undoubtedly, migraine and primary nocturnal enuresis (PNE) are different diseases, normally diagnosed and evaluated in independent way even if it is possible to find some common points.The possible consequences of our ideas are that PNE could be considered as migraine equivalent, such as a “periodic syndrome”, and the treatment and care of migraine cannot exclude the causal role of sleep disorders.</description><dc:title>Migraine and enuresis in children: An unusual correlation? - Corrected Proof</dc:title><dc:creator>M. Carotenuto, M. Esposito, Antonio Pascotto</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.004</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-25</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-25</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000290/abstract?rss=yes"><title>Gastric tubes as vectors of Helicobacter pylori transmission - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000290/abstract?rss=yes</link><description>Abstract: Peptic ulcer was a rare disease before 1850. The prevalence of peptic ulcer increased gradually in persons born between 1870 and 1900. A similar decay in opposite direction of the prevalence occurred after the 1960–1970s. Although the pathogenesis of peptic ulcer is readily explained by the Helicobacter pylori infection, the bacterium occurred many thousands years ago and followed the migrations of human populations; consequently, its presence does not explain the increase in peptic ulcer prevalence. Gastric tubes for secretory testing were introduced from 1871 and their use was extended gradually in the then growing departments of gastroenterology, becoming a very popular, though unpleasant method. There is circumstantial evidence from the pre-H. pylori era that gastric/enteral infections could be transmitted though contaminated gastric tubes/electrodes. The author’s hypothesis is based on the temporary overlap of the increased peptic ulcer prevalence and the extensive use of gastric secretory testing. The use of contaminated gastric tubes in sick persons harbouring pathogenic strains of the bacterium could have led to the transmission of the infection by gastro-oral route to the patients’ ward-mates and on, to their family members: years later, new ulcer or dyspeptic patients may have come from such groups. The current decay in peptic ulcer prevalence could be due to the decreased use of secretory testing and implementation of rigorous disinfection rules.</description><dc:title>Gastric tubes as vectors of Helicobacter pylori transmission - Corrected Proof</dc:title><dc:creator>György Miklós Buzás</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.025</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-24</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-24</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000320/abstract?rss=yes"><title>The straight line hypothesis elaborated: Case reference obesity, an argument for acidosis, oxidative stress, and disease conglomeration? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000320/abstract?rss=yes</link><description>Summary: Studies report on the association between obesity and oxidative stress, with and without additional diseases. Macrophages in adipocytes, and hypoxia in adipose tissue have been suggested to explain how obesity can relate to oxidative stress. The straight line hypothesis using the lactic acid trap construct has been put forward to explain how proton imbalance can relate to obesity. Proton imbalance has been also reported to associate with the production of reactive oxygen species by inhibition of mitochondrial energy production. This review brings together existing literature and concepts to explain how obesity can relate to oxidative stress via protons, uniquely for itself or, as often observed, in conglomeration of additional diseases.</description><dc:title>The straight line hypothesis elaborated: Case reference obesity, an argument for acidosis, oxidative stress, and disease conglomeration? - Corrected Proof</dc:title><dc:creator>Shoma Berkemeyer</dc:creator><dc:identifier>10.1016/j.mehy.2009.12.034</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-24</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-24</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000368/abstract?rss=yes"><title>Glioblastoma and dementia may share a common cause - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000368/abstract?rss=yes</link><description>Summary: The cause of most glioblastomas is unknown. One cause might lie in the surrounding brain tissue. The interactions between glioblastoma cells and their micro- and macro-environment could create a context that promotes or suppresses tumor growth and protects or exposes the malignant cells to immune attack. Alzheimer’s disease has been identified as a protein misfolding disorder (proteopathy), caused by accumulation of abnormally folded A-beta and tau proteins in the brain. These or other changed proteins or as yet unrecognized biochemical brain changes of dementia might promote glioblastoma development. Published data indicate that there is an association between Alzheimer’s disease prevalence and malignant brain tumor incidence in 19 US states. Hypothetically, Alzheimer’s and glioblastoma may share an as yet unknown peripheral tissue pathway that can promote the progression of both diseases. If this pathway can be identified, new treatments for both conditions may follow.