Irreversible Brain Damage Research Articles

Hyperhomocysteinemia And Pathogenetic Mechanisms Of Ischemic Stroke

The article is intended to give basic information and the role of homocysteine in the human body. The amino acid homocysteine is a product of methionine demethylation. When the level of homocysteine increases, it damages the tissue structures of the arteries, initiating the release of cytokines, cyclins and other inflammatory mediators. Its accumulation leads to loosening of the arterial walls, the formation of local defects in the endothelium, which, in turn, leads to the deposition of cholesterol and calcium on the vascular wall. Hyperhomocysteinemia as a consequence of impaired homocysteine metabolism is considered an independent risk factor for stroke in humans. The role of neuroprotective therapy in interrupting or slowing down the sequence of damaging biochemical and molecular processes that can cause irreversible ischemic brain damage is shown.

Development of a wearable device for the early diagnosis of neurodegenerative diseases

The progressive evolution of information and sensing technologies is giving pulse to the development of wearable mobile devices in search of life quality improvement. A relevant field of application is healthcare, with the development of wireless unobtrusive wearable solutions for the continuous remote health monitoring of patients. These wearable devices are particularly important for neurodegenerative diseases due to the possibility of early stage diagnoses through continuous monitoring to collect earlier significant data. Discovering specific symptoms and early defining medical treatments can delay, if not stop, the pathology progress whereas, once major symptoms like restricted or impaired mobility has appeared, the patients already underwent relevant and irreversible brain damage. The aim of this work is to show the development of the Neuroglass, a wearable smart glasses device for early stage diagnosis and monitoring of Parkinsonian-type neurodegenerative diseases. The designed frame is compliant to the standards and in order to embed the sensors to collect data from head and eyes movements since one of the early symptoms of Parkinson’s disease has proven to be eye tremors. Preliminary laboratory tests, e.g. head accelerations measurements for different body movements, were carried out in order to choose properly the characteristics and positioning of the sensors; afterwards the device’s frame was designed by means of a 3D parametric CAD and built by additive manufacturing. The design was validated by first experimental test on monitoring eye movements and blinks.

Tetrahydrobiopterin deficiencies: Lesson from clinical experience.

ObjectivesThe present study describes clinical, biochemical, molecular genetic data, current treatment strategies and follow‐up in nine patients with tetrahydrobiopterin (BH4) deficiency due to various inherited genetic defects.MethodsWe analyzed clinical, biochemical, and molecular data of nine patients with suspected BH4 deficiency. All patients were diagnosed at Ege University Faculty of Medicine in Izmir, Turkey and comprised data collected from 2006 to 2019. The diagnostic laboratory examinations included blood phenylalanine and urinary or plasma pterins, dihydropteridine reductase (DHPR) enzyme activity measurement in dried blood spots, folic acid and monoamine neurotransmitter metabolites in cerebrospinal fluid, as well as DNA sequencing.ResultsAmong the nine patients, we identified one with autosomal recessive GTP cyclohydrolase I (ar GTPCH) deficiency, two with 6‐pyruvoyl‐tetrahydropterin synthase (PTPS) deficiency, three with sepiapterin reductase (SR) deficiency, and three with DHPR deficiency. Similar to previous observations, the most common clinical symptoms are developmental delay, intellectual disability, and movement disorders. All patients received treatment with l‐dopa and 5‐hydroxytryptophan, while only the ar GTPCH, the PTPS, and one DHPR deficient patients were supplemented in addition with BH4. The recommended dose range varies among patients and depends on the type of disease. The consequences of BH4 deficiencies are quite variable; however, early diagnosis and treatment will improve outcomes.ConclusionsAs BH4 deficiencies are rare group of treatable neurometabolic disorders, it is essential to diagnose the underlying (genetic) defect in newborns with hyperphenylalaninemia. Irreversible brain damage and progressive neurological deterioration may occur in untreated or late diagnosed patients. Prognosis could be satisfying in the cases with early diagnose and treatment.

