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Medical council of India has made remarkable modifications in the curriculum of medical students after a long period of more than 20 years with regulations on Graduate Medical Education 1997. Innovative and interactive teaching methods have taken center place in the implementation of the new curriculum nationwide. Small group teaching and problem-assisted learning have brought a paradigm shift in biochemistry teaching, which was earlier teacher cantered and was taught by only didactic lectures due to which biochemistry was considered a boring and dry subject. The present interventional study was conducted in the Department of Biochemistry, Vardhman Mahavir Medical College and Safdarjung Hospital, Delhi. All the students of MBBS first professional Batch 2018-2019 were enrolled in the present study. After sensitizing the faculty and students regarding jigsaw method of learning, it was undertaken in two different batches on 4 different days, with faculty and senior residents acting as facilitators. The groups were named according to rainbow colors. The topics were taught by power point presentation before the conduction of jigsaw activity that was discussed in form of seven clinical cases. Post jigsaw, a prevalidated feedback questionnaire was filled by the students. The faculty and senior residents gave a constructive feedback via focused group discussion. In our study 100% students opined that teaching and being taught by peers was beneficial in enhancing the in depth knowledge of the topic. Ninety-two percent students opined jigsaw learning helpful in promoting self-directed learning in the student, whereas 88.5% students felt that this teaching learning tool to be made a the regular part of the curriculum. Jigsaw groups create many opportunities for creative interchange of ideas and lively and meaningful participations. But due to limitation of time and logistics, it can be used in conjunction with routine methods of learning., (© 2020 International Union of Biochemistry and Molecular Biology.)

Young children are often hyperreactive to somatosensory inputs hardly noticed by adults, as exemplified by irritation to seams or labels in clothing. The neurodevelopmental mechanisms underlying changes in sensory reactivity are not well understood. Based on the idea that neurodevelopmental changes in somatosensory processing and/or changes in sensory adaptation might underlie developmental differences in somatosensory reactivity, high-density electroencephalography was used to examine how the nervous system responds and adapts to repeated vibrotactile stimulation over childhood. Participants aged 6-18 yr old were presented with 50-ms vibrotactile stimuli to the right wrist over the median nerve at 5 blocked interstimulus intervals (ranging from ∼7 to ∼1 stimulus per second). Somatosensory evoked potentials (SEPs) revealed three major phases of activation within the first 200 ms, with scalp topographies suggestive of neural generators in contralateral somatosensory cortex. Although overall SEPs were highly similar for younger, middle, and older age groups (6.1-9.8, 10.0-12.9, and 13.0-17.8 yr old), there were significant age-related amplitude differences in initial and later phases of the SEP. In contrast, robust adaptation effects for fast vs. slow presentation rates were observed that did not differ as a function of age. A greater amplitude response in the later portion of the SEP was observed for the youngest group and may be related to developmental changes in responsivity to somatosensory stimuli. These data suggest the protracted development of the somatosensory system over childhood, whereas adaptation, as assayed in this study, is largely in place by ∼7 yr of age., (Copyright © 2016 the American Physiological Society.)

Background: The genetics of autism spectrum disorder (hereafter referred to as "autism") are rapidly unfolding, with a significant increase in the identification of genes implicated in the disorder. Many of these genes are part of a complex landscape of genetic variants that are thought to act together to cause the behavioral phenotype associated with autism. One of the few single-locus causes of autism involves a mutation in the SH3 and multiple ankyrin repeat domains 3 (SHANK3) gene. Previous electrophysiological studies in mice with Shank3 mutations demonstrated impairment in synaptic long-term potentiation, suggesting a potential disruption at the synapse., Methods: To understand how variants in SHANK3 would lead to such impairments and manifest in the brain of patients with autism, we assessed the presence of synaptic pathology in Shank3-deficient mice at 5 weeks and 3 months of age, focusing on the stratum radiatum of the CA1 field. This study analyzed both Shank3 heterozygous and homozygous mice using an electron microscopy approach to determine whether there is a morphological correlate to the synaptic functional impairment., Results: As both synaptic strength and plasticity are affected in Shank3-deficient mice, we hypothesized that there would be a reduction in synapse density, postsynaptic density length, and perforated synapse density. No differences were found in most parameters assessed. However, Shank3 heterozygotes had significantly higher numbers of perforated synapses at 5 weeks compared to 3 months of age and significantly higher numbers of perforated synapses compared to 5-week-old wildtype and Shank3 homozygous mice., Conclusions: Although this finding represents preliminary evidence for ultrastructural alterations, it suggests that while major structural changes seem to be compensated for in Shank3-deficient mice, more subtle morphological alterations, affecting synaptic structure, may take place in an age-dependent manner.