</description><dc:title>Glioblastoma and dementia may share a common cause - Corrected Proof</dc:title><dc:creator>Steven Lehrer</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.031</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-24</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-24</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000526/abstract?rss=yes"><title>Alcohol-induced acute pancreatitis: The ‘critical mass’ concept - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000526/abstract?rss=yes</link><description>Summary: The association of alcohol consumption and acute pancreatitis (AP) has been well documented. Extensive research in the field of alcohol-induced AP has allowed scientists to understand the different aspects by which ethanol may alter pancreatic cellular function. However, despite the recognition and understanding of these proposed mechanisms, the basic question that remains unanswered is that although alcohol is consumed the world over, why is it that only some people develop AP? Epidemiologic data indicates a higher frequency of alcohol-induced AP in geographical locations where surrogate/home-brewed alcoholic beverages are freely available. These surrogate/home-brewed alcoholic beverages contain in addition to ethanol, higher alcohols (e.g. propanol and butanol) and other by-products/contaminants (e.g. acids, aldehydes and esters), the potential of which to induce pancreatic damage has been incompletely studied. Mutations in genes that metabolise alcohol as well as those that protect the acinar cells and the extra-acinar milieu from prematurely activated digestive enzymes (e.g. genetic mutations in SPINK1 or PRSS1 genes) have also been noted in these geographical locations. Based on the available epidemiologic, clinical and basic research data available at the present time, we propose a unifying hypothesis presenting for the first time the ‘critical mass’ concept. We hypothesise that it is the achievement of a ‘critical mass’ of damaged acinar cells that is required to trigger off the inflammatory cascade leading to a clinically recognised attack of AP. The consequence of a critical mass of damaged acinar cells is the generation of sufficient mediators to result in clinical AP. While the consumption of alcohol does damage acinar cells, the number of damaged acinar cells does not necessarily reach the ‘critical mass’ with every binge. Co-factors such a high fat or protein meals are required to sensitize the acinar cells by raising the metabolic state to a high level which compromises the viability of the cells. In addition, the existence of genetic mutations and / or the consumption of surrogate alcoholic beverages, by facilitating acinar cell damage, directly or indirectly, potentially hasten the achievement of the ‘critical mass’, leading to an attack of AP.</description><dc:title>Alcohol-induced acute pancreatitis: The ‘critical mass’ concept - Corrected Proof</dc:title><dc:creator>Savio G. Barreto, Gino T.P. Saccone</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.036</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-24</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-24</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000678/abstract?rss=yes"><title>Are Duchenne muscular dystrophy patients more likely to develop carpal tunnel syndrome? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000678/abstract?rss=yes</link><description>In an interesting hypothesis, Zenian  has reported the possibility of development of the carpal tunnel syndrome during sexual intercourse when the hands are repeatedly exposed to high pressure from the weight of the upper body.</description><dc:title>Are Duchenne muscular dystrophy patients more likely to develop carpal tunnel syndrome? - Corrected Proof</dc:title><dc:creator>Devesh V. Oberoi, Bilal Ahmed</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.002</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-24</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-24</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000708/abstract?rss=yes"><title>Impairment of telomeric quadruple helix formation – A possible event involved in the carcinogenicity of aromatic amines from the thermodynamic point of view? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000708/abstract?rss=yes</link><description>Summary: Occupational exposure to aromatic amines (in particular, benzidine, 2-naphthylamine, and possibly 1-naphthylamine) has been linked to the development of bladder cancer due to the “carcinogenicity” of these compounds. However, little detailed knowledge is currently available concerning the interaction between these molecules and human DNA which might explain subsequent neoplastic transformation. Telomeres are protective DNA–protein complexes at the ends of human chromosomes which are functionally implicated in the maintenance of the chromosomal structural integrity. Telomeric DNA is composed of noncoding guanine-rich tandem sequences. Since covalent adduction of modified aromatic amines (protonated nitrenium ions) basically involves the nucleobase guanine, it appears reasonable to assume that telomeres represent the “hot spot” of the human DNA at which pertinent molecular interactions are likely to take place. Therefore, the present hypothesis focusses on thermodynamical aspects of possible molecular interactions between aromatic amines and telomeric DNA suggesting unfolding and destabilization of intramolecular telomeric quadruple helices inevitably accompanied by a loss of telomeric protective functions.