CASE REPORTS OF JAPANESE ENCEPHALITIS:AN UNDERDIAGNOSED ENTITY IN AN ENDEMIC REGION OF UTTAR PRADESH, INDIA

Emerging viruses causing Acute Encephalitis Syndrome (AES) can be more damaging due to irreversible brain damage, irrespective of the identical medical characteristics created by all agents. We report two cases of acute encephalitis syndrome caused by Japanese encephalitis virus from a usually under-reported geographic region of India. Both patients were managed conservatively with favourable outcome in one of them.There should be considerable effort to identify the particular causative agent that triggers AES, bearing in mind the various clinical manifestations of Japanese encephalitis virus. Although there is no significant impact on management, it is possible to prevent transmission to healthy contacts and the community through vector control and vaccination.

Clinical Aspects of Neonatal Hypoglycemia: A Mini Review.

Introduction: Neonatal hypoglycemia is common and a preventable cause of brain damage. The goal of management is to prevent or minimize brain injury. The purpose of this mini review is to summarize recent advances and current thinking around clinical aspects of transient neonatal hypoglycemia.Results: The groups of babies at highest risk of hypoglycemia are well defined. However, the optimal frequency and duration of screening for hypoglycemia, as well as the threshold at which treatment would prevent brain injury, remains uncertain. Continuous interstitial glucose monitoring in a research setting provides useful information about glycemic control, including the duration, frequency, and severity of hypoglycemia. However, it remains unknown whether continuous monitoring is associated with clinical benefits or harms. Oral dextrose gel is increasingly being recommended as a first-line treatment for neonatal hypoglycemia. There is some evidence that even transient and clinically undetected episodes of neonatal hypoglycemia are associated with adverse sequelae, suggesting that prophylaxis should also be considered. Mild transient hypoglycemia is not associated with neurodevelopmental impairment at preschool ages, but is associated with low visual motor and executive function, and with neurodevelopmental impairment and poor literacy and mathematics achievement in later childhood.Conclusion: Our current management of neonatal hypoglycemia lacks a reliable evidence base. Randomized trials are required to assess the effects of different prophylactic and treatment strategies, but need to be adequately powered to assess outcomes at least to school age.

RETRACTED ARTICLE: Mesenchymal stem cell-derived exosome miR-542-3p suppresses inflammation and prevents cerebral infarction

BackgroundCerebral infarction ranks as the second leading cause of disability and death globally, and inflammatory response of glial cells is the main cause of brain damage during cerebral infarction.MethodsStudies have shown that mesenchymal stem cells (MSCs) can secrete exosomes and contribute to cerebral disease. Here, we would explore the function of MSC-derived exosome in cerebral infarction.ResultsMicroarray indicated a decrease of miR-542-3p and an increase of Toll-Like Receptor 4 (TLR4) in middle cerebral artery occlusion (MCAO) mice comparing with sham mice. And luciferase and RIP analysis indicated a binding of miR-542-3p and TLR4. Then, we injected AAV9-miR-542-3p into paracele of sham or MCAO mice. Functional analysis showed that AAV9-miR-542-3p inhibited infarction area and the number of degenerating neurons and suppressed inflammatory factors’ expression and inflammatory cell infiltration. As well, transfection of miR-542-3p mimics into HA1800 cells underwent oxygen and glucose deprivation (OGD). Similarly, overexpression of miR-542-3p alleviated OGD induced cell apoptosis, ROS, and activation of inflammation response. Moreover, miR-542-3p could be packaged into MSCs and secreted into HA1800 cells. The extractive exosome-miR-21-3p treatment relieved MCAO- or OGD-induced cerebral injury and inflammation through targeting TLR4.ConclusionThese results confirmed that MSC-derived exosome miR-542-3p prevented ischemia-induced glial cell inflammatory response via inhibiting TLR4. These results suggest possible therapeutic strategies for using exosome delivery of miR-542-3p to cure cerebral ischemic injury.