The anterior cingulate cortex, which is involved in cognitive and affective functioning, is important in investigating disorders in which individuals exhibit impairments in higher-order functions. In this study, we examined the anterior midcingulate cortex (aMCC) at the cellular level in patients with autism and in controls. We focused our analysis on layer V of the aMCC because it contains von Economo neurons, specialized cells thought to be involved in emotional expression and focused attention. Using a stereologic approach, we determined whether there were neuropathologic changes in von Economo neuron number, pyramidal neuron number, or pyramidal neuron size between diagnostic groups. When the groups were subdivided into young children and adolescents, pyramidal neuron and von Economo neuron numbers positively correlated with autism severity in young children, as measured by the Autism Diagnostic Interview-Revised. Young children with autism also had significantly smaller pyramidal neurons than their matched controls. Because the aMCC is involved in decision-making during uncertain situations, decreased pyramidal neuron size may reflect a potential reduction in the functional connectivity of the aMCC.

Background: While most neuropathologic studies focus on regions involved in behavioral abnormalities in autism, it is also important to identify whether areas that appear functionally normal are devoid of pathologic alterations. In this study we analyzed the posteroinferior occipitotemporal gyrus, an extrastriate area not considered to be affected in autism. This area borders the fusiform gyrus, which is known to exhibit functional and cellular abnormalities in autism., Findings: No studies have implicated posteroinferior occipitotemporal gyrus dysfunction in autism, leading us to hypothesize that neuropathology would not occur in this area. We indeed observed no significant differences in pyramidal neuron number or size in layers III, V, and VI in seven pairs of autism and controls., Conclusions: These findings are consistent with the hypothesis that neuropathology is unique to areas involved in stereotypies and social and emotional behaviors, and support the specificity of the localization of pathology in the fusiform gyrus.

Introduction: There is now a consensus that atherosclerosis represents a state of heightened oxidative stress which is characterized by lipid and protein oxidation in the vascular wall. Inspite of many efforts which were made to explain the role of oxidative stress in progression of CAD (Coronary Artery Disease), its predictive role is still not clear. In order to fill these lacunae and to establish the utility of antioxidant vitamins in delaying the progression of CAD from stable angina (SA) towards myocardial Infarction (MI), the present study was conducted., Materials and Methods: In this study, we compared the lipid profile and oxidant antioxidant status in 50 patients of CAD and 50 controls. The 50 patients of CAD were further grouped into those with SA, unstable angina (USA) and MI and the values of blood reduced glutathione (GSH) and lipid peroxidation marker Malonyldialdehyde (MDA) were studied and compared in these three subgroups of CAD., Results: The values of MDA were significantly increased in patients of CAD as compared to those in controls. Plasma MDA values of patients who presented with unstable angina and acute MI were significantly higher than those in patients who presented with SA and in controls, whereas there was no significant difference between values in those with unstable angina and non Q wave MI. The values of GSH showed a significant depletion in patients of CAD as compared to those in controls. A clearly significant depletion in GSH levels was observed in SA patients as compared to those in unstable angina and MI. But no such variations were observed between unstable angina and MI patients., Conclusion: From the present study, it was concluded that there was a significant negative correlation between blood glutathione and serum MDA. This may have occurred due to utilization of GSH in quenching free radicals and still persisting oxidative stress, which may have caused an increase in MDA levels due to increased lipid peroxidation. Further, the enhanced depletion of GSH and the increase in the levels of MDA in patients of USA and MI as compared to those in SA patients confirms the role of oxidative stress in progression of CAD from SA through USA to MI.