</description><dc:title>Impairment of telomeric quadruple helix formation – A possible event involved in the carcinogenicity of aromatic amines from the thermodynamic point of view? - Corrected Proof</dc:title><dc:creator>Sven Gunia</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.005</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-24</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-24</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000174/abstract?rss=yes"><title>Drug-induced gingival hyperplasia and scaffolds: They may be valuable for horizontal food impaction - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000174/abstract?rss=yes</link><description>Summary: Food impaction is a severe clinical trouble that bothers most people especially middle aged and old people. It is reported that the rate of food impaction is 92.2%. The incidence of 40–59years old is 98.9%. It is a disease of high prevalence in population. It has influenced people’s social intercourse and everyday life because it may cause halitosis, gingivalitis, periodontitis, gingival abscess, alveolar bone absorption, root caries, eventually lead to severe results from teeth loose to deletion and so on. Several reasons are involved with food impaction such as gingival recession, periodontal disease, caries, age, excessive attrition, etc. Food impaction can be divided into two kinds: vertical and horizontal food impaction. At present, there are some clinical methods such as crown or dental filling for vertical one, but horizontal food impaction is still difficult to deal with. Though some methods are being adopted like making crowns and removable obstructers, the problems have never been settled effectively for the injury to teeth and inconvenience of these treatments. Here we put forward a hypothesis that periodontal tissues can regenerate much the same as normal situation by way of using drug to induce gingiva hyperplasia initiatively and implanting scaffolds. Then horizontal food impaction will be cured when the interproximal clearance is filled with periodontal tissues. It will bring the patient hope.</description><dc:title>Drug-induced gingival hyperplasia and scaffolds: They may be valuable for horizontal food impaction - Corrected Proof</dc:title><dc:creator>Huali Du, Mingying Gao, Congcong Qi, Shaochen Liu, Yinghe Lin</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.013</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000307/abstract?rss=yes"><title>Swine flu vaccine adjuvants and multiple sclerosis – Is there potential for harmful effect? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000307/abstract?rss=yes</link><description>Summary: Vaccines are generally considered a simple compound and clinicians are sometimes unaware of the possible dangers related to the new adjuvanted vaccine approach. Due to their cost effectiveness and in order to obtain stronger response with a lower antigen dose, adjuvanted vaccines are preferred during pandemics. Adjuvants are strong immunostimulants and may be harmful in some special patient groups, such as in multiple sclerosis. There is a significant need for the effort among clinicians to heighten the awareness of the potential harms. In patient groups like multiple sclerosis, it is very important to advise vaccination with non-adjuvanted vaccines. Pure vaccine (without adjuvant) must be obtained for these groups.</description><dc:title>Swine flu vaccine adjuvants and multiple sclerosis – Is there potential for harmful effect? - Corrected Proof</dc:title><dc:creator>Şerefnur Öztürk</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.026</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000332/abstract?rss=yes"><title>Atypical trigeminal neuralgia: A consequence of central sensitization? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000332/abstract?rss=yes</link><description>Summary: Trigeminal neuralgia (TN) is characterized by sudden, recurrent, usually unilateral, severe brief stabbing pains in the distribution of trigeminal nerve. Although it is widely accepted that blood vessel or tumor compression contributes to paroxysms of TN, the pathogenesis of persistent background pain in atypical TN patient is unclear. Central sensitization is pain hypersensitivity caused by central neural plasticity. It is responsible for many temporal and symptomatic features of acute and chronic pain. We hypothesize that central sensitization might account for some symptoms of atypical TN. Based on this hypothesis, we postulate that early medical intervention predicts good outcomes in TN and medicines which are effective on central sensitization may be potential agents for the treatment of atypical TN.