EFFICACY OF YOGA ON TRAUMA IN ORPHAN CHILDREN DWELLING IN ORPHANAGE HOMES: An EXPERIMENTAL PRE POST STUDY

Orphans and vulnerable children (OVC) are at increased risk for post-traumatic stress disorder (PTSD), depression and anxiety. They are at a substantially greater risk for developmental problems in cognitive, physiological, social, emotional, and behavioural domains. The aim of present study is to diagnosed the presence of trauma and  to study the effect of Integrated Approach of Yoga therapy on participants with post trauma stress disorder. Three orphanages were chosen for the study. The children were divided in to two groups experimental (n=21) and control group (n=21). The children were in the age group 7 to 12. CAPS-CA-5 for DSM-5 (Clinician Administered PTSN Scale child/Adolescent version for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) was administered prior to the intervention. Only children who satisfied the diagnostic criteria were selected. Yoga group underwent three months of Yoga program in a schedule of 90 min per day, five days per week whereas the Control group followed the routine activities Intervention was given by trained Yoga teachers at the Orphanage. The yoga module included Loosening Practices, Breathing practices, Asanas, Surya Namaskaras, Pranayama, Yogic Games, Devotional songs and Bhajans. Practices were given on weekdays and the participants were assessed after three months

YOGIC MANAGEMENT FOR HYPOTHYROIDISM: A CASE STUDY

The thyroid is butterfly shaped gland, and the pituitary gland (another gland located in the brain) regulates it. Hypothyroidism (underactive thyroid) refers to any state in which a person's thyroid hormone production is below normal. In Modern medicine Standard treatment for hypothyroidism involves daily use of the synthetic thyroid hormone levothyroxine (Levothroid, Synthroid, others). A patient might become dependent on these drugs for life.. We present a case where a patient was suffering from hypothyroidism for the last 6 months and got positive results by integrated approach with yoga therapy. The Patient was suffering for hypothyroidism with TSH level of 36.6. After the end of the yoga therapy the TSH level was reduced to 5.82.The patient did not undergo treatment with modern medicine

Knowledge, practices and gender discrepancies of migrant labours concerning malaria in Bhubaneswar, Odisha, India

Background: Bhubaneswar, the capital of Odisha is an up-coming city since 1960s. The capital is undergoing various developmental activities and rapid industrialization. This is leading to migration of labours from various districts of Odisha including malaria endemic districts. The records available in central malaria laboratory, Bhubaneswar revealed high malaria incidence (ranged from 5% to 11% during last five years).Methods: The study was undertaken in Bhubaneswar, Odisha, India, on migrant laboures (300 samples) through a pre-structured schedule.Results: The study revealed the migrated respondents were from malaria endemic districts of Odisha. The malaria endemicity of the districts ranged from 2.2-9.8. It was also found that only 6% of the migrants were from low endemic areas i.e. SPR5. Study of the awareness of the respondents showed 31% males and 9% females knew mosquito bite as a cause of malaria. Rapid Diagnostic Test showed twenty seven numbers of respondents tested positive for malaria (24 positive for PF and 3 positive for PV), out of them 6 were males and 21 were females. The study of their sleeping habits and personal protection methods showed that 32% respondents slept outdoor and 73% did not use anything as protection against mosquito bite. The study regarding knowledge of malaria signs and symptoms among respondents showed that the most commonly recognized signs and symptoms of malaria were headache (23%).  Vector incrimination study showed that per man hour density of an. stephensi is 5.7.Conclusions: Thus presence of efficient malaria vectors and inadequate knowledge in the migrant labour community and emphatically among female migrant labours regarding cause, symptoms, prevention, control measures and risks associated with malaria is the major reason of malaria transmission.

Yoga therapy for Metabolic Syndrome - A Review

Metabolic syndrome is a collection of risk factors that increase the chance of developing heart disease, stroke, and diabetes. Lifestyle changes like losing weight, exercise, and dietary changes can help prevent or reverse metabolic syndrome. Metabolic syndrome is now considered as a serious public health problem. It is estimated that 20 - 25% of the world adult population is suffering from this disorder. Yet most recommendations currently focus on diet and exercise and do not consider stress reduction strategies. Yoga is a effective tool for stress management, that may reduce blood pressure (BP) increase parasympathetic activation. In this review, we examined the basic principles of Pancha Kosha (five sheaths of human existence) concept from an Indian scripture Taittiriya Upanishad and the pathophysiology of a disease from the Yogic approach of Yoga Vasistha’s Adhi (originated from mind) and Vyadhi (ailment/disease) concept and focused on Yoga and HPA axis. Based on these concepts, a Yoga module is recommended as a remedial therapy to manage Metabolic Syndrome

