Investigation of Renal Protective Effect of Euphorbia antiquorum L.(Stem) in Animal Model

Introduction: Euphorbia antiquorum is a fleshy shrub belonging to the family Euphorbiaceae. It is widely distributed in the hotter parts of India. It is used as a substitute for the Ayurvedic drug ‘Snuhee’ whose accepted botanical source is Euphorbia neriifolia Linn. The leaf, stem, latex and root of Snuhee are used in treatment of diseases and conditions like, diabetes, coryza, and oedema. Objective: The present study is aimed to investigate the renal protective effect of  E. antiquorum alcoholic extracts of the stem   on alloxan (150mg/kg) induced diabetic Wistar rats. Methods: All animals were treated for 21 days and sacrificed on the last day. Unwanted placebo effect in case of the control group was blocked by executing appropriate vehicle treatment and same animal handling pattern. Extract and standard drug doses given orally were suspended in 0.9% normal saline. Blood samples were drawn from retro orbital sinus using Diethyl-ether anesthesia at weekly intervals for 3 weeks. Blood samples were labeled in such a way that analysis team was kept blind about groups and nature of the study design. Body weight measurement and blood sampling were done on 1st, 7th, 14th and 21st day of the study. Conclusion: 21 days daily treatment with a test drug of ethanolic extract of stems of Euphorbia antiquorum significantly reduced the elevated Blood glucose level, Urinary Albumin, urine creatinine, serum creatinine in alloxan induced diabetic rats. Keywords: Nephropathy, Glomerulonephritis, Creatinine, Albumin, Oedem

Estimation of population mean in two– stage sampling under a deterministic response mechanism in the presence of non-response

In the present paper, we have considered the problem of estimation of population mean in the presence of non-response under two-stage sampling. Two different models of non-response with deterministic response mechanism have been discussed in the paper. The estimators under two non-response models have been developed by using Hansen and Hurwitz (1946) technique. The expressions for the variances and estimates of variance of these estimators have been derived. The optimum values of sample sizes have been obtained by considering a suitable cost function for a fixed variance. A limited simulation study has been carried out to examine the magnitude of percent relative loss (% RL) in standard error due to non-response. An empirical study with the real populations has also been carried out to assess the % RL in standard error due to non-response

An apparatus for quantification of light and temperature cutting ability of curtains

An apparatus has been designed and developed to measure the light cutting/absorbing ability of curtains and to provide useful information on their temperature cutting ability. The apparatus is provided with various light sources with light, temperature and humidity detectors. The reproducibility of results, and effect of intensity of light (MBTL light source) on light and temperature cutting ability of six different fabric samples have been studied. The light and temperature cutting ability of the knitted fabric is found to be lower than that of woven and black out curtain fabric samples

Development of fabric smoothness tester

An instrument has been designed and developed to measure the smoothness behavior of finished cotton fabrics. The instrument is based on pendulum principle. The weight (hang on string) comprises a frictionless wheel movable along arc shaped platform. The platform acts as a sample holder. When the weight is subjected to push, it swings back and forth in the platform. The amplitude of the swing reduces due to friction of the fabric. The amplitude is inversely proportional to the friction or roughness of the fabric. Various types of finished cotton fabrics are tested on the developed instrument. The results are compared with Kawabata system to verify the working of instrument. These results are also compared with the bending length and crease recovery behavior of the particular fabric sample. It is found that the lesser the bending length the more will be the smoothness. If the crease recovery angle is high, the fabric will be smoother. One way analysis of variance has been applied to find out effect of different processes on fabric surface smoothness property

Endogenous expression of FAD-linked PS1 impairs proliferation, neuronal differentiation and survival of adult hippocampal progenitors

BACKGROUND: Alzheimer’s disease (AD) is characterized by progressive memory loss and impaired cognitive function. Early-onset familial forms of the disease (FAD) are caused by inheritance of mutant genes encoding presenilin 1 (PS1) variants. We have demonstrated that prion promoter (PrP)-driven expression of human FAD-linked PS1 variants in mice leads to impairments in environmental enrichment (EE)-induced adult hippocampal neural progenitor cell (AHNPC) proliferation and neuronal differentiation, and have provided evidence that accessory cells in the hippocampal niche expressing PS1 variants may modulate AHNPC phenotypes, in vivo. While of significant interest, these latter studies relied on transgenic mice that express human PS1 variant transgenes ubiquitously and at high levels, and the consequences of wild type or mutant PS1 expressed under physiologically relevant levels on EE-mediated AHNPC phenotypes has not yet been tested. RESULTS: To assess the impact of mutant PS1 on EE-induced AHNPC phenotypes when expressed under physiological levels, we exposed adult mice that constitutively express the PSEN1 M146V mutation driven by the endogenous PSEN1 promoter (PS1 M146V “knock-in” (KI) mice) to standard or EE-housed conditions. We show that in comparison to wild type PS1 mice, AHNPCs in mice carrying homozygous (PS1(M146V/M146V)) or heterozygous (PS1(M146V/+)) M146V mutant alleles fail to exhibit EE-induced proliferation and commitment towards neurogenic lineages. More importantly, we report that the survival of newborn progenitors are diminished in PS1 M146V KI mice exposed to EE-conditions compared to respective EE wild type controls. CONCLUSIONS: Our findings reveal that expression at physiological levels achieved by a single PS1 M146V allele is sufficient to impair EE-induced AHNPC proliferation, survival and neuronal differentiation, in vivo. These results and our finding that microglia expressing a single PS1 M146V allele impairs the proliferation of wild type AHNPCs in vitro argue that expression of mutant PS1 in the AHNPC niche impairs AHNPCs phenotypes in a dominant, non-cell autonomous manner