</description><dc:title>Atypical trigeminal neuralgia: A consequence of central sensitization? - Corrected Proof</dc:title><dc:creator>Wen-han Hu, Kai Zhang, Jian-guo Zhang</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.028</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS030698771000037X/abstract?rss=yes"><title>Mona Lisa’s smile: A hypothesis based on a new principle of art neuroscience - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS030698771000037X/abstract?rss=yes</link><description>Summary: The smile on Mona Lisa’s face remains enigmatous and a topic of much discussion in art circle over the centuries. In this essay the author proposes a new principle of art neuroscience or the science of aesthetics namely ‘dynamism’ which artists often employ to impart an illusion of movement in their art works which are essentially static. This illusion is possibly generated through imaginative thinking which involves frontal cortical activation in the viewer’s brain coupled with activation of the motion area (area V5/MT) of the viewer’s visual cortex. It is suggested that this principle of dynamism is somewhat different from the previously described concept of kinetic art. The author hypothesizes that the great painter Leonardo da Vinci very intelligently painted the angles of the mouth of Mona Lisa’s face to evoke this illusion of movement (smile) to increase the aesthetic value of this great work of art.</description><dc:title>Mona Lisa’s smile: A hypothesis based on a new principle of art neuroscience - Corrected Proof</dc:title><dc:creator>Ambar Chakravarty</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.032</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000502/abstract?rss=yes"><title>A proposal to rename and classify aplastic anemia as Myeloaplastic syndrome (MAS) Type I and II - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000502/abstract?rss=yes</link><description>“Names are important chiefly from the symbolic standpoint; they project images!”Dameshek W    The term “Aplastic Anemia (AA)” is a misnomer, as generations of medical students have discovered. Firstly, it is not just anemia – all 3 lineages are affected, leading to pancytopenia . Secondly, the term suggests a single disease, rather than the end result of spectra of etiologies and pathologies leading to bone marrow aplasia.</description><dc:title>A proposal to rename and classify aplastic anemia as Myeloaplastic syndrome (MAS) Type I and II - Corrected Proof</dc:title><dc:creator>A. Venniyoor</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.034</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS030698771000054X/abstract?rss=yes"><title>Treatment-induced stress syndromes - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS030698771000054X/abstract?rss=yes</link><description>Abstract: Placebo controlled trials in disease states as currently constituted are designed to show a drug “works” when in fact it may not. Efficacy of this type may be constructed in trials that demonstrate some marginal superiority of a drug over placebo in disease states that do not take into account any potentialities of the drugs being tested to cause dependence and consequent deleterious effects on withdrawal. This paper reviews the history of the concept of physical dependence. While outlined in terms of the psychotropic drugs, it will be clear that such has been the neglect of this feature of drug actions that it must, until proven otherwise, be assumed to apply to all drugs. Filling the gap in our knowledge would require studies of new compounds in healthy volunteers. In the absence of such studies, any clinical information on therapeutic agents should point to the lack of information on this matter.</description><dc:title>Treatment-induced stress syndromes - Corrected Proof</dc:title><dc:creator>David Healy</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.038</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000551/abstract?rss=yes"><title>Autism and anorexia nervosa: Two facets of the same disease? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000551/abstract?rss=yes</link><description>Abstract: We compiled data included in the Primal Health Research Database (www.primalhealthresearch.com) to test the hypothesis that when two pathological conditions or personality traits share the same critical period for gene–environment interaction, we should expect further similarities, particularly from clinical and pathophysiological perspectives. The keywords ‘autism’ and ‘anorexia nervosa’ (but not bulimia nervosa) lead to studies suggesting that for both conditions the perinatal period is critical. We take this example to look at other possible links between these pathological entities.From a clinical perspective, several teams have independently emphasized the importance of autistic traits in anorexia nervosa. Deficits in the processing of oxytocin have been demonstrated in both cases. Autistic groups have significantly lower blood oxytocin levels than normal groups, and oxytocin levels increase with age in the normal group only. In autistic groups there is a high ratio of intermediates of