Von Economo neurons (VENs) are projection neurons located in layer V of the anterior cingulate and frontoinsular cortex that are increasingly attracting the interest of the scientific community as many studies point to their involvement in neuropsychiatric conditions. In this review we provide a critical appraisal of both historic and recent literature on VENs that highlights the importance of clinicopathological studies in areas of research where animal models are not available. Current data suggest that VENs represent a specialized neuronal type with a characteristic morphology that evolved only in a restricted number of species most likely from a population of pyramidal neurons present in ancestral mammals in the context of specific adaptive pressures. VENs, which evolved among primates only in the hominoid lineage, are particularly vulnerable in neuropsychiatric conditions characterized by deficits in social skills and emotional function. Moreover, recent evidence on the neurochemical profile, morphologic features, and laminar and regional distribution of VENs suggests that this intriguing neuronal population could be critically involved in autonomic regulation., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Autism is a neurodevelopmental disorder characterized by deficits in social interaction and social communication, as well as by the presence of repetitive and stereotyped behaviors and interests. Brodmann areas 44 and 45 in the inferior frontal cortex, which are involved in language processing, imitation function, and sociality processing networks, have been implicated in this complex disorder. Using a stereologic approach, this study aims to explore the presence of neuropathological differences in areas 44 and 45 in patients with autism compared to age- and hemisphere-matched controls. Based on previous evidence in the fusiform gyrus, we expected to find a decrease in the number and size of pyramidal neurons as well as an increase in volume of layers III, V, and VI in patients with autism. We observed significantly smaller pyramidal neurons in patients with autism compared to controls, although there was no difference in pyramidal neuron numbers or layer volumes. The reduced pyramidal neuron size suggests that a certain degree of dysfunction of areas 44 and 45 plays a role in the pathology of autism. Our results also support previous studies that have shown specific cellular neuropathology in autism with regionally specific reduction in neuron size, and provide further evidence for the possible involvement of the mirror neuron system, as well as impairment of neuronal networks relevant to communication and social behaviors, in this disorder.

The presence of von Economo neurons (VENs) in the frontoinsular cortex (FI) has been linked to a possible role in the integration of bodily feelings, emotional regulation, and goal-directed behaviors. They have also been implicated in fast intuitive evaluation of complex social situations. Several studies reported a decreased number of VENs in neuropsychiatric diseases in which the "embodied" dimension of social cognition is markedly affected. Neuropathological analyses of VENs in patients with autism are few and did not report alterations in VEN numbers. In this study we re-evaluated the possible presence of changes in VEN numbers and their relationship with the diagnosis of autism. Using a stereologic approach we quantified VENs and pyramidal neurons in layer V of FI in postmortem brains of four young patients with autism and three comparably aged controls. We also investigated possible autism-related differences in FI layer V volume. Patients with autism consistently had a significantly higher ratio of VENs to pyramidal neurons (p=0.020) than control subjects. This result may reflect the presence of neuronal overgrowth in young patients with autism and may also be related to alterations in migration, cortical lamination, and apoptosis. Higher numbers of VENs in the FI of patients with autism may also underlie a heightened interoception, described in some clinical observations., (Copyright © 2010 Elsevier B.V. All rights reserved.)

We directly prepared insoluble silk films by blending with glycerol and avoiding the use of organic solvents. The ability to blend a plasticizer like glycerol with a hydrophobic protein like silk and achieve stable material systems above a critical threshold of glycerol is an important new finding with importance for green chemistry approaches to new and more flexible silk-based biomaterials. The aqueous solubility, biocompatibility, and well-documented use of glycerol as a plasticizer with other biopolymers prompted its inclusion in silk fibroin solutions to assess impact on silk film behavior. Processing was performed in water rather than organic solvents to enhance the potential biocompatibility of these biomaterials. The films exhibited modified morphologies that could be controlled on the basis of the blend composition and also exhibited altered mechanical properties, such as improved elongation at break, when compared with pure silk fibroin films. Mechanistically, glycerol appears to replace water in silk fibroin chain hydration, resulting in the initial stabilization of helical structures in the films, as opposed to random coil or beta-sheet structures. The use of glycerol in combination with silk fibroin in materials processing expands the functional features attainable with this fibrous protein, and in particular, in the formation of more flexible films with potential utility in a range of biomaterial and device applications.

Material systems are needed that promote stabilization of entrained molecules, such as enzymes or therapeutic proteins, without destroying their activity. We demonstrate that the unique structure of silk fibroin protein, when assembled into the solid state, establishes an environment that is conducive to the stabilization of entrained proteins. Enzymes (glucose oxidase, lipase, and horseradish peroxidase) entrapped in these films over 10 months retained significant activity, even when stored at 37 degrees C, and in the case of glucose oxidase did not lose any activity. Further, the mode of processing of the silk protein into the films could be correlated to the stability of the enzymes. The relationship between processing and stability offers a large suite of conditions within which to optimize such stabilization processes. Overall, the techniques reported here result in materials that stabilize enzymes to an extent, without the need for cryoprotectants, emulsifiers, covalent immobilization, or other treatments. Further, these systems are amenable to optical applications and characterization, environmental distribution without refrigeration, are ingestible, and offer potential use in vivo, because silk materials are biocompatible and FDA approved, degradable with proteases, and currently used in biomedical devices.