Regulation of hippocampal progenitor cell survival, proliferation and dendritic development by BDNF

<p>Abstract</p> <p>Background</p> <p>Environmental enrichment (EE) is known to enhance BDNF levels and neurogenesis in the adult hippocampus. To examine the role of BDNF in modulating EE-mediated adult hippocampal neurogenesis, we conditionally ablated <it>BDNF </it>expression in the hippocampus (cKO mice) and have assessed proliferation, survival, differentiation and dendritic development of hippocampal progenitors.</p> <p>Results</p> <p>We show that while the extent of cell proliferation and neuronal fate differentiation in the hippocampus of cKO mice is not different from wild-type (WT) littermates maintained in either standard or enriched conditions, reduced BDNF levels significantly impaired the survival of newborn cells in both housing conditions. In addition, while highly active enriched WT mice exhibited a robust increase in progenitor cell proliferation, highly active cKO mice showed a modest increase in cell proliferation compared to standard housed or underactive cKO mice.</p> <p>Conclusions</p> <p>There results argue that while BDNF plays a role in exercise-induced cell proliferation, other factors must contribute to this phenomenon. We also show that dendritic development was impaired in cKO mice maintained in standard housing conditions, and that EE rescued this phenotype.</p

Towards reducing tension-compression yield and cyclic asymmetry in pure magnesium and magnesium-aluminum alloy with cerium addition

In this study, we report the effect of cerium (Ce) addition on the tension-compression yield and cyclic asymmetry in commercially pure magnesium (Cp-Mg) and Mg-Al alloy at room temperature (RT). The materials examined include extruded and annealed Cp-Mg, Mg-0.5Ce, and Mg-3Al-0.5Ce alloys. Incorporation of 0.5wt.% Ce in pure Mg results in the weakening of its basal texture, uniform distribution of Mg12Ce precipitates, and refinement of the grain size. Consequently, the tensile yield strength and ductility of pure Mg increase, and tension-compression yield asymmetry is eliminated. However, the presence of 3wt.% Al in Mg suppresses the beneficial effects of Ce addition. The formation of complex precipitates, such as Mg-Al-Ce and Al11Ce3, limits the weakening of the basal texture, reduction in grain size, improvement in ductility, and elimination of tension-compression yield asymmetry observed in Mg-0.5Ce. Nevertheless, Al contributes to the solid solution strengthening in Mg, resulting in the highest tensile yield strength of Mg-3Al-0.5Ce. Finally, the addition of 0.5wt.% Ce enhances the cyclic strength, stabilizes cyclic stress response, reduces inelastic strain, and minimizes cyclic asymmetry in both pure Mg and Mg-Al alloy while maintaining a comparable fatigue life. Overall, Ce addition positively impacts the microstructure and mechanical behavior of pure Mg and its investigated alloy. The reasons for these improvements are discussed in detail

Lungs deposition and pharmacokinetic study of submicron budesonide particles in Wistar rats intended for immediate effect in asthma

The purpose of the present investigation was to study the aerosolization, lungs deposition and pharmacokinetic study of inhalable submicron particles of budesonide in male Wistar rats. Submicron particles were prepared by antisolvent nanoprecipitation method and freeze-dried to obtain free flowing powder. The freeze-drying process yielded dry powder with desirable aerodynamic properties for inhalation therapy. An in-house model inhaler was designed to deliver medicine to lungs, optimized at dose level of 10 mg for 30 sec of fluidization. The in vitro aerosolization study demonstrates that submicron particles dissolve faster with improved aerosolization effect as compared to micronized budesonide. Both submicron and micron particles were compared for in vivo lungs dep- osition. The results showed that relatively high quantity of submicron particles reaches deep into the lungs as compared to micron particles. Most pronounced effect observed with submicron particles from pharmacokinetic parameters was the enhancement in peak plasma concentration (Cmax) by 28.85 %, and increase in area under concentration curve (AUC0–8h) by 30.33 % compared to micron sized particles. The results suggested that devel- oped submicronized formulation of budesonide can be used for pulmonary drug delivery for high deposition to deep lungs tissues

Sex-specific effects of microbiome perturbations on cerebral Aβ amyloidosis and microglia phenotypes.

We demonstrated that an antibiotic cocktail (ABX)-perturbed gut microbiome is associated with reduced amyloid-β (Aβ) plaque pathology and astrogliosis in the male amyloid precursor protein (APP)SWE /presenilin 1 (PS1)ΔE9 transgenic model of Aβ amyloidosis. We now show that in an independent, aggressive APPSWE/PS1L166P (APPPS1-21) mouse model of Aβ amyloidosis, an ABX-perturbed gut microbiome is associated with a reduction in Aβ pathology and alterations in microglial morphology, thus establishing the generality of the phenomenon. Most importantly, these latter alterations occur only in brains of male mice, not in the brains of female mice. Furthermore, ABX treatment lead to alterations in levels of selected microglial expressed transcripts indicative of the "M0" homeostatic state in male but not in female mice. Finally, we found that transplants of fecal microbiota from age-matched APPPS1-21 male mice into ABX-treated APPPS1-21 male restores the gut microbiome and partially restores Aβ pathology and microglial morphology, thus demonstrating a causal role of the microbiome in the modulation of Aβ amyloidosis and microglial physiology in mouse models of Aβ amyloidosis