Autistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum. We propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions.

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Psychosis and autism as diametrical disorders of the social brain

This is a very good book and a very important one. The list of authors (107) reads like the ‘Who’s Who’ of spinal cord medicine. The volume is much more than an update of previous volumes of the ‘Handbook’, which also dealt with this topic and were published in 1976 and 1992. New developments have produced important and exciting changes that have altered the subject almost beyond recognition. This statement is true as regards the clinical achievments including diagnosis, prognosis and rehabilitation, but not quite so accurate as regards pre-clinical research. The 38 chapters form five sections. The first section, on development and anatomical perspectives, deals with the growth and maturation of the spinal cord. A good overview of the embryology, both cellular and molecular, is followed by a description of maldevelopment and the implications of molecular and genetic defects. The anatomy and biomechanisms are dealt with in terms of fundamental principles applied to the spinal column and spinal cord, and lead on to spinal cord injury. This is a good base for the following chapters that form the second section and which deal with the diagnosis, prognosis and monitoring of spinal cord trauma. Hopefully, in the future, there will be clinical trials of therapeutic interventions (but more of that later), and this will require accurate and quantitative measurement. The standard and recognized method is the ASIA scale, but this has limitations, and the best potential lies with neurophysiology and with advanced high-resolution neuroimaging techniques.This is dealt with in two excellent and comprehensive chapters. The majority of spinal cord injury outcome measures are understandably related to the younger population. However, the increasingly ageing population in most countries has to be addressed. This is a problem in the entire field of medicine. Specifically, in spinal cord injury, the average age of injury has increased and is still increasing. A short but notable chapter deals with the pathophysiology of the ageing nervous system, the aetiology and clinical presentation, complications and mortality and outcome. The third section deals with acute spinal cord injury: medical and surgical treatment, management and rehabilitation. These are useful straightforward reviews but are also good accounts of exciting developments. It is pointed out, and it cannot be over-emphasized, that spinal cord injury, although interrupting motor and sensory long tracts, still leaves neuronal networks intact below the site of the lesion. This is potentially a much more fruitful area of study than the conventional, and so far fruitless, pursuit of axonal repair. Chapter 20, on the changing field of rehabilitation, gives a brief account of how neural activity has a role in central nervous system (CNS) development and plasticity, but this important subject could have been improved to a great extent. A chapter on spinal cord stimulation (SCS) should have given more prominence to Cook, who, in the early 1970s, was the first to demonstrate improvement in neurological deficit with SCS. He was carrying out this procedure for pain on a young sufferer with multiple sclerosis when to his great surprise he saw a marked improvement in spasticity with consequent improvement in ambulation. The speed of change suggested that this was almost certainly due to an increase in inhibition. Cook took his observations to the neurologists in his hospital and later to the neurological societies in New York. They refused to even investigate this. Subsequent studies (elsewhere) demonstrated recordable and reproducible neurophysiologcal changes at spinal and brain-stem levels and eventually led to the formation of the International Neuromodulation Society. What Cook had observed was no more than that reported by Frohlich and Sherrington in 1902: after decerebration in cat, dog and Macaque, stimulation of the lower thoracic and lumbar region of the spinal cord showed ‘..an effect...constant and regular...evoked marked inhibition of the rigidity..’. Cook deserves much greater recognition. Section 4 is concerned with chronic-stage rehabilitation, and overlaps with the previous section. In fact, it is difficult to see why the two sections were separated. ‘Rehabilitation strategies that optimize spontaneous repair and promote neurological recovery are becoming mainstream’. Is this perhaps rather optimistic? ‘Spontaneous repair’ and ‘neurological recovery’ risks undue raising of hopes. This is based on a single case report about 11 years ago. Nevertheless, this is an interesting section that, in this chapter, deals with the effect of activity including electrical stimulation on synapses. Although the field is not exactly comprehensively covered, a good trenchant point is made: that conventional rehabilitation of spinal cord disease ignores the beneficial effects of afferent feedback and stimulation, which is aninteresting and potentially exciting concept that brings into focus the undamaged, but altered, central nervous system. The final section, section 5, deals with preclinical research ‘bridging the gap between bench and bedside.’ This is the longest section in 15 chapters and approximately one-third of the total volume.The first chapter in this section sets out the goals for therapy, discusses protocols and gives an algorithm for discovery through to clinical use. The authors point out that no clinical trial so far has been shown to be effective (reviewer’s emphasis). An outstanding and thoughtful chapter follows, again emphasizing the improvement in animals and man with appropriate afferent input, and discusses the challenges to be met. However, there is some inconsistency among the contributors, which, though understandable, is somewhat confusing. Chapter 25 states that ‘basic research in spinal cord repair is promising’. A more realistic description might state the opposite. Further chapters point out that there are no satisfactory solutions. Indeed, chapter 33 begins with ‘so far, there is no clinical procedure for inducing severed nerve fibres to regenerate’. Further on, the authors state that ‘the grandfather of the transplantation strategies was espoused by Santiago Ramon y Cajal in the 19th century’. Spinal Cord (2013) 51, 797–799 & 2013 International Spinal Cord Society All rights reserved 1362-4393/13

