Treatment of vaginal prolapse in cows and buffaloes.
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Biomedical subjects
Publications and source records attributed to B B Singh.
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A random survey was conducted to study the epidemiology of brucellosis in Punjab (India), using the 'Survey Toolbox' sampling software. A two-stage sampling procedure was adopted: in the first stage, villages were selected, and in the second the selection of animals was made. In all, 52 villages were selected randomly from a sampling frame of all the villages of Punjab. The total number of animals in these villages was 18,644, out of which 973 animals (approximately 5%) belonging to various owners were randomly selected. Serum samples collected from the animals were screened for Brucella antibodies by an avidinbiotin enzyme-linked immunosorbent assay, which showed the apparent overall prevalence of brucellosis to be 12.09% (true prevalence, 11.23%). The prevalence varied from a low of 0% to a high of 24.3% in various districts. Higher variance (0.08) was noted within villages than between different villages (0.03). The prevalence rates among buffaloes and cattle were 13.4% and 9.9%, respectively. The seroprevalence of brucellosis was found to be significantly higher (chi square = 24.50, p < 0.001) in animals with a history of abortion (33.87%) than in those without such a history (11.63%).
The present paper discusses a general expression for determining the minimum sample size (plants) for a given number of seeds or vice versa for capturing multiple allelic diversity. The model considers sampling from a large 2 k-ploid population under a broad range of mating systems. Numerous expressions/results developed for germplasm collection/regeneration for diploid populations by earlier workers can be directly deduced from our general expression by assigning appropriate values of the corresponding parameters. A seed factor which influences the plant sample size has also been isolated to aid the collectors in selecting the appropriate combination of number of plants and seeds per plant. When genotypic multiplicity of seeds is taken into consideration, a sample size of even less than 172 plants can conserve diversity of 20 alleles from 50,000 polymorphic loci with a very large probability of conservation (0.9999) in most of the cases.
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The Ran-binding protein 2 (RanBP2) is a vertebrate mosaic protein composed of four interspersed RanGTPase binding domains (RBDs), a variable and species-specific zinc finger cluster domain, leucine-rich, cyclophilin, and cyclophilin-like (CLD) domains. Functional mapping of RanBP2 showed that the domains, zinc finger and CLD, between RBD1 and RBD2, and RBD3 and RBD4, respectively, associate specifically with the nuclear export receptor, CRM1/exportin-1, and components of the 19 S regulatory particle of the 26 S proteasome. Now, we report the mapping of a novel RanBP2 domain located between RBD2 and RBD3, which is also conserved in the partially duplicated isoform RanBP2L1. Yet, this domain leads to the neuronal association of only RanBP2 with two kinesin microtubule-based motor proteins, KIF5B and KIF5C. These kinesins associate directly in vitro and in vivo with RanBP2. Moreover, the kinesin light chain and RanGTPase are part of this RanBP2 macroassembly complex. These data provide evidence of a specific docking site in RanBP2 for KIF5B and KIF5C. A model emerges whereby RanBP2 acts as a selective signal integrator of nuclear and cytoplasmic trafficking pathways in neurons.
Ca(2+) influx via plasma membrane Trp3 channels is proposed to be regulated by a reversible interaction with inositol trisphosphate receptor (IP(3)R) in the endoplasmic reticulum. Condensation of the cortical actin layer has been suggested to physically disrupt this interaction and inhibit Trp3-mediated Ca(2+) influx. This study examines the effect of cytoskeletal reorganization on the localization and function of Trp3 and key Ca(2+) signaling proteins. Calyculin-A treatment resulted in formation of condensed actin layer at the plasma membrane; internalization of Trp3, Galpha(q/11), phospholipase Cbeta, and caveolin-1; and attenuation of 1-oleoyl-2-acetyl-sn-glycerol- and ATP-stimulated Sr(2+) influx. Importantly, Trp3 and IP(3)R-3 remained co-localized inside the cell and were co-immunoprecipitated. Jasplakinolide also induced internalization of Trp3 and caveolin-1. Pretreatment of cells with cytochalasin D or staurosporine did not affect Trp3 but prevented calyculin-A-induced effects. Based on these data, we suggest that Trp3 is assembled in a caveolar Ca(2+) signaling complex with IP(3)R, SERCA, Galpha(q/11), phospholipase Cbeta, caveolin-1, and ezrin. Furthermore, our data demonstrate that conditions which stabilize cortical actin induce loss of Trp3 activity due to internalization of the Trp3-signaling complex, not disruption of IP(3)R-Trp3 interaction. This suggests that localization of the Trp3-associated signaling complex, rather than Trp3-IP(3)R coupling, depends on the status of the actin cytoskeleton.