Calm the raging hormone - a new therapeutic strategy involving progesterone-signaling for hemorrhagic CCMs

Cerebral cavernous malformations (CCMs), one of the most common vascular malformations, are characterized by abnormally dilated intracranial microvascular capillaries resulting in increased susceptibility to hemorrhagic stroke. As an autosomal dominant disorder with incomplete penetrance, the majority of CCMs gene mutation carriers are largely asymptomatic but when symptoms occur, the disease has typically reached the stage of focal hemorrhage with irreversible brain damage, while the molecular "trigger" initiating the occurrence of CCM pathology remain elusive. Currently, the invasive neurosurgery removal of CCM lesions is the only option for the treatment, despite the recurrence of the worse symptoms frequently occurring after surgery. Therefore, there is a grave need for identification of molecular targets for therapeutic treatment and biomarkers as risk predictors for hemorrhagic stroke prevention. Based on reported various perturbed angiogenic signaling cascades mediated by the CCM signaling complex (CSC), there have been many proposed candidate drugs, targeting potentially angiogenic-relevant signaling pathways dysregulated by loss of function of one of the CCM proteins, which might not be enough to correct the pathological phenotype, hemorrhagic CCMs. In this review, we describe a new paradigm for the mechanism of hemorrhagic CCM lesions, and propose a new concept for the assurance of the CSC-stability to prevent the devastating outcome of hemorrhagic CCMs.

The plasminogen activating system in the pathogenesis of Alzheimer's disease.

Dementia is a clinical syndrome that affects approximately 47 million people worldwide and is characterized by progressive and irreversible decline of cognitive, behavioral and sesorimotor functions. Alzheimer’s disease (AD) accounts for approximately 60–80% of all cases of dementia, and neuropathologically is characterized by extracellular deposits of insoluble amyloid-β (Aβ) and intracellular aggregates of hyperphosphorylated tau. Significantly, although for a long time it was believed that the extracellular accumulation of Aβ was the culprit of the symptoms observed in these patients, more recent studies have shown that cognitive decline in people suffering this disease is associated with soluble Aβ-induced synaptic dysfunction instead of the formation of insoluble Aβ-containing extracellular plaques. These observations are translationally relevant because soluble Aβ-induced synaptic dysfunction is an early event in AD that precedes neuronal death, and thus is amenable to therapeutic interventions to prevent cognitive decline before the progression to irreversible brain damage. The plasminogen activating (PA) system is an enzymatic cascade that triggers the degradation of fibrin by catalyzing the conversion of plasminogen into plasmin via two serine proteinases: tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). Experimental evidence reported over the last three decades has shown that tPA and uPA play a role in the pathogenesis of AD. However, these studies have focused on the ability of these plasminogen activators to trigger plasmin-induced cleavage of insoluble Aβ-containing extracellular plaques. In contrast, recent evidence indicates that activity-dependent release of uPA from the presynaptic terminal of cerebral cortical neurons protects the synapse from the deleterious effects of soluble Aβ via a mechanism that does not require plasmin generation or the cleavage of Aβ fibrils. Below we discuss the role of the PA system in the pathogenesis of AD and the translational relevance of data published to this date.

Primary hypothyroidism and autoimmune thyroiditis alter the transcriptional activity of genes regulating neurogenesis in the blood of patients.

Objective. Thyroid hormones play an important role in the development and maturation of the central nervous symptom and their failure in the prenatal period leading to an irreversible brain damage. Their effect on the brain of adult, however, has not been fully studied. With the discovery of neurogenesis in the adult brain, many recent studies have been focused on the understanding the basic mechanisms controlling this process. Many neurogenesis regulatory genes are not only transcribed but also translated into the blood cells. The goal of our study was to analyze the transcriptional activity of neurogenesis regulatory genes in peripheral blood cells in patients with thyroid pathology.Methods. The pathway-specific PCR array (Neurotrophins and Receptors RT2 Profiler PCR Array, QIAGEN, Germany) was used to identify and validate the neurogenesis regulatory genes expression in patients with thyroid pathology and control group.Results. The results showed that GFRA3, NGFR, NRG1, NTF3, NTRK1, and NTRK2 significantly decreased their expression in patients with autoimmune thyroiditis with rising serum of autoantibodies. The patients with primary hypothyroidism, as a result of autoimmune thyroiditis and postoperative hypothyroidism, had significantly lower expression of FGF2, NGFR, NRG1, and NTF3. The mRNA level of CNTFR was markedly decreased in the group of patients with postoperative hypothyroidism. No change in the ARTN, PSPN, TFG, MT3, and NELL1 expression was observed in any group of patients.Conclusion. The finding indicates that a decrease in thyroid hormones and a high level of autoantibodies, such as anti-thyroglobulin antibody and anti-thyroid peroxidase antibody, affect the expression of mRNA neurogenesis-regulated genes in patients with thyroid pathology.