oxytocin synthesis (OX-T) to the nonapeptide oxytocin (OT). On the other hand, it has been reported that the level of oxytocin in the cerebrospinal fluid of anorexic women is significantly lower than the level of oxytocin in bulimic and control subjects. Scanning data reveal similar asymmetric functions with left hemisphere preponderance in autistic spectrum disorders and anorexia. A comparative study of the mirror neurons systems is another promising avenue for research.Such an accumulation of similarities from a great diversity of perspectives suggests that anorexia nervosa might be considered a female variant of the autistic spectrum. A plausible interpretation is that prenatal exposure to male hormones might protect against the expression of this disease: girls who have a twin brother are at low risk for anorexia nervosa, compared with girls who have a twin sister, and with controls; furthermore genetic linkage analyses do not detect change on the X chromosome.From an overview of the database, the perinatal period appears to be critical for all disorders related to the capacity to love (including love of oneself), to the potential for aggression (including self-destructive behaviours), or to sociability. Is the perinatal period critical for the organisation of the oxytocin system? This is an important question at a time when we learn that the widely used synthetic oxytocin can probably diffuse across the placenta. On the other hand, where the genesis of metabolic types is concerned, it is prenatal life that appears to be critical.</description><dc:title>Autism and anorexia nervosa: Two facets of the same disease? - Corrected Proof</dc:title><dc:creator>Michel Odent</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.039</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000563/abstract?rss=yes"><title>Possible testable correlations between passive smoking and bipolar/cyclothymic disorder, depression and ADD/ADHD - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000563/abstract?rss=yes</link><description>In a previous article, mostly dedicated to organic ‘civilization diseases’, I have suggested possible connections between interferences of various kinds in the neural reward system and some typical mental disorders . Since then, I have identified some precise patterns of passive smoking which I suspect may be at the origin of certain variants of some frequent mental disorders. In principle, the corresponding statistical correlations, which I have observed in a few cases, should be easy to test on a much larger scale by researchers with access to a sufficient number of cases:</description><dc:title>Possible testable correlations between passive smoking and bipolar/cyclothymic disorder, depression and ADD/ADHD - Corrected Proof</dc:title><dc:creator>M.C. Gracia</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.040</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000587/abstract?rss=yes"><title>Pathogenesis of leukoaraiosis: Role of jugular venous reflux - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000587/abstract?rss=yes</link><description>Summary: Leukoaraiosis (LA) is a major cause of vascular dementia and disability in the elderly. Age and hypertension are the most two important risk factors. Despite its clinical significance, the etiology is so far unclear. Chronic cerebral hypoperfusion associated with vasogenic edema, microbleeding or/and endothelial dysfunction found in LA favors venous ischemia, in stead of arterial ischemia, as its pathogenesis. The involved regions in LA, periventricular and subcortical regions, are the drainage territory of deep cerebral venous system and the watershed region between the superficial and deep cerebral venous system respectively. Adding the facts that periventricular venule collagenosis, and retinal and intraparenchymal venules dilatation are related to the severity of LA, cerebral venous hypertension caused by downstream venous outflow impairment might play a major role in the pathogenesis of LA.Internal jugular vein is the main venous outflow pathway for cerebral venous drainage. The frequency of jugular venous reflux (JVR) is increased with aging. Hypertension, which has a decreased venous distensibility, might further exacerbate the sustained or long-term repetitive retrograde-transmitted cerebral venous pressure and venous outflow insufficiency caused by JVR. Clinically, JVR caused by a dural AV fistula does lead to cerebral hypoperfusion, white matter abnormalities, vasogenic edema and cognitive impairment in several published reports.JVR is suggested to play a key role in the pathogenesis of LA through a sustained or long-term repetitive retrograde-transmitted cerebral venous pressure and venous outflow insufficiency, which might lead to chronic cerebral venous hypertensions, abnormal cerebral venules structural changes, decreased cerebral blood flow, endothelial dysfunction, and vasogenic edema in cerebral white matters.