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Handbook of clinical neurology

Laterality: Functional Asymmetry in the Intact Brain.

The authors of this text are both plastic surgeons. Dr Dellon has studied sensory nerves extensively, sensibility testing and sensory reeducation in particular. Dr Mackinnon has had a long-term interest in nerve physiology as it relates to surgery on peripheral nerves and, particularly, grafting with autografts and allografts. Both authors are international authorities in their fields, and they also have a large experience with various peripheral nerve problems that are treated surgically. In order to be logical, comprehensive, and nonrepetitious, the authors have chosen to write this text themselves, and this appears to be a very good decision. The focus of this text is the surgery of peripheral nerve disorders, with which the authors have extensive, either clinical or research, experience. They have chosen a strict organization of the contents that starts with a macroscopic, microscopic, and ultrastructural description of the anatomy of peripheral nerves. The physiology of peripheral nerves

Surgery of the Peripheral Nerve

Mammalian spermatogenesis is a complex biological process occurring in the seminiferous tubules in the testis. This process represents a delicate balance between cell proliferation, differentiation, and apoptosis. In most mammals, the testicles are kept in the scrotum 2 to 7°C below body core temperature, and the spermatogenic process proceeds with a blood and oxygen supply that is fairly independent of changes in other vascular beds in the body. Despite this apparently well-controlled local environment, pathologies such as varicocele or testicular torsion and environmental exposure to low oxygen (hypoxia) can result in changes in blood flow, nutrients, and oxygen supply along with an increased local temperature that may induce adverse effects on Leydig cell function and spermatogenesis. These conditions may lead to male subfertility or infertility. Our literature analyses and our own results suggest that conditions such as germ cell apoptosis and DNA damage are common features in hypoxia and varicocele and testicular torsion. Furthermore, oxidative damage seems to be present in these conditions during the initiation stages of germ cell damage and apoptosis. Other mechanisms like membrane-bound metalloproteinases and phospholipase A2 activation could also be part of the pathophysiological consequences of testicular hypoxia.

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The hypoxic testicle: physiology and pathophysiology.

We report the case of 44-year-old woman with a left-sided Bochdalek hernia (BH) with concomitant partial situs inversus The patient was presented from the outpatient clinic with lower chest discomfort She had suffered from abdominal pain for one year, with no history of trauma, previous surgery, or extreme physical exertion Chest radiograph revealed a large left-sided BH The patient underwent thoracotomy Intestinal organs, containing bowel, small intestine, caecum, and appendix were seen in the left hemithorax Because of the failure to reduce the intestinal organs into the peritoneal cavity, laparotomy was performed The right side of the abdominal cavity was empty In conclusion, partial situs inversus was diagnosed The diaphragmatic defect was repaired with non-absorbable sutures via laparotomy, and with a prolene mesh via thoracotomy Bochdalek hernia with partial situs inversus is a rare clinical entity with none reported in medical literature

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Bochdalek hernia with concomitant partial situs inversus in an adult.

