Energy determines broad pattern of plant distribution in Western Himalaya

Several factors describe the broad pattern of diversity in plant species distribution. We explore these determinants of species richness in Western Himalayas using high‐resolution species data available for the area to energy, water, physiography and anthropogenic disturbance. The floral data involves 1279 species from 1178 spatial locations and 738 sample plots of a national database. We evaluated their correlation with 8‐environmental variables, selected on the basis of correlation coefficients and principal component loadings, using both linear (structural equation model) and nonlinear (generalised additive model) techniques. There were 645 genera and 176 families including 815 herbs, 213 shrubs, 190 trees, and 61 lianas. The nonlinear model explained the maximum deviance of 67.4% and showed the dominant contribution of climate on species richness with a 59% share. Energy variables (potential evapotranspiration and temperature seasonality) explained the deviance better than did water variables (aridity index and precipitation of the driest quarter). Temperature seasonality had the maximum impact on the species richness. The structural equation model confirmed the results of the nonlinear model but less efficiently. The mutual influences of the climatic variables were found to affect the predictions of the model significantly. To our knowledge, the 67.4% deviance found in the species richness pattern is one of the highest values reported in mountain studies. Broadly, climate described by water–energy dynamics provides the best explanation for the species richness pattern. Both modeling approaches supported the same conclusion that energy is the best predictor of species richness. The dry and cold conditions of the region account for the dominant contribution of energy on species richness.     

Biosorptive removal of arsenic from drinking water

A biomass derived from the plant Momordica charantia has been found to be very efficient in arsenic(III) adsorption. An attempt was made to use this biomass for arsenic(III) removal under different conditions. The parameters optimized were contact time (5-150 min), pH (2-11), concentration of adsorbent (1-50 g/l), concentration of adsorbate (0.1-100mg/l), etc. It was observed that the pH had a strong effect on biosorption capacity. The optimum pH obtained for arsenic adsorption was 9. The influence of common ions such as Ca(2+), Mg(2+), Cd(2+), Se(4+), Cl(-), SO(4)(2-), and HCO(3)(-), at concentrations varying from 5 to 1000 mg/l was investigated. To establish the most appropriate correlation for the equilibrium curves, isotherm studies were performed for As(III) ion using Freundlich and Langmuir adsorption isotherms. The pattern of adsorption fitted well with both models. The biomass of M. charantia was found to be effective for the removal of As(III) with 88% sorption efficiency at a concentration of 0.5mg/l of As(III) solution, and thus uptake capacity is 0.88 mg As(III)/gm of biomass. It appears that this biomass should be used as a palliative food item. Further it also appears that the dietary habits may play a role in the toxic effects of ingested arsenic.     

Analysis of interaction between etoricoxib and tramadol against mechanical hyperalgesia of spinal cord injury in rats

Drug combinations have the potential advantage of greater analgesia over monotherapy. The present study was aimed to assess any possible interaction (additive or potentiation) in the antinociceptive effects of etoricoxib; a novel cyclooxygenase-2 inhibitor, and tramadol; a typical opioid agonist when administered in combination against mechanical hyperalgesia induced by spinal cord injury in rats. The nature of interaction was analyzed using surface of synergistic interaction (SSI) analysis and an isobolographic analysis. Etoricoxib or tramadol when administered alone to rats, exhibited different antihyperalgesic potencies (ED50 etoricoxib: 0.58+/-0.19 mg/kg, po; ED50 tramadol: 9.85+/-0.57 mg/kg, po). However, both the drugs were found to be long acting against this model of hyperalgesia. Further, etoricoxib and tramadol were co-administered in fixed ratios of ED50 fractions. One combination (0.29/4.79 mg/kg, po: etoricoxib/tramadol) exhibited additivity and other three combinations (0.15/2.39, 0.08/1.19, and 0.04/0.59 mg/kg, po: etoricoxib/tramadol) resulted in potentiation when analyzed by SSI. The SSI was calculated from the total antihyperalgesic effect produced by the combination after the subtraction of the antihyperalgesic effect produced by each of the individual drug. In the isobolographic analysis, the experimental ED50 was found to be far below the line of additivity also indicating a significant (P < 0.05) synergistic antihyperalgesic effect when etoricoxib and tramadol was co-administered to rats. The synergistic antihyperalgesic effect of etoricoxib and tramadol combination suggests that these combinations may have clinical utility in mechanical hyperalgesia associated with spinal injury.     