A study of clinical and management profile of Hyponatraemia in the department of surgery

A serum level of less than 135mmol/lit is defined as Hyponatraemia. It can be due to be either hypervolemia, euvolemia or hypervolemia condition. It has a high prevalence especially with patients with metabolic disorders. Diabetes is one such condition. Over correction of dehydration is the leading cause of the illness. Acute is a state where the whole scenario arises and manifests within 48 hours. Hyponatraemia causes neurological deficits and the patients come with a plethora of symptoms. Pinpoint diagnosis is the need of the hour as any delay in identifying can actually cause fatal irreversible brain damage to the patients. The correction also if identified has to be done in a graded manner, if not may again be fatal by causing osmotic demyelination. This study puts in an effort to study the clinical and management profile of Hyponatraemia cases. This study is intended to help the physicians and also clinical practitioners to identify and also help the patients so as to stall the always fatal outcome if treatment is delayed.

Brain damage caused by neonatal hypoxia-ischemia and the effects of hypothermia in severe combined immunodeficient (SCID) mice

Neonatal hypoxic-ischemic encephalopathy (HIE) is a major cause of brain damage in newborns. Although therapeutic hypothermia has been shown to be neuroprotective against neonatal HIE in clinical trials, its effect is not satisfactory. Cell-based therapies have attracted much attention as novel treatments for HIE. Preclinical studies on a variety of human cell transplantation methods have been performed in immunodeficient/immunosuppressed animals, such as severe combined immunodeficient (SCID) mice, which lack functional T and B lymphocytes. The detailed characteristics of neonatal HIE in SCID mice, however, have not been delineated. In preclinical studies, novel therapies for neonatal HIE should be evaluated in combination with hypothermia, which has become a standard treatment for neonatal HIE. However, the effects of hypothermia in SCID mice have not been delineated. In the present study, we compared neonatal hypoxic-ischemic (HI) brain damage in SCID mice and wild-type mice treated with or without hypothermia. Male and female mouse pups were subjected to HI insult induced by unilateral common carotid artery ligation combined with systemic hypoxia on postnatal day 12. In the first 4 h after HI insult, body temperature was maintained at 36 °C for the normothermia groups or 32 °C for the hypothermia groups. The severity of brain damage in SCID mice did not differ from that in wild-type mice based on most evaluations, i.e., cerebral blood flow, hemiparesis, muscle strength, spontaneous activity, cerebral hemispheric volume, neuropathological injury, and serum cytokine levels, although spleen weight, brain weight, leukocyte counts and the levels of some cytokines in the peripheral blood were different between genotypes. The effects of hypothermia in SCID mice were comparable to those in wild-type mice based on most evaluations. Taken together, these findings indicate that SCID mice can be used as an appropriate preclinical model for cell therapies for neonatal HIE.