</description><dc:title>Pathogenesis of leukoaraiosis: Role of jugular venous reflux - Corrected Proof</dc:title><dc:creator>Chih-Ping Chung, Han-Hwa Hu</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.042</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000599/abstract?rss=yes"><title>Spoken language can have its impact on the respiratory passage - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000599/abstract?rss=yes</link><description>Summary: Spoken language, due its chronic impact, could be looked upon as one of the factors for its role, either in prevention or causation of respiratory illnesses. There will be variations in articulatory–aerodynamics and respiratory system dynamics among the spoken languages. Geographic variation of disease patterns and uncertain etiologies of some respiratory illnesses, which occur due to insult to the mucosal barrier or the defense mechanism of the respiratory passage, may be explained by the hypothesis of unhealthy language. Habituation to a particular spoken language could mask the symptoms of phonotrauma. Other respiratory illnesses could initiate from the phonotrauma by spoken language. There exist lacunae in the research of languages. Finding out the healthy language could mean relative freedom from respiratory illnesses. Healthy spoken language could relieve the stress on vocal cords and improve the defense mechanism of the respiratory passage.</description><dc:title>Spoken language can have its impact on the respiratory passage - Corrected Proof</dc:title><dc:creator>Jyothi M.P. D’Souza, Deepak Herald D’Souza</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.043</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000605/abstract?rss=yes"><title>Evolutionary support for the hypothesis about uric acid as a neurotransmitter - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000605/abstract?rss=yes</link><description>Uric acid (urate) is generated during the metabolisms of purines. Uric acid has been demonstrated to possess radical scavenging and reducing activities . However, the physiological functions of uric acid should go beyond the antioxidant potential for this ubiquitous compound in humans . In a recent interesting paper, Bucay hypothesizes that uric acid may act as a neurotransmitter based on the findings that high levels of uric acid can prevent neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease . Here, further support is provided for this hypothesis from an evolutionary point of view.</description><dc:title>Evolutionary support for the hypothesis about uric acid as a neurotransmitter - Corrected Proof</dc:title><dc:creator>Liang Shen</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.044</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000617/abstract?rss=yes"><title>Percutaneous femoral head arthroplasty using calcium phosphate cement maybe a more feasible way to cure avascular necrosis of femoral head: Comment on “Calcium phosphate cement to prevent collapse in avascular necrosis of the femoral head” - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000617/abstract?rss=yes</link><description>In one hypotheses published recently, the author described a novel way to treat avascular necrosis of the femoral head – calcium phosphate cement combining with standard decompression of osteonecrotic femoral head lesion. As mentioned in this paper, “Calcium phosphate cement would both provide structural support and allow for bony substitution over time” . This hypotheses sheds a light on the cure of avascular necrosis of the femoral head, however, we think it may be more feasible after some steps were taken firstly.</description><dc:title>Percutaneous femoral head arthroplasty using calcium phosphate cement maybe a more feasible way to cure avascular necrosis of femoral head: Comment on “Calcium phosphate cement to prevent collapse in avascular necrosis of the femoral head” - Corrected Proof</dc:title><dc:creator>Jun Wan, Xiang-sheng Zhang</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.045</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000629/abstract?rss=yes"><title>Carpal tunnel syndrome, sexual intercourse and physical shape - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000629/abstract?rss=yes</link><description>Recently, this journal has published a very interesting article  suggesting that many cases of bilateral carpal tunnel syndrome might result from postures and movements necessary to perform sexual intercourse. In my opinion, the evidence presented in this paper is rather convincing, and I would want only to add that, according to my research, whatever posture or movement occurring simultaneously with an intense pleasure must be considered to have ‘special health status’ and carefully watched for possible health problems. The reason is that, according to my research, during intense pleasure, tissue damages of whatever kind may not elicit the appropriate pain sensations, because this pain is compensated by the pleasure. In other words, the brain ‘thinks’ that this pain is necessary to obtain the pleasure. Hence my observations and recommendations:</description><dc:title>Carpal tunnel syndrome, sexual intercourse and physical shape - Corrected Proof</dc:title><dc:creator>M.C. Gracia</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.046</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000642/abstract?rss=yes"><title>Did viral disease of humans wipe out the