Mercury sensing and toxicity studies of novel latex fabricated silver nanoparticles

Safe and eco-friendly alternatives to currently used hazardous chemico-physical methods of silver nanoparticles (AgNPs) synthesis are need of time. Rapid, low cost, selective detection of toxic metals in environmental sample is important to take safety action. Toxicity assessment of engineered AgNPs is essential to avoid its side effects on human and non-target organisms. In the present study, biologically active latex from Euphorbia heterophylla (Poinsettia) was utilized for synthesis of AgNPs. AgNPs was of spherical shape and narrow size range (20–50 nm). Occurrence of elemental silver and crystalline nature of AgNPs was analyzed. Role of latex metabolites in reduction and stabilization of AgNPs was analyzed by FT-IR, protein coagulation test and phytochemical analysis. Latex-synthesized AgNPs showed potential in selective and sensitive detection of toxic mercury ions (Hg²⁺) with limit of detection around 100 ppb. Addition of Hg²⁺ showed marked deviation in color and surface plasmon resonance spectra of AgNPs. Toxicity studies on aquatic non-target species Daphnia magna showed that latex-synthesized AgNPs (20.66 ± 1.52 % immobilization) were comparatively very less toxic than chemically synthesized AgNPs (51.66 ± 1.52 % immobilization). Similarly, comparative toxicity study on human red blood cells showed lower hemolysis (4.46 ± 0.01 %) by latex-synthesized AgNPs as compared to chemically synthesized AgNPs causing 6.14 ± 0.01 % hemolysis.     

Characterization of a High-Affinity Mg2+-Independent Ca2+-ATPase from Rat Brain Synaptosomal Membranes

A high-affinity Mg2+-independent Ca2+-ATPase (Ca2+-ATPase) has been differentiated from the Mg2+-dependent, Ca2+-stimulated ATPase (Ca2+,Mg2+-ATPase) in rat brain synaptosomal membranes. Using ATP as a substrate, the K0.5 of Ca2+ for Ca2+-ATPase was found to be 1.33 microM with a Km for ATP of 19 microM and a Vmax of 33 nmol/mg/min. Using Ca-ATP as a substrate, the Km for Ca-ATP was found to be 0.22 microM. Unlike Ca2+,Mg2+-ATPase, Ca2+-ATPase was not inhibited by N-ethylmaleimide, trifluoperazine, lanthanum, zinc, or vanadate. La3+ and Zn2+, in contrast, stimulated the enzyme activity. Unlike Ca2+, Mg2+-ATPase activity, ATP-dependent Ca2+ uptake was negligible in the absence of added Mg2+, indicating that the Ca2+ transport into synaptosomal endoplasmic reticulum may not be a function of the Ca2+-ATPase described. Ca2+-ATPase activity was not stimulated by the monovalent cations Na+ or K+. Ca2+, Mg2+-ATPase demonstrated a substrate preference for ATP and ADP, but not GTP, whereas Ca2+-ATPase hydrolyzed ATP and GTP, and to a lesser extent ADP. The results presented here suggest the high-affinity Mg2+-independent Ca2+-ATPase may be a separate form from Ca2+,Mg2+-ATPase. The capacity of Mg2+-independent Ca2+-ATPase to hydrolyze GTP suggests this protein may be involved in GTP-dependent activities within the cell.     

Hepatic Deficiency of Augmenter of Liver Regeneration Exacerbates Alcohol-Induced Liver Injury and Promotes Fibrosis in Mice

Why only a subpopulation (about 15%) of humans develops liver cirrhosis due to alcohol is a critical as yet unanswered question. Liver-specific depletion of augmenter of liver regeneration (ALR) protein in mice causes robust steatosis and hepatocyte apoptosis by 2 weeks; these pathologies regress subsequently with return of ALR expression even at lower than control levels, but the mice develop modest steatohepatitis by 8 weeks. We aimed to investigate whether chronic alcohol ingestion promotes excessive hepatic fibrosis in these ALR-deficient mice. Liver-specific ALR-deficient and wild type (WT) female mice (8–10 weeks old) were placed on 4% alcohol-supplemented or isocaloric diet for 4 weeks. Liver sections were examined for histopathology, and parameters of steatosis and fibrosis were quantified. The mRNA expression of alcohol dehydrogenase-1, acetaldehyde dehydrogenase-1 and cytochrome P450-2E1 increased in WT mice but decreased in ALR-deficient mice upon alcohol ingestion. While alcohol induced steatosis and mild inflammation in WT mice, ALR-deficient mice showed minimal steatosis, strong hepatocellular injury and inflammation, prominent ductular proliferation, and robust fibrosis. Compared to the WT mice, alcohol feeding of ALR-deficient mice resulted in significantly greater increase in hepatic TNFα and TGFβ, and oxidative stress; there was also hepatic iron accumulation, robust lipid peroxidation and mitochondrial DNA damage. Importantly, similar to ALR-deficient mice, lower hepatic ALR levels in human alcoholic liver cirrhosis were associated with increased iron content, reduced expression of alcohol dehydrogenase and acetaldehyde dehydrogenase, and elevated fibrogenic markers. We conclude that ALR deficiency or anomaly can play a critical role in alcohol-induced hepatic fibrosis/cirrhosis, mechanisms of which may involve dysregulation of alcohol metabolism and iron homeostasis, mitochondrial damage and oxidative injury.     