Aging-induced microbleeds of the mouse thalamus compared to sensorimotor and memory defects

The aim of this study is to investigate the relationship between aging and brain vasculature health. Three groups of mice, 3, 17–18, and 24 months, comparable to young adult, middle age, and old human were studied. Prussian blue histology and fast imaging with steady precession T2∗-weighted magnetic resonance imaging were used to quantify structural changes in the brain across age groups. The novel object recognition test was used to assess behavioral changes associated with anatomical changes. This study is the first to show that the thalamus is the most vulnerable brain region in the mouse model for aging-induced vascular damage. Magnetic resonance imaging data document the timeline of accumulation of thalamic damage. Histological data reveal that the majority of vascular damage accumulates in the ventroposterior nucleus and mediodorsal thalamic nucleus. Functional studies indicate that aging-induced vascular damage in the thalamus is associated with memory and sensorimotor deficits. This study points to the possibility that aging-associated vascular disease is a factor in irreversible brain damage as early as middle age.

Evaluation of Antemortem Diagnostic Techniques in Goats Naturally Infected With Scrapie.

Scrapie is a naturally occurring transmissible spongiform encephalopathy (TSE) that affects sheep and goats. Sheep and goats can be infected with scrapie as lambs or kids via contact with the placenta or placental fluids, or from ingestion of prions shed in the environment and/or bodily fluids (e.g., saliva, urine, and feces). Like other TSEs, scrapie is generally not diagnosed before extensive and irreversible brain damage has occurred. Therefore, a reliable method to screen animals may facilitate diagnosis. Additionally, while natural scrapie in sheep has been widely described, naturally acquired goat scrapie is less well-characterized. The purpose of this study was to better understand natural goat scrapie in regard to disease phenotype (i.e., incubation period, clinical signs, neuroanatomical deposition patterns of PrPSc, and molecular profile as detected by Western blot) and to evaluate the efficacy of antemortem tests to detect scrapie-positive animals in a herd of goats. Briefly, 28 scrapie-exposed goats were removed from a farm depopulated due to previous diagnoses of scrapie on the premises and observed daily for 30 months. Over the course of the observation period, antemortem biopsies of recto-anal mucosa-associated lymphoid tissue (RAMALT) were taken and tested using immunohistochemistry and real-time quaking-induced conversion (RT-QuIC), and retinal thickness was measured in vivo using optical coherence tomography (OCT). Following the observation period, immunohistochemistry and Western blot were performed to assess neuroanatomical deposition patterns of PrPSc and molecular profile. Our results demonstrate that antemortem rectal biopsy was 77% effective in identifying goats naturally infected with scrapie and that a positive antemortem rectal biopsy was associated with the presence of clinical signs of neurologic disease and a positive dam status. We report that changes in retinal thickness are not detectable over the course of the observation period in goats naturally infected with scrapie. Finally, our results indicate that the accumulation of PrPSc in central nervous system (CNS) and non-CNS tissues is consistent with previous reports of scrapie in sheep and goats.

White Cerebellum Sign: case series and literature review

Introduction: The white cerebellum sign is a rare radiological finding, seen in severe traumatic brain injury and severe hypoxia. Radiologically, it is characterized by cerebellar hyperdensity, associated with diffuse cerebral hemispheres hypoattenuation. This paper aims to guide the white cerebellum sign diagnosis in traumatic craniocerebral injuries or not in pediatric patients. Patients and Methods: The authors present a series of five cases that showed the white cerebellum sign from the period about 2007 and 2010, associated with a literature review. Results: The white cerebellum sign was present in 5 patients, three of them were male and 2 female. The mean age was 22 months. The causes of which were: traumatic brain injury (3), drowning (1) and metabolic encephalopathy (1). The skull computerized tomography scan was performed in all cases. All patients were submitted to conservative treatment. There were four deaths and one survived with severe neurological sequelae. Conclusion: The white cerebellum sign is associated with irreversible brain damage, and its pathophysiology is controversial. The imaging tests are important to diagnosis. It has a poor prognosis, associated with the development of diffuse cerebral atrophy or cystic encephalomalacia in those who survive.

The Gut Microbiota and Oxidative Stress in Autism Spectrum Disorders (ASD).

