Evaluation of total LDH and its isoenzymes as markers in preeclampsia

BackgroundPreeclampsia, a rapidly progressing pregnancy-specific multi-systemic syndrome is globally the leading cause of maternal and neonatal morbidity and mortality. This study aims to evaluate the serum total Lactate dehydrogenase levels in women with preeclampsia when compared to normotensive pregnant women and assess the electrophoretic pattern of the LDH isoenzymes in normal pregnancy, preeclampsia and eclampsia.MethodsThe study, carried out in the Department of Biochemistry of MVJ Medical College, included 30 patients of preeclampsia and 30 normotensive gestational age-matched pregnant women admitted to the Department of OBG. Serum total LDH was analysed by DGKC method. Serum and cord blood samples for isoenzyme distribution analysis were collected from a normal pregnant woman undergoing delivery, a woman with mild eclampsia, two women with eclampsia, and analysed by slab gel electrophoresis followed by activity staining.ResultsLDH was significantly elevated in cases as well as between the case (mild and severe) groups, showed a moderate positive statistically significant correlation with systolic, diastolic blood pressure and a sensitivity of 50% and a specificity of 80%. Further, the isoenzyme pattern showed a decreasing distribution of aerobic forms of LDH in preeclampsia-eclampsia.ConclusionsSerum total LDH may serve as a robust and affordable marker of preeclampsia. Serum total LDH, along with its isoenzyme profile, might serve as a predictor and a stronger marker of preeclampsia when compared to serum LDH analysis alone. It may also be used to assess the severity of preeclampsia and hence help in predicting and preventing adverse maternal and foetal outcomes.     

Augmented Phytoextraction of Lead (Pb2+)-Polluted Soils: A Comparative Study of the Effectiveness of Plant Growth Regulators,EDTA, and Plant Growth–Promoting Rhizobacteria

Abstract

The role of gibberellic acid (GA3), indole-3-acetic acid (IAA), plant growth–promoting bacteria (Rhizobium and Azotobacter), and a synthetic chelator (EDTA; ethylenediaminetetraacetic acid) in lead (Pb) phytoextraction was evaluated using Parthenium hysterophorus (dicot, unpalatable noncrop) and Zea mays (monocot food/forage crop) plants at the flowering stage. Various plant parts were analyzed by atomic absorption/flame spectrophotometer for their Pb content. Both plant growth regulators and both growth-promoting bacteria significantly increased the plant growth in Pb-polluