Community empowerment - a successful model for prevention of non-communicable diseases in India - the Chennai Urban population study (CUPS - 17)

Background and objective: Randomized clinical trials have documented that lifestyle changes through physical activity can prevent diabetes. However there is no data whether such strategies are applicable at community level, that is, in a real life setting. This study demonstrates the first attempt in India, to our knowledge, of increasing physical activity through community empowerment in an attempt at primary prevention of non communicable diseases. Methods: The Chennai Urban Population Study [CUPS] was conducted in the year 1996 in two residential areas: a middle income group the Asiad colony at Tirumangalam, and a low income group at Bharathi Nagar in T. Nagar. The Asiad colony was selected for this study. Of the 524 eligible individuals available at baseline in 1998 [age ≥ 20 years], 479 individuals consented for the study (response rate:91.4%). After seven years, in 2004, the number of eligible individuals increased to 712 of whom 705 consented for the study (response rate:99%). Education regarding the benefits of physical activity was provided by mass awareness programmes like public lectures and video clippings. Both at baseline and during follow-up, details about the physical activity were collected using a validated questionnaire, which included job related and leisure time activities, and specific questions on exercise. Study individuals were then graded as having light, moderate and heavy physical activity using a scoring system. Results: In response to the awareness programmes given by our research team, the colony residents constructed a unique public park with their own funds. Though the occupation grades did not change, there was a significant change in the pattern of physical activity. At baseline, only 14.2% of the residents did some form of exercise more than three times a week, which presently increased to 58.7%[p<0.001]. The number of subjects who walked more than three times a week increased from 13.8% at baseline to 52.1% during follow-up [p<0.001]. Conclusion: This study is a demonstration of how community empowerment with increased physical activity could possibly lead to prevention of diabetes and other non communicable diseases at the community level. This study also highlights the importance of sharing the results of research studies with the community

Association of A1C with cardiovascular disease and metabolic syndrome in Asian Indians with normal glucose tolerance.

OBJECTIVE: This study examines the association of A1C with cardiovascular disease (CVD) risk factors, coronary artery disease (CAD), and metabolic syndrome in Asian Indians with normal glucose tolerance (NGT). RESEARCH DESIGN AND METHODS: This cross-sectional study recruited subjects from phase III of the Chennai Urban Rural Epidemiology Study (CURES), an epidemiological study in a representative population of Chennai (formerly Madras) in South India, conducted between January 2003 and June 2004. Included were 1,644 subjects with NGT, i.e., fasting plasma glucose <100 mg/dl (5.6 mmol/l) and 2-h postload plasma glucose <140 mg/dl (7.8 mmol/l). A1C was measured using the Biorad Variant machine. Metabolic syndrome was defined based on modified Adult Treatment Panel III guidelines. RESULTS: The mean +/- SD A1C value in the study cohort was 5.5 +/- 0.4%. A1C showed a significant association with BMI (beta = 0.017, P < 0.001), systolic (beta = 0.002, P = 0.028) and diastolic (beta = 0.202, P = 0.017) blood pressure, waist circumference (beta = 0.007, P < 0.001), serum cholesterol (beta = 0.002, P < 0.001), triglycerides (beta = 0.001, P < 0.001), LDL cholesterol (beta = 0.002, P < 0.001), fasting insulin (beta = 0.009, P < 0.001), and homeostasis model assessment of insulin resistance (beta = 0.047, P < 0.001) after adjusting for age and sex. Regression analysis showed that A1C had a strong association with metabolic syndrome that persisted after adjusting for age and sex (odds ratio [OR] 2.9 [95% CI 2.08-4.00]; P < 0.001). A1C also had a strong association with CAD (2.6 [1.23-5.63]; P = 0.01), but the significance was lost when adjusted for age and sex. CONCLUSIONS: There is a strong association of A1C with prevalent CVD risk factors in Asian-Indian subjects with NGT

An aetiological evaluation of short stature

Background: Short stature can be a normal variant or secondary to an underlying disorder. It is necessary to evaluate short stature to differentiate a normal from pathological short stature and thus decide the further treatment needed. This study was conducted at a tertiary care hospital to find out the various etiologies of short statureMethods: An observational study was conducted on 49 children in age of 2-12 years with short stature. They were grouped as normal variants and pathological short stature depending on upper-lower segment ratio the study group was later divided into proportionate and disproportionate short stature. They were further investigated to find out the etiology of the short stature. The bone age of all groups was compared with the chronological age to calculate the bone age retardation.Results: Out of 49 children 26.5% were normal variants and 73.4% as pathological type. 77.7% of pathological short stature were proportionate type. The male:female ratio was 1:1.4. Chronic systemic disorders were detected in 24.48% while malnutrition and endocrine disorders constituted 12% each. The bone age retardation in endocrine disorders was 0.47.Conclusions: Chronic systemic disorders were commonest cause of pathological short stature in this study. Females were predominantly affected in all groups and bone age retardation was maximum in endocrine disorders, thus indicating that early diagnosis and management of these disorders is necessary to decrease the growth retardation in these children. An understanding of short stature not only permits to differentiate a normal variant from an underlying disorder but also helps in modifying the course by means of early intervention