Neandertals? - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000642/abstract?rss=yes</link><description>Summary: Neandertals were an anatomically distinct hominoid species inhabiting a vast geographical area ranging from Portugal to western Siberia and from northern Europe to the Middle East. The species became extinct 28,000years ago, coinciding with the arrival of anatomically modern humans (AMHs) in Europe 40,000years ago. There has been considerable debate surrounding the main causes of the extinction of Neandertals. After at least 200,000years of successful adaption to the climate, flora and fauna of Eurasia, it is not clear why they suddenly failed to survive. For many years, climate change or competition with anatomically modern human (AMH) have been the leading hypotheses. Recently these hypotheses have somewhat fallen out of favour due to the recognition that Neandertals were a highly developed species with complex social structure, culture and technical skills.Were AMHs lucky and survived some catastrophe that eradicated the Neandertals? It seems unlikely that this is the case considering the close timing of the arrival of AMHs and the disappearance of Neandertals. Perhaps the arrival of AMHs also brought additional new non-human microscopic inhabitants to the regions where Neandertals lived and these new inhabitants contributed to the disappearance of the species.We introduce a medical hypothesis that complements other recent explanations for the extinction of Neandertals. After the ancestors of Neandertals left Africa, their immune system adapted gradually to the pathogens in their new Eurasian environment. In contrast, AMHs continued to co-evolve with east African pathogens. More than 200,000years later, AMHs carried pathogens that would have been alien to pre-historic Europe. First contact between long separated populations can be devastating. Recent European and American history provides evidence for similar events, where introduction of viral, protozoan or bacterial pathogens to immunologically naïve populations lead to mass mortality and local population extinction. We propose that a virus, possibly from the family Herpesviridae, contributed to Neandertal extinction.</description><dc:title>Did viral disease of humans wipe out the Neandertals? - Corrected Proof</dc:title><dc:creator>Horst Wolff, Alex D. Greenwood</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.048</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000654/abstract?rss=yes"><title>There’s something about passive movement… - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000654/abstract?rss=yes</link><description>Summary: The recognised (funded) stand-alone clinical status for therapeutic methods of passive movement has become increasingly threatened in recent times as the preference for active treatment (specific exercise) gains hold. This is in part due to the equivocal results for clinical trials of passive movement, queries regarding its cost-benefit and negative findings for many of the fundamental claims and recommendations of its clinical process. Linked to these issues has been the profession’s difficulty in demonstrating plausible science-based mechanisms for anything more than transient effects. The present proposal is that the manual application of graduated oscillatory tensile loading to healing (or unhealed) soft tissues in the form of passive movement could facilitate optimal repair and tissue integrity (and so protection against subsequent ‘stress’). The mechanism depends on the intrinsic ability for non-excitable connective tissue cells to ‘sense’ mechanical stimuli and to transduce mechanical into chemical signals. This leads to gene transcription and subsequent adaptive remodelling of the extracellular matrix (ECM). An outline of these events is given, emphasising their dependence on the effective interplay between internally (cellular) and externally (matrix) generated mechanical forces. In principle, it ought to be possible to investigate the proposal and other clinical passive movement issues using modern soft tissue imaging and biological techniques with suitable human subjects and animal models.</description><dc:title>There’s something about passive movement… - Corrected Proof</dc:title><dc:creator>Max Zusman</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.049</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS030698771000068X/abstract?rss=yes"><title>Waist circumference as an indicator of adiposity and the relevance of body height - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS030698771000068X/abstract?rss=yes</link><description>Summary: Waist circumference (WC) is an obvious indicator of adiposity, but there is a confusing diversity of approaches to its quantitative use. Because taller people of any given relative fat content tend to have bigger WCs, indices of adiposity commonly take the form WC/heightq, where q is 1 or less. Sometimes the influence of height is regarded as insignificant, so that q is taken as zero. More attention has been given to such indices than to establishing how to use them for predicting adiposity. The usual approach has been empirical and statistical, but many published findings can be integrated using a more analytical