Nickel has a number of adverse biological effects that have made the use of nickel in biomedical implants controversial. Yet information about the distribution of nickel in tissues around nickel-containing implants is scarce. The purpose of the current study was to use a laser ablation technique, combined with inductively coupled mass spectroscopy, to assess the spatial distribution of nickel around nickel-containing implants in vivo. Polyethylene, pure nickel wire, or a nickel-containing alloy (Ni-Cr) were implanted subcutaneously into rats for 7 days. The tissues were analyzed for Ni content and inflammation at 1-mm intervals up to 5 mm away from the implants. The sham surgery sites and the polyethylene caused mild to moderate inflammation 1-2 mm from the implant site with no detectable nickel in the tissue. The nickel wire caused severe inflammation up to 5 mm away from the implant site with necrosis for 1 mm around the implant. Nickel concentrations reached 48 microg/g near the implants, falling exponentially to undetectable levels at 3-4 mm from the implants. The Ni-Cr wire caused inflammation equivalent to polyethylene, with less than 4 microg/g of nickel present in the tissue for 1-2 mm around the implants. The current study showed that the laser-ablation technique was well suited for the analysis of soft tissues for metal-ion content, and that the nickel distribution in tissues correlated well with overt tissue inflammation.
OBJECTIVES: We developed a prognostic strategy for quantifying the long-term risk of coronary heart disease (CHD) events in survivors of acute coronary syndromes (ACS). BACKGROUND: Strategies for quantifying long-term risk of CHD events have generally been confined to primary prevention settings. The Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) study, which demonstrated that pravastatin reduces CHD events in ACS survivors with a broad range of cholesterol levels, enabled assessment of long-term prognosis in a secondary prevention setting. METHODS: Based on outcomes in 8,557 patients in the LIPID study, a multivariate risk factor model was developed for prediction of CHD death or nonfatal myocardial infarction. Prognostic indexes were developed based on the model, and low-, medium-, high- and very high-risk groups were defined by categorizing the prognostic indexes. RESULTS: In addition to pravastatin treatment, the independently significant risk factors included: total and high density lipoprotein cholesterol, age, gender, smoking status, qualifying ACS, prior coronary revascularization, diabetes mellitus, hypertension and prior stroke. Pravastatin reduced coronary event rates in each risk level, and the relative risk reduction did not vary significantly between risk levels. The predicted five-year coronary event rates ranged from 5% to 19% for those assigned pravastatin and from 6.4% to 23.6% for those assigned placebo. CONCLUSIONS: Long-term prognosis of ACS survivors varied substantially according to conventional risk factor profile. Pravastatin reduced coronary risk within all risk levels; however, absolute risk remained high in treated patients with unfavorable profiles. Our risk stratification strategy enables identification of ACS survivors who remain at very high risk despite statin therapy.
Ferredoxins are small iron sulfur proteins necessary for electron donation. FdxH1 and FdxH2 are associated with two different nif gene clusters where they transfer electrons for the reduction of nitrogenase complex. FdxH1 was observed to be stable towards oxygen, whereas, FdxH2 was relatively unstable. We had identified the amino acid involved in oxygen sensitivity of ferredoxin protein using protein modeling. The exchange of valine to leucine at position 77 was critical for ferredoxin proteins in relation to its oxygen sensitivity. This exchange leads to a longer side chain, which inhibits the accessibility of oxygen to the iron sulfur cluster. Site directed mutagenesis and in vitro experiments confirms that valine indeed is involved in the oxygen sensitivity. The exchange of leucine to valine in FdxH1 makes it oxygen unstable. Thus, from the above results we can conclude that the position of leucine at position 77 is critical for oxygen sensitivity of ferredoxin and protein modeling can be used to identify specific amino acids in other oxygen-sensitive proteins.
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BACKGROUND: Adhesion molecules have been implicated in the pathogenesis of rheumatoid arthritis and may also play a role in the pathogenesis of periodontal disease by promoting the recruitment and retention of leukocytes in gingival tissue. METHODS: The aim of the present study was to evaluate the capacity of interleukin-1beta (IL-1beta) to regulate adhesion molecule expression on clinically healthy human gingival (HGF) and periodontal ligament (PDL) fibroblasts. The HGF (n = 6) and PDL (n = 3) fibroblasts were treated with 1.0 ng/ml of IL-1beta for 24 hours and then incubated with primary intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) antibodies followed by FITC-conjugated secondary antibodies. The expression of ICAM-1 and VCAM-1 was measured by immunofluorescence flow cytometry. RESULTS: The levels of ICAM-1 expression in IL-1beta treated HGF and PDL fibroblasts were statistically significant (P < or = 0.05) compared to normal untreated controls using log-transformed data and 3-way analysis of variance. Both cells expressed VCAM-1 after IL-1beta treatment, but the levels were not statistically different from controls. CONCLUSIONS: This study demonstrated that IL-1beta upregulated ICAM-1 expression in both HGF and PDL fibroblasts. Even though the level of VCAM-1 was not statistically different from both HGF and PDL fibroblasts treated with IL-1beta compared to controls, both cells do express the VCAM-1 molecules. These results suggest that ICAM-1 and VCAM-1 might be involved in the pathogenesis of periodontal disease.