Co-operation between humoral and cellular immunity in pulmonary lung inflammation

Master'sMASTER OF SCIENC

Insecticidal factors from the seeds of Erythrina indica Lam against Hyblaea puera, the most serious defoliator pest of teak

The organic solvent extracts from the seeds of Erythrina indica were tested for their insecticidal action against Hyblaea puera, the most important defoliator pest of teak. The larvicidal activity of the petroleum ether, chloroform, methanol, ethyl alcohol, ethyl acetate, acetone and water extracts from the seeds of E. indica on the 3rd instar larvae of H. puera showed 100% mortality even with least concentration (0.25%). The ovicidal activity was exhibited by chloroform and ethyl acetate extract. Both the extracts exhibited highest egg hatch inhibition (56%) at highest concentration (2%). The least LC50 (1.15%) shows that ethyl acetate extract is better than chloroform extract (1.78). Two compounds were isolated from the ethyl acetate extract of the seeds of Erythrina indica by column chromatography. The compounds were identified using HPLC, GC MS, and NMR. Compound 1 was a mixture of linoleic acid and oleic acid. Compound 2 was a mixture of linoleic acid and oleic acid ester with a glycerol unit attached to it. Compounds 1 and 2 were biologically active and exhibited potent insecticidal activity against the 3rd instar larvae of H. puera. The result showed that Compound 2 isolated from E. indica exhibited highest mortality (72%) at concentration (0.125%). At highest concentration (0.5%) highest mortality (92%) was exhibited by Compound 2 which on comparison is on par with the Neemark (Azadirachtin) exhibiting highest mortality (100%). The study is complementary with earliar works and proves that the seeds of E. indica has immense potential to be utilized as botanical insecticide

Tunable Nanostructures and Crystal Structures in Titanium Oxide Films

Controllable nanostructures in spin coated titanium oxide (TiO2) films have been achieved by a very simple means, through change of post deposition annealing temperature. Electron beam imaging and reciprocal space analysis revealed as-deposited TiO2films to be characterized by a dominant anatase phase which converts to the rutile form at 600 °C and reverts to the anatase modification at 1,200 °C. The phase changes are also accompanied by changes in the film microstructure: from regular nanoparticles (as-deposited) to nanowires (600 °C) and finally to dendrite like shapes at 1,200 °C. Photoluminescence studies, Raman spectral results, and X-ray diffraction data also furnish evidence in support of the observed solid state phase transformations in TiO2

ECG Recordings as Predictors of Very Early Autism Likelihood: A Machine Learning Approach

In recent years, there has been a rise in the prevalence of autism spectrum disorder (ASD). The diagnosis of ASD requires behavioral observation and standardized testing completed by highly trained experts. Early intervention for ASD can begin as early as 1–2 years of age, but ASD diagnoses are not typically made until ages 2–5 years, thus delaying the start of intervention. There is an urgent need for non-invasive biomarkers to detect ASD in infancy. While previous research using physiological recordings has focused on brain-based biomarkers of ASD, this study investigated the potential of electrocardiogram (ECG) recordings as an ASD biomarker in 3–6-month-old infants. We recorded the heart activity of infants at typical and elevated familial likelihood for ASD during naturalistic interactions with objects and caregivers. After obtaining the ECG signals, features such as heart rate variability (HRV) and sympathetic and parasympathetic activities were extracted. Then we evaluated the effectiveness of multiple machine learning classifiers for classifying ASD likelihood. Our findings support our hypothesis that infant ECG signals contain important information about ASD familial likelihood. Amongthe various machine learning algorithms tested, KNN performed best according to sensitivity (0.70 ± 0.117), F1-score (0.689 ± 0.124), precision (0.717 ± 0.128), accuracy (0.70 ± 0.117, p-value = 0.02), and ROC (0.686 ± 0.122, p-value = 0.06). These results suggest that ECG signals contain relevant information about the likelihood of an infant developing ASD. Future studies should consider the potential of information contained in ECG, and other indices of autonomic control, for the development of biomarkers of ASD in infanc