RESVERATROL PROTECTS WHOLE BODY HEAT STRESS-INDUCED TESTICULAR DAMAGE IN RAT MODEL

Objective: The local thermoregulation in testis is important for optimum spermatozoa development. Excessive heat hampers this regulation resulting in alteration of normal testicular function. The present investigation confirms the role of free radicals in hyperthermia induced oxidative damage in testis and elucidates the dose-dependent ameliorating effect of resveratrol (RSV) against testicular oxidative damage. The aim of the present investigation is also to observe the role of selective concentration of RSV on heat induced oxidative changes in the damaged tissue. Methods: 48 male Wister rats were exposed to hyperthermic condition for the past 7 days of the total 21 days of experiment. RSV was pre- and co-treated with heat stress daily in a dose-dependent manner (1 mg, 5 mg, and 10 mg/kg body weight) for 21days. Results: Reactive oxygen species level was estimated using flow cytometry. Enhancement of hepatotoxicity markers in serum, lipid peroxidation and decreasing antioxidant status in the testis homogenate demonstrated that the oxidative damage in heat exposed tissue. Conclusion: Histological study along with biochemical and molecular assessment of the redox balance of testicular tissue in the present study revealed that RSV significantly ameliorated the heat induced damage in testis. The findings suggest that RSV is an effective antioxidant polyphenolic compound that can protect testis against hyperthermia induced oxidative damage

Mycobacterium tuberculosis lipoarabinomannan-mediated IRAK-M induction negatively regulates toll-like receptor-dependent interleukin-12 p40 production in macrophages

Mannose-capped lipoarabinomannans (Man-LAMs) are members of the repertoire of Mycobacterium tuberculosis modulins that the bacillus uses to subvert the host innate immune response. Interleukin-12 (IL-12) production is critical for mounting an effective immune response by the host against M. tuberculosis. We demonstrate that Man-LAM inhibits IL-12 p40 production mediated by subsequent challenge with lipopolysaccharide (LPS). Man-LAM inhibits LPS-induced IL-12 p40 expression in an IL-10-independent manner. It attenuates LPS-induced NF-κB-driven luciferase gene expression, suggesting that its effects are likely directly related to inhibition of NF-κB. This is probably because of dampening of the Toll-like receptor signaling. Man-LAM inhibits IL-1 receptor-associated kinase (IRAK)-TRAF6 interaction as well as IκB-α phosphorylation. It directly attenuates nuclear translocation and DNA binding of c-Rel and p50. Man-LAM exerts these effects by inducing the expression of Irak-M, a negative regulator of TLR signaling. Knockdown of Irak-M expression by RNA interference reinstates LPS-induced IL-12 production in Man-LAM-pretreated cells. The fact that Irak-M expression could be elicited by yeast mannan suggested that ligation of the mannose receptor by the mannooligosaccharide caps of LAM was the probable trigger for IRAK-M induction

Toll-like receptor 2 and mitogen- and stress-activated kinase 1 are effectors of Mycobacterium avium-induced cyclooxygenase-2 expression in macrophages

Understanding how pathogenic mycobacteria subvert the protective immune response is crucial to the development of strategies aimed at controlling mycobacterial infections. Prostaglandin E2 exerts an immunosuppressive function in the context of mycobacterial infection. Because cyclooxygenase-2 (COX-2) is a rate-limiting enzyme in prostaglandin biosynthesis, there is a need to delineate the mechanisms through which pathogenic mycobacteria regulate COX-2 expression in macrophages. Our studies demonstrate that the NF-κB and CRE elements of the COX-2 promoter are critical to Mycobacterium avium-induced COX-2 gene expression. M. avium-triggered signaling originates at the Toll-like receptor 2 (TLR2). Ras associates with TLR2 and activates the mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK), whereas tumor necrosis factor receptor-associated factor 6 (TRAF6)/transforming growth factor β -activated kinase 1 (TAK1)-dependent signaling activates p38 MAPK. Both ERK and p38 MAPK activation converge to regulate the activation of mitogen- and stress-activated kinase 1 (MSK1). MSK1 mediates the phosphorylation of the transcription factor CREB accounting for its stimulatory effect on CRE-dependent gene expression. M. avium-triggered cytoplasmic NF-κB activation following IκB phosphorylation is necessary but not sufficient for COX-2 promoter-driven gene expression. MSK1 activation is also essential for M. avium-triggered NF-κB-dependent gene expression, presumably mediating nucleosomal modifications. These studies demonstrate that the nuclear kinase MSK1 is necessary in regulating the pathogen-driven expression of a gene by controlling two transcription factors. The attenuation of MSK1 may therefore have potential benefit in restricting survival of pathogenic mycobacteria in macrophages