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Ayurveda, the science of life, is a comprehensive medical system that has been the traditional system of healthcare in India for more than 5000 years. This medical system was well established around 2500 to 600 BC, when it evolved into 2 schools: the School of Physicians and the School of Surgeons, similar to allopathy. Charak Samhita, Susrut Samhita, and Ashtang Hridaya Samhita are the Senior Triad texts, and Madhav Nidan Samhita, Sarangdhar Samhita, and Bhavprakash Samhita are the Junior Triad texts. Around 600 BC. Ayurveda was branched into internal medicine; pediatrics; psychiatry; surgery; eye, ear, nose, and throat; toxicology; geriatrics; and eugenics/aphrodisiacs. The body is composed of 3 body doshas, 3 mental doshas, 7 dhatus, and malas. The harmony among the body doshas of vata (nervous system), pitta (enzymes), and kapha (mucus) and the gunas, or mental doshas (which are human attributes: satogun [godly], rajas [kingly], and tamas [evil]), constitutes health, and their disharmony constitutes disease. The management of illness requires balancing the doshas back into a harmonious state through lifestyle interventions, spiritual nurturing, and treatment with herbo-mineral formulas based on one's mental and bodily constitution.
Because the disharmony of mental doshas (satogun, rajogun, and tamogun) and body doshas (vata, pitta, and kapha) are the major cause of illness, the goal of illness management in Ayurveda is to bring back harmony among the doshas. The management includes clinical examination, diagnosis, and dietary and lifestyle interventions and treatment. The clinical examination consists of Astha Sthana Pariksha (8-point diagnosis: pulse-diagnosis, urine, stool, tongue, voice and body sound, eye, skin, and total body appearance examinations) and examination of the digestive system and the patient's physical strength. The treatment consists of cleansing (Panchkarma), palliation (improve digestion, remove toxic waste, fasting, observe thirst, exercise, sunbathing, and meditation), mental nurturing, and spiritual healing depending on the disturbed doshas and the patient's constitution. The preferred use of bhasms and herbal formulas over the respective metallic salts or the single herbs is discussed. This review suggests a great potential for integration of Ayurvedic therapies into the healthcare system in the United States.
The nitrite reductase gene (nirA) from the filamentous, heterocyst-forming cyanobacterium Anabaena sp. PCC 7120 (A. PCC 7120) was expressed in Escherichia coli using the pET-system. Co-expression of the cysG gene encoding siroheme synthase of Salmonella typhimurium increased the amount of soluble, active nitrite reductase four fold. Nitrite reductase was purified to homogeneity. In order to identify amino acid residues involved in ferredoxin (PetF)-nitrite reductase electron transfer in A. PCC 7120, we performed a sequence comparison between ferredoxin-dependent nitrite reductases from various species. The alignment revealed a number of conserved residues possibly involved in ferredoxin nitrite reductase interaction. The position of these residues relative to the [4Fe4S]-cluster as the primary electron acceptor was tentatively localized in a three dimensional structure of the sulfite reductase from E. coli, which is closest related to nitrite reductase among the proteins with known tertiary structure. The exchange of certain positively charged amino acid residues of the nitrite reductase with uncharged residues revealed the influence of these residues on the interaction of nitrite reductase with reduced ferredoxin. We identified at least two separate regions of nitrite reductase that contribute to the binding of ferredoxin.
Transient receptor potential protein 1 (Trp1) has been proposed as a component of the store-operated Ca(2+) entry (SOCE) channel. However, the exact mechanism by which Trp1 is regulated by store depletion is not known. Here, we examined the role of the Trp1 C-terminal domain in SOCE by expressing hTrp1alpha lacking amino acids 664-793 (DeltaTrp1alpha) or full-length hTrp1alpha in the HSG (human submandibular gland) cell line. Both carbachol (CCh) and thapsigargin (Tg) activated sustained Ca(2+) influx in control (nontransfected), DeltaTrp1alpha-, and Trp1alpha-expressing cells. Sustained [Ca(2+)](i), following stimulation with either Tg or CCh in DeltaTrp1alpha-expressing cells, was about 1.5-2-fold higher than in Trp1alpha-expressing cells and 4-fold higher than in control cells. Importantly, (i) basal Ca(2+) influx and (ii) Tg- or CCh-stimulated internal Ca(2+) release were similar in all the cells. A similar increase in Tg-stimulated Ca(2+) influx was seen in cells expressing Delta2Trp1alpha, lacking the C-terminal domain amino acid 649-793, which includes the EWKFAR sequence. Further, both inositol 1,4,5-trisphosphate receptor-3 and caveolin-1 were immunoprecipitated with DeltaTrp1alpha and Trp1alpha. In aggregate, these data suggest that (i) the EWKFAR sequence does not contribute significantly to the Trp1-associated increase in SOCE, and (ii) the Trp1 C-terminal region, amino acids 664-793, is involved in the modulation of SOCE.