approach. This leads to several hypotheses that are supported by published evidence, but which remain to be fully tested. Testing mainly requires data sets of the kind that have already been used for related purposes. The main hypotheses are as follow. For adults, the preferred index is WC/height0.5, while for adolescents and children it is WC/height. However, to obtain equations for the prediction of percentage body fat, the latter should be regressed on the reciprocals of the squares of these indices, namely 1/(WC2/height) and 1/(WC/height)2 respectively. These expressions decrease with increasing percentage body fat, but should do so in a linear manner. Two other hypotheses are that the non-fat content of the abdomen tends to increase with percentage body fat and that the ratio WC2/height is approximately proportional to the body mass index. The analysis is based mainly on the following ideas: firstly, that the area of fat or adipose tissue in a transverse computed tomogram of the abdomen equals the total area less the fat-free area, the former being the main determinant of WC and the latter being partly determined by fat-free body size as represented by height; secondly, that guidance can be usefully be sought in simple, dimensionally-correct models of body form, but that parameters in the resulting equations may become attenuated by the necessary use of regression analysis or the maximizing of correlations. There may be a better measure of fat-free body size with which to replace height in these indices, but the waist-to-hip ratio is unhelpful. It is hoped that this analysis can be usefully extended to the problem of estimating intra-abdominal (visceral) fat from waist circumference.</description><dc:title>Waist circumference as an indicator of adiposity and the relevance of body height - Corrected Proof</dc:title><dc:creator>R.F. Burton</dc:creator><dc:identifier>10.1016/j.mehy.2010.02.003</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000289/abstract?rss=yes"><title>The origin of pre-eclampsia: From decidual “hyperoxia” to late hypoxia - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000289/abstract?rss=yes</link><description>Summary: Normal gestation implants on a relatively hypoxic deciduas so that trophoblast deeply invades endometrium and angiogenesis seeks for oxygen supply. If implantation occurs before those hypoxic conditions occur, trophoblast invasion is defective, due to the relatively high oxygen tension in the decidual environment, laying the foundations for subsequent pre-eclampsia.</description><dc:title>The origin of pre-eclampsia: From decidual “hyperoxia” to late hypoxia - Corrected Proof</dc:title><dc:creator>Andrea L. Tranquilli, Beatrice Landi</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.024</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-19</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-19</prism:publicationDate></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000356/abstract?rss=yes"><title>Frailty and resilience from physics to medicine - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000356/abstract?rss=yes</link><description>Medicine makes use of an extremely ample and flexible range of terms, reshaping existing concepts and deriving others from scientific and popular sectors. The well known and widely used term “stress” is a good example and, more recently, other terms deriving from physics are becoming more and more employed in biomedicine and in medical humanities. Frailty and resilience are two of them.</description><dc:title>Frailty and resilience from physics to medicine - Corrected Proof</dc:title><dc:creator>Andrea A. Conti, Antonio Conti</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.030</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-18</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-18</prism:publicationDate><prism:section>CORRESPONDENCE</prism:section></item><item rdf:about="http://www.medical-hypotheses.com/article/PIIS0306987710000277/abstract?rss=yes"><title>Immigration, mental health and suicidal behavior - Corrected Proof</title><link>http://www.medical-hypotheses.com/article/PIIS0306987710000277/abstract?rss=yes</link><description>The term “immigration” is usually used to denote international immigration. The United Nations considers a long term international migrant to be “A person who moves to a country other than that of his or her usual residence for a period of at least a year (12months), so that the country of destination effectively becomes his or her new country of usual residence. From the perspective … of the country of arrival the person will be a long-term immigrant” . The International Organization for Migration has reported that there are more than 200 million immigrants around the world today .</description><dc:title>Immigration, mental health and suicidal behavior - Corrected Proof</dc:title><dc:creator>Leo Sher</dc:creator><dc:identifier>10.1016/j.mehy.2010.01.023</dc:identifier><dc:source>Medical Hypotheses (2010)</dc:source><dc:date>2010-02-17</dc:date><prism:publicationName>Medical Hypotheses</prism:publicationName><prism:publicationDate>2010-02-17</prism:publicationDate><prism:section>EDITORIAL</prism:section></item></rdf:RDF>