Vhl deficiency in osteocytes produces high bone mass and hematopoietic defects

Tissue oxygen (O2) levels vary during development and disease; adaptations to decreased O2 (hypoxia) are mediated by hypoxia-inducible factor (HIF) transcription factors. HIFs are active in the skeleton, and stabilizing HIF-α isoforms cause high bone mass (HBM) phenotypes. A fundamental limitation of previous studies examining the obligate role for HIF-α isoforms in the skeleton involves the persistence of gene deletion as osteolineage cells differentiate into osteocytes. Because osteocytes orchestrate skeletal development and homeostasis, we evaluated the influence of Vhl or Hif1a disruption in osteocytes. Osteocytic Vhl deletion caused HBM phenotype, but Hif1a was dispensable in osteocytes. Vhl cKO mice revealed enhanced canonical Wnt signaling. B cell development was reduced while myelopoiesis increased in osteocytic Vhl cKO, revealing a novel influence of Vhl/HIF-α function in osteocytes on maintenance of bone microarchitecture via canonical Wnt signaling and effects on hematopoiesis

Sostdc1 deficiency accelerates fracture healing by promoting the expansion of periosteal mesenchymal stem cells

Loss of Sostdc1, a growth factor paralogous to Sost, causes the formation of ectopic incisors, fused molars, abnormal hair follicles, and resistance to kidney disease. Sostdc1 is expressed in the periosteum, a source of osteoblasts, fibroblasts and mesenchymal progenitor cells, which are critically important for fracture repair. Here, we investigated the role of Sostdc1 in bone metabolism and fracture repair. Mice lacking Sostdc1 (Sostdc1−/−) had a low bone mass phenotype associated with loss of trabecular bone in both lumbar vertebrae and in the appendicular skeleton. In contrast, Sostdc1−/− cortical bone measurements revealed larger bones with higher BMD, suggesting that Sostdc1 exerts differential effects on cortical and trabecular bone. Mid-diaphyseal femoral fractures induced in Sostdc1−/− mice showed that the periosteal population normally positive for Sostdc1 rapidly expands during periosteal thickening and these cells migrate into the fracture callus at 3 days post fracture. Quantitative analysis of mesenchymal stem cell (MSC) and osteoblast populations determined that MSCs express Sostdc1, and that Sostdc1−/− 5 day calluses harbor > 2-fold more MSCs than fractured wildtype controls. Histologically a fraction of Sostdc1-positive cells also expressed nestin and α-smooth muscle actin, suggesting that Sostdc1 marks a population of osteochondral progenitor cells that actively participate in callus formation and bone repair. Elevated numbers of MSCs in D5 calluses resulted in a larger, more vascularized cartilage callus at day 7, and a more rapid turnover of cartilage with significantly more remodeled bone and a thicker cortical shell at 21 days post fracture. These data support accelerated or enhanced bone formation/remodeling of the callus in Sostdc1−/− mice, suggesting that Sostdc1 may promote and maintain mesenchymal stem cell quiescence in the periosteum

Conditional Deletion of Sost in MSC‐derived lineages Identifies Specific Cell Type Contributions to Bone Mass and B Cell Development

Sclerostin (Sost) is a negative regulator of bone formation and blocking its function via antibodies has shown great therapeutic promise by increasing both bone mass in humans and animal models. Sclerostin deletion in Sost knockout mice (Sost‐/‐) causes high bone mass (HBM) similar to Sclerosteosis patients. Sost‐/‐ mice have been shown to display an up to 300% increase in bone volume/total volume (BV/TV), relative to aged matched controls, and it has been postulated that the main source of skeletal Sclerostin is the osteocyte. To understand the cell‐type specific contributions to the HBM phenotype described in Sost‐/‐ mice, as well as to address the endocrine and paracrine mode of action of sclerostin, we examined the skeletal phenotypes of conditional Sost loss‐of‐function (SostiCOIN/iCOIN) mice with specific deletions in (1) the limb mesenchyme (Prx1‐Cre; targets osteoprogenitors and their progeny); (2) mid‐stage osteoblasts and their progenitors (Col1‐Cre); (3) mature osteocytes (Dmp1‐Cre) and (4) hypertrophic chondrocytes and their progenitors (ColX‐Cre). All conditional alleles resulted in significant increases in bone mass in trabecular bone in both the femur and lumbar vertebrae, but only Prx1‐Cre deletion fully recapitulated the amplitude of the HBM phenotype in the appendicular skeleton and the B cell defect described in the global knockout. Despite wildtype expression of Sost in the axial skeleton of Prx1‐Cre deleted mice, these mice also had a significant increase in bone mass in the vertebrae, but the Sclerostin released in circulation by the axial skeleton did not affect bone parameters in the appendicular skeleton. Also, both Col1 and Dmp1 deletion resulted in a similar 80% significant increase in trabecular bone mass, but only Col1 and Prx1 deletion resulted in a significant increase in cortical thickness. We conclude that several cell types within the Prx1‐osteoprogenitor derived lineages contribute significant amounts of Sclerostin protein to the paracrine pool of Sost, in bone