Autism spectrum disorders (ASDs) are a kind of neurodevelopmental disorder with rapidly increasing morbidity. In recent years, many studies have proposed a possible link between ASD and multiple environmental as well as genetic risk factors; nevertheless, recent studies have still failed to identify the specific pathogenesis. An analysis of the literature showed that oxidative stress and redox imbalance caused by high levels of reactive oxygen species (ROS) are thought to be integral parts of ASD pathophysiology. On the one hand, this review aims to elucidate the communications between oxidative stress, as a risk factor, and ASD. As such, there is also evidence to suggest that early assessment and treatment of antioxidant status are likely to result in improved long-term prognosis by disturbing oxidative stress in the brain to avoid additional irreversible brain damage. Accordingly, we will also discuss the possibility of novel therapies regarding oxidative stress as a target according to recent literature. On the other hand, this review suggests a definite relationship between ASD and an unbalanced gastrointestinal tract (GIT) microbiota (i.e., GIT dysbiosis). A variety of studies have concluded that the intestinal microbiota influences many aspects of human health, including metabolism, the immune and nervous systems, and the mucosal barrier. Additionally, the oxidative stress and GIT dysfunction in autistic children have both been reported to be related to mitochondrial dysfunction. What is the connection between them? Moreover, specific changes in the GIT microbiota are clearly observed in most autistic children, and the related mechanisms and the connection among ASD, the GIT microbiota, and oxidative stress are also discussed, providing a theory and molecular strategies for clinical practice as well as further studies.

Electrocorticography in patients with severe traumatic brain injury

Introduction. The frequency of adverse outcomes in patients with severe traumatic brain injury (TBI) exceeds 25%. Epileptic seizures and vasospasm, in the absence of pathogenetic treatment, cause irreversible brain damage and thus complicate the course of severe TBI. Bedside electroencephalography (EEG) is traditionally used to diagnose these conditions. However, its low spatial resolution when recording from the scalp and a large number of artefacts that make it challenging to analyse the data. Materials and methods. Electrocorticography (ECoG) monitoring was performed using subdural electrodes implanted in the traumatic brain lesion during TBI surgery in 11 patients during the acute period of severe TBI. All patients were concurrently monitored using scalp EEG with subdermal needle electrodes. Results. Analysis of scalp recordings showed frequency disturbances and oscillation asymmetry in all patients, while sporadic epileptiform activity and rhythmic and periodic patterns were detected in 18% and 64% of subjects, respectively. Analysis of invasive EEG showed sporadic epileptiform activity in 27% of patients, while rhythmic and periodic patterns were present in 91%. Moreover, epileptiform activity was registered only by the subdural leads in 3 patients. The total percentage of subjects in whom we registered clinical and electrographic signs of convulsive and non-convulsive status epilepticus using EEG and ECoG was 55%. We found indirect EEG signs of slow-spreading cortical depolarization in one patient whose level of consciousness was coma, followed by an electrographic pattern of status epilepticus on ECoG. Conclusion. ECoG recording, while patients with severe TBI are in the intensive care unit, increases the diagnostic capabilities of this method, allowing electrographic seizures to be recorded more often and more accurately, but also to detect indirect signs of slow-spreading cortical depolarization using standard EEG amplifiers. Electrode implantation during TBI surgery is safe and does not significantly change the surgical approach.

Assessment of students' knowledge on iodine supplementation by women planning pregnancy

Introduction: Iodine is essential for the synthesis of the thyroid hormones. Proper thyroid function in a pregnant woman depends on the accumulated reserves of iodine in the pre-pregnancy period. If they are sufficient, the production of thyroid hormones is adequate even in the case of increased demand. Adequate iodine status during pregnancy is crucial for maternal health and foetal growth. Severe iodine deficiency causes maternal and foetal hypothyroxinaemia, leading to irreversible brain damage, manifested by mental retardation and neurological disorders. The daily requirement for iodine for pregnant women has been determined by The World Health Organization (WHO) at 250 µg. Most likely, the demand for it cannot be covered only by dietary iodine intake, so iodine should be supplemented in the form of tablets at a dose of 150-200 µg daily.Purpose: The aim of the study is to assess students' knowledge on iodine supplementation by women planning pregnancy and pregnant women.Material and method: Students' knowledge regarding the importance of iodine supplementation was verified using anonymous Internet questionnaire. The obtained results were analysed and checked on the basis of scientific literature.Results: The percentage of students who think iodine supplementation should be recommended is 22.7%, and 9.7% believe it is not necessary. Only 8.8% of the respondents chose the correct recommended dose of iodine. Surprisingly, most of the respondents do not know the recommended iodine dose, as much as 71.7% of them.Conclusions: The proper supply of iodine has a decisive impact on the proper functioning of the body, and its deficiency has serious consequences, especially in the womb. The problem of iodine deficiency is serious. This is also confirmed by the results of our surveys. It is important to educate students on the recommendations for iodine supplementation in women of childbearing age.

