Detection of Bovine Papilloma Viruses in Wart‐Like Lesions of Upper Gastrointestinal Tract of Cattle and Buffaloes

In present investigation, etiopathological characterization of upper gastrointestinal tract (GIT) tumours of cattle and buffaloes was undertaken. A total of 27 GIT wart‐like lesions in rumen, reticulum, mouth and oesophagus of cattle and buffaloes revealed the presence of small nodular to larger spherical or slender growths with thin base present on mucosa and ruminal pillar. Histopathologically, these cases were diagnosed as fibropapilloma/papilloma. This is the first world record on ruminal papillomatosis in buffaloes. Ruminal warts of cattle and buffaloes revealed the presence of BPV‐5, ‐1 & ‐2, which is the first report of presence of these BPVs in the ruminal warts from India. Quantitative real‐time PCR revealed that DNA samples of different GIT wart‐like lesions contained varying amount of BPV DNA copy numbers. Immunohistochemistry revealed that the PCNA and Ki67 immunopositivity was present in the basal and spinosum layer of the fibropapilloma/papilloma, indicating these as the cellular proliferation site. In conclusion, the present investigation revealed that BPV‐5, ‐1 & ‐2 are associated with certain ruminal wart‐like lesions/growths in cattle and buffaloes, and the basal and spinosum layer of the ruminal fibropapilloma/papilloma were cellular proliferation sites.     

Prediction Model for Low Birth Weight and its Validation

Objective

To evaluate the factors associated with low birth weight (LBW) and to formulate a scale to predict the probability of having a LBW infant.

Methods

This hospital based case–control study was conducted in a tertiary care university hospital in North India. The study included 250 LBW neonates and 250 neonates with birth weight ≥2,500 g. Data were collected by interviewing mothers using pre-designed structured questionnaire and from hospital records.

Results

Factors significantly associated with LBW were inadequate weight gain by the mother during pregnancy (<8.9 kg), inadequate proteins in diet (<47 g/d), previous preterm baby, previous LBW baby, anemic mother and passive smoking. The prediction model made on these six variables has a sensitivity of 71.6 %, specificity 67.0 %, positive LR 2.17 and negative LR of 0.42 for a cut-off score of ≥29.25. On validation, it has a sensitivity of 72 % and specificity of 64 %.

Conclusions

It is possible to predict LBW using a prediction model based on significant risk factors associated with LBW.     

Reserpine modulates neurotransmitter release to extend lifespan and alleviate age-dependent Aβ proteotoxicity in Caenorhabditis elegans

Aging is a debilitating process often associated with chronic diseases such as diabetes, cardiovascular and neurodegenerative diseases like Alzheimer's disease (AD). AD occurs at a very high incidence posing a huge burden to the society. Model organisms such as C. elegans become essential to understand aging or lifespan extension - the etiology, molecular mechanism and identification of new drugs against age associated diseases. The AD model, manifesting Aβ proteotoxicity, in C. elegans is well established and has provided valuable insights. Earlier, we have reported that Reserpine, an FDA-approved antihypertensive drug, increases C. elegans lifespan with a high quality of life and ameliorates Aβ toxicity in C. elegans. But reserpine does not seem to act through the known lifespan extension pathways or inhibition of its known target, vesicular monoamine transporter, VMAT. Reserpine's mode of action and the pathways it activates are not known. Here, we have evaluated the presynaptic neurotransmitter(s) release pathway and identified acetylcholine (ACh) as the crucial player for reserpine's action. The corroborating evidences are: i) lack of lifespan extension in the ACh loss of function (hypomorphic) - synthesis (cha-1) and transport (unc-17) mutants; ii) mitigation of chronic aldicarb effect; iii) lifespan extension in dopamine (cat-2) and dopamine and serotonin (bas-1) biosynthetic mutants; iv) no rescue from exogenous serotonin induced paralysis in the AD model worms; upon reserpine treatment. Thus, modulation of acetylcholine is essential for reserpine's action.