Execution of macrophage apoptosis by PE_PGRS33 of Mycobacterium tuberculosis is mediated by toll-like receptor 2-dependent release of tumor necrosis factor-α

Combating tuberculosis requires a detailed understanding of how mycobacterial effectors modulate the host immune response. The role of the multigene PE family of proteins unique to mycobacteria in the pathogenesis of tuberculosis is still poorly understood, although certain PE_PGRS genes have been linked to virulence. Tumor necrosis factor-α (TNF-α ) is essential for successfully combating tuberculosis. In this study we provide evidence that PE_PGRS33, a surface exposed protein, elicits TNF-α release from macrophages in a TLR2 (Toll-like receptor 2)-dependent manner. ASK1 (apoptosis signal-regulating kinase 1) is activated downstream of TLR2. ASK1 activates the MAPKs p38 and JNK. PE_PGRS33-induced signaling leads to enhanced expression of TNF-α and TNF receptor I (TNFRI) genes. Mycobacterium smegmatis expressing PE_ PGRS33 elicits the same effects as purified PE_PGRS33. TNF-α release occurs even when internalization of the bacteria is blocked by cytochalasin D, suggesting that interaction of PE_ PGRS33 with TLR2 is sufficient to trigger the effects described. Release of TNF-α plays the determining role in triggering apoptosis in macrophages challenged with PE_PGRS33. The death receptor-dependent signals are amplified through classical caspase 8-dependent mitochondrial release of cytochrome c, leading to the activation of caspases 9 and 3. An important aspect of our findings is that deletions within the PGRS domain (simulating those occurring in clinical strains) attenuate the TNF-α-inducing ability of PE_PGRS33. These results provide the first evidence that variations in the polymorphic repeats of the PGRS domain modulate the innate immune response

Xenia studies in exotic and indigenous almond (Prunus amygdalus L.) varieties of Kashmir, India

Pollination is very important to obtain an economic yield, and the selection of pollinizer with suitable quality and quantity of pollen is an essential practice in different fruit plants. The effects of pollen parent on kernel and nut characters are known to occur in several nut crops and to determine the best pollinizer and effect of pollen source on the nut and kernel quality of almond (Prunus amygdalus L.). The present investigation was carried out at the experiment farm of Dryland Agriculture Research Station (DARS), SKUAST-Kashmir for two consecutive years, i.e. 2008 and 2009. Various cross combinations were made among nine almond (three exotic and six indigenous) varieties/selections which are compatible with each other. Their nut and kernel characteristics were determined and observed maximum nut weight (2.21 g), nut length (39.78 mm) and nut breadth (20.33 mm), kernel weight (1.28 g), kernel length (28.63 mm) and kernel breadth (12.61 mm) and shelling percentage (57.99 %). In the present study it has been observed that the parent with big nut and kernel size and weight influenced the nut and kernel size; nut and kernel weight of the recipient parent significantly (p?0.05)

Global burden of 288 causes of death and life expectancy decomposition in 204 countries and territories and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021