DNA-Encoded Glutamine Synthetase Enzyme as Ammonia-Lowering Therapeutic for Hyperammonemia.

Hyperammonemia is a dangerous life-threatening metabolic complication characterized by markedly elevated ammonia levels that can lead to irreversible brain damage if not carefully monitored. Current pharmacological treatment strategies available for hyperammonemia patients are suboptimal and associated with major side effects. In this study, we focus on developing and evaluating the in vivo delivery of novel DNA-encoded glutamine synthetase (GS) enzymes for the treatment of hyperammonemia. Direct in vivo delivered DNA-encoded GS enzyme was evaluated in ammonium acetate-induced hyperammonemia and thioacetamide-induced acute liver injury (ALI) models in C57BL/6 mice. In ammonium acetate-induced hyperammonemia model, we achieved a 30.5% decrease in blood ammonia levels 15 min postadministration of ammonium acetate, with DNA-encoded GS-treated group. Significant increase in survival was observed in ALI model with the treated mice. A comparison of the secreted versus intracellular DNA-encoded GS enzyme demonstrated similar increases in survival in the ALI model, with 40% mortality in the secreted enzymes and 30% mortality in the intracellular enzymes, as compared with 90% mortality in the control group. Direct in vivo delivery of DNA-encoded GS demonstrated important ammonia-lowering potential. These results provide the initial steps toward development of delivered DNA as a potential new approach to ammonia-lowering therapeutics.

Malnutrition Alleviation of Selenium by Agronomic Bio-Fortification

Selenium an micro-nutrient causes malnutrition in human health if the recommended level 55 μg day-1 is not consumed. The disorders such as thyroid gland dysfunctions, irreversible brain damage, peripheral vascular diseases, chronic and Kashin–Beck disease, impaired immune response to viral infections, male infertility, pre-eclampsia in women, heart diseases and cancer. The rectification strategy is by increasing the element content in edible parts of staple food by agronomic bio-fortification strategies which overcomes the selenium availability in soils influenced by soil pH and redox potential of soil. The success reports of eminent research workers confirms the feasibility of the approach enhancing the nutrient content in grains and alleviating malnutrition.

Assessment of iodine deficiency disorder among school going children aged 5-10 years in Sagar district of Madhya Pradesh: an observational cross sectional study

Background: Iodine deficiency (IDD) is the world’s most prevalent cause of brain damage. glaciations, flooding, rivers lead to deficiency of iodine in crops grown on iodine. Diet low in iodine can result in stillbirth and abortions and many more sequelae. Objectives of the research work were to study the prevalence of IDD amongst 6-12 years children by clinical examination and to determine the concentration of iodine in salt sample at consumer level. Also, to determine the urinary iodine excretion amongst 6-12 years age group children.Methods: It was a cross sectional study conducted in the government schools of Sagar district among school children of 6-12 years of age. Total 2700 school children from 30 villages were included using PPS sampling. Students were clinically examined and their urine samples were taken for MUIC estimation.Results: Prevalence of goiter was more in 10 to 11 years of age (14.07%) and less in 8 to 9 years age group (7.59%). Overall prevalence of goiter in district Sagar is 10.51%.Conclusions: Despite NIDDCP, there is still dearth of awareness among general public about the usage and storage of iodized salt which is the root cause of Iodine deficiency.