/pdf/inmunoexpresion-del-factor-de-crecimiento-endotelial-1hrhidh3f7.pdf

Inmunoexpresión del Factor de Crecimiento Endotelial Vascular, Linfoma de Células β 2 y Grupo de Diferenciación 68 en Tejido Cerebeloso de Ratas Tratadas con Ganoderma lucidum

Comparison of the clinical efficacy of two different types of post systems which were restored with composite restorations

SUMMARY: We aimed to investigate the potential harmful effects of maternal valproic acid (VPA) on fetal sciatic nerve, and the protective effects of vitamin E (Vit E) and folic acid (FA) on fetal rats. Valproic acid (400mg/kg), folic acid (400mg/kg) and vitamin E (250 mg/kg) were administered to rats on each of gestation days 8-10. All fetuses were collected on gestation day 20. With thin sections of biopsies, sciatic nerve of fetuses were stained with uranyl acetat and were examined under transmission electron microscope. The fetuses (n:36) were divided into five groups: control, vpa, vpa+fa, vpa+vit e and vpa+fa+vit e groups. In each group; drug procedure, surgical procedure and histological methods were performed. Later, weights and lengths of fetuses in each group were compared and analyzed by One-Way Anova test. Administration of single doses of valproic acid (400 mg/kg) resulted in weight and length loss between control and vpa group. However, length and weight differences between the other groups were not significant. The histopathological findings of control group was normal. In vpa group, it showed extensive degenerative changes especially in myelin coat. In addition, most prominent finding in this group was condensation of collagen fibers in extensively demyelinated samples, while moderately effected areas were relatively nor- mal. Both vpa+fa and vpa+ vit e groups exhibited similar ultrastructural changes, reflecting minimal to moderate degenerative changes. In vpa+fa+vit e group had almost the normal structure. Administration of single doses of valproic acid (400 mg/kg) resulted in a deteriorative effect on sciatic nerve at ultrastructural level. Administration of FA and Vit E had a protective effect to prevent the degenerative changes to a certain degree. Combination of FA and Vit E together following VPA administration had a more potent protective effect. The objective of the present study is to analyze histopathologic changes which may occur in a high risk experimental model after the administration of valproic acid. In addition, protective roles of the administration of folic acid and vitamin E are assessed.

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The Effects of Valproic Acid on Sciatic Nerve of Fetal Rats and Protective Effects of Folic Acid and Vitamin E Efectos del Ácido Valproico sobre el Nervio Ciático de Fetos de Ratas y Efectos de Protección del Ácido Fólico y Vitamina E

The aim of this study was to determine the effects of recombinant human interleukin-4 (rhIL-4) on hypoxia-induced lung injury in immature rats. The study was performed on 1-day-old Sprague Dawley rat pups. Group 1 (n = 7) served as nonhypoxic controls. Group 2 (untreated, n = 7) rats were subjected to hypoxia-reoxygenation (H/O) and were then returned to their mothers. Group 3 (rhIL-4 treated, n = 7) rats were subjected to H/O, were returned to their mothers, and were treated with rhIL-4 (75 microg/kg subcutaneously) for the next 3 days. All animals were killed on day 4 and lung specimens were obtained to determine the tissue level of malondialdehyde (MDA) and histological changes. In the untreated group, MDA levels were significantly increased compared to control and rhIL-4 groups. In the rhIL-4 treated group, MDA levels were not significantly different compared to control group. The rhIL-4 treated group had a significantly lower score of pathological lesions and alveolar hemorrhage grade values than the untreated group. The untreated animals had areas marked intraalveolar hemorrhage, capillary congestion, interstitial edema, and hypercellularity of lung that were not seen in the rhIL-4 treated rats. In conclusion, this study found beneficial effects of rhIL-4 in an experimental model on the hypoxia-induced lung injury.

Mehmet Cudi Tuncer

Papers

Bochdalek hernia with concomitant partial situs inversus in an adult.

Inmunoexpresión del Factor de Crecimiento Endotelial Vascular, Linfoma de Células β 2 y Grupo de Diferenciación 68 en Tejido Cerebeloso de Ratas Tratadas con Ganoderma lucidum

Comparison of the clinical efficacy of two different types of post systems which were restored with composite restorations

The Effects of Valproic Acid on Sciatic Nerve of Fetal Rats and Protective Effects of Folic Acid and Vitamin E Efectos del Ácido Valproico sobre el Nervio Ciático de Fetos de Ratas y Efectos de Protección del Ácido Fólico y Vitamina E

The effects of exogenous interleukin-4 on hypoxia-induced lung injury