BACKGROUND Regular, detailed reporting on population health by underlying cause of death is fundamental for public health decision making. Cause-specific estimates of mortality and the subsequent effects on life expectancy worldwide are valuable metrics to gauge progress in reducing mortality rates. These estimates are particularly important following large-scale mortality spikes, such as the COVID-19 pandemic. When systematically analysed, mortality rates and life expectancy allow comparisons of the consequences of causes of death globally and over time, providing a nuanced understanding of the effect of these causes on global populations. METHODS The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 cause-of-death analysis estimated mortality and years of life lost (YLLs) from 288 causes of death by age-sex-location-year in 204 countries and territories and 811 subnational locations for each year from 1990 until 2021. The analysis used 56 604 data sources, including data from vital registration and verbal autopsy as well as surveys, censuses, surveillance systems, and cancer registries, among others. As with previous GBD rounds, cause-specific death rates for most causes were estimated using the Cause of Death Ensemble model-a modelling tool developed for GBD to assess the out-of-sample predictive validity of different statistical models and covariate permutations and combine those results to produce cause-specific mortality estimates-with alternative strategies adapted to model causes with insufficient data, substantial changes in reporting over the study period, or unusual epidemiology. YLLs were computed as the product of the number of deaths for each cause-age-sex-location-year and the standard life expectancy at each age. As part of the modelling process, uncertainty intervals (UIs) were generated using the 2·5th and 97·5th percentiles from a 1000-draw distribution for each metric. We decomposed life expectancy by cause of death, location, and year to show cause-specific effects on life expectancy from 1990 to 2021. We also used the coefficient of variation and the fraction of population affected by 90% of deaths to highlight concentrations of mortality. Findings are reported in counts and age-standardised rates. Methodological improvements for cause-of-death estimates in GBD 2021 include the expansion of under-5-years age group to include four new age groups, enhanced methods to account for stochastic variation of sparse data, and the inclusion of COVID-19 and other pandemic-related mortality-which includes excess mortality associated with the pandemic, excluding COVID-19, lower respiratory infections, measles, malaria, and pertussis. For this analysis, 199 new country-years of vital registration cause-of-death data, 5 country-years of surveillance data, 21 country-years of verbal autopsy data, and 94 country-years of other data types were added to those used in previous GBD rounds. FINDINGS The leading causes of age-standardised deaths globally were the same in 2019 as they were in 1990; in descending order, these were, ischaemic heart disease, stroke, chronic obstructive pulmonary disease, and lower respiratory infections. In 2021, however, COVID-19 replaced stroke as the second-leading age-standardised cause of death, with 94·0 deaths (95% UI 89·2-100·0) per 100 000 population. The COVID-19 pandemic shifted the rankings of the leading five causes, lowering stroke to the third-leading and chronic obstructive pulmonary disease to the fourth-leading position. In 2021, the highest age-standardised death rates from COVID-19 occurred in sub-Saharan Africa (271·0 deaths [250·1-290·7] per 100 000 population) and Latin America and the Caribbean (195·4 deaths [182·1-211·4] per 100 000 population). The lowest age-standardised death rates from COVID-19 were in the high-income super-region (48·1 deaths [47·4-48·8] per 100 000 population) and southeast Asia, east Asia, and Oceania (23·2 deaths [16·3-37·2] per 100 000 population). Globally, life expectancy steadily improved between 1990 and 2019 for 18 of the 22 investigated causes. Decomposition of global and regional life expectancy showed the positive effect that reductions in deaths from enteric infections, lower respiratory infections, stroke, and neonatal deaths, among others have contributed to improved survival over the study period. However, a net reduction of 1·6 years occurred in global life expectancy between 2019 and 2021, primarily due to increased death rates from COVID-19 and other pandemic-related mortality. Life expectancy was highly variable between super-regions over the study period, with southeast Asia, east Asia, and Oceania gaining 8·3 years (6·7-9·9) overall, while having the smallest reduction in life expectancy due to COVID-19 (0·4 years). The largest reduction in life expectancy due to COVID-19 occurred in Latin America and the Caribbean (3·6 years). Additionally, 53 of the 288 causes of death were highly concentrated in locations with less than 50% of the global population as of 2021, and these causes of death became progressively more concentrated since 1990, when only 44 causes showed this pattern. The concentration phenomenon is discussed heuristically with respect to enteric and lower respiratory infections, malaria, HIV/AIDS, neonatal disorders, tuberculosis, and measles. INTERPRETATION Long-standing gains in life expectancy and reductions in many of the leading causes of death have been disrupted by the COVID-19 pandemic, the adverse effects of which were spread unevenly among populations. Despite the pandemic, there has been continued progress in combatting several notable causes of death, leading to improved global life expectancy over the study period. Each of the seven GBD super-regions showed an overall improvement from 1990 and 2021, obscuring the negative effect in the years of the pandemic. Additionally, our findings regarding regional variation in causes of death driving increases in life expectancy hold clear policy utility. Analyses of shifting mortality trends reveal that several causes, once widespread globally, are now increasingly concentrated geographically. These changes in mortality concentration, alongside further investigation of changing risks, interventions, and relevant policy, present an important opportunity to deepen our understanding of mortality-reduction strategies. Examining patterns in mortality concentration might reveal areas where successful public health interventions have been implemented. Translating these successes to locations where certain causes of death remain entrenched can inform policies that work to improve life expectancy for people everywhere. FUNDING Bill & Melinda Gates Foundation