Heightened NTPDase-1/CD39 expression and angiogenesis in radiation proctitis

Radiation proctitis is an inflammatory process associated with persistent and refractory lower gastrointestinal bleeding. Purinergic signaling regulates hemostasis, inflammation, and angiogenesis. For example, CD39, the vascular ectonucleotidase, blocks platelet activation and is required for angiogenesis. Whether CD39 expression is affected by radiation injury is unknown. The aim of this work was to study CD39 expression patterns after clinical radiation injury to the rectum. We prospectively enrolled eight patients with radiation proctitis and five gender-matched controls. Biopsies were taken from normal-appearing rectal mucosa of controls and from the normal sigmoid and abnormal rectum of patients. Expression patterns of CD39, P2Y2 receptor, CD31, CD61 integrin, and vascular endothelial growth factor receptor 2 were examined by immunostaining; levels of CD39 were further evaluated by Western blots. Chronic inflammatory lesions of radiation proctitis were associated with heightened levels of angiogenesis. Immunohistochemical stains showed increased vascular expression of CD39, as confirmed by Western blots. CD39 was co-localized with vascular endothelial markers CD31 and CD61 integrin, as well as expressed by stromal tissues. Development of neovasculature and associated CD39 expression in radiation proctitis may be associated with the chronic, refractory bleeding observed in this condition.     

Force spectroscopy and fluorescence microscopy of dsDNA–YOYO-1 complexes: implications for the structure of dsDNA in the overstretching region

When individual dsDNA molecules are stretched beyond their B-form contour length, they reveal a structural transition in which the molecule extends 1.7 times its contour length. The nature of this transition is still a subject of debate. In the first model, the DNA helix unwinds and combined with the tilting of the base pairs (which remain intact), results in a stretched form of DNA (also known as S-DNA). In the second model the base pairs break resulting effectively in two single-strands, which is referred to as force-induced melting. Here a combination of optical tweezers force spectroscopy with fluorescence microscopy was used to study the structure of dsDNA in the overstretching regime. When dsDNA was stretched in the presence of 10 nM YOYO-1 an initial increase in total fluorescence intensity of the dye–DNA complex was observed and at an extension where the dsDNA started to overstretch the fluorescence intensity leveled off and ultimately decreased when stretched further into the overstretching region. Simultaneous force spectroscopy and fluorescence polarization microscopy revealed that the orientation of dye molecules did not change significantly in the overstretching region (78.0°± 3.2°). These results presented here clearly suggest that, the structure of overstretched dsDNA can be explained accurately by force induced melting.     

Modulatory effect of diclofenac on antispasmodic effect of pitofenone in cholinergic spasm

Biliary, ureteric and intestinal colic are extremely common clinical conditions associated with smooth muscle spasm. In the present study, antispasmodic activity was carried out against acetylcholine (10-640 ng/ml)-induced contractions on guinea pig ileum. Acetylcholine (10-640 ng/ml) induced concentration-dependent contraction of smooth muscle. Diclofenac, in varying concentration (9.4 x 10(-5) mol/l and 14.1 x 10(-5) mol/l) shifted the concentration response curve of acetylcholine to the right without suppressing the maximal response. However, in higher concentration diclofenac (18.9 x 10(-5) mol/l) blocked the response in an unsurmountable fashion. Further, analgin (11.09 x 10(-5), 16.63 x 10(-5) and 22.18 x 10(-5) mol/l) in equimolar concentrations did not alter the concentration response curve of acetylcholine, but in higher concentration analgin (44.36 x 10(-5) mol/l) also blocked the response in an unsurmountable fashion. Pitofenone (2.5 x 10(-6) mol/l) also, shifted the concentration response curve of acetylcholine to right in a parallel fashion with no change in maximal response. The present study confirms the potent antispasmodic activity of diclofenac-pitofenone combination in comparison to analgin-pitofenone in molar equivalent concentration (in comparison to diclofenac) against acetylcholine-induced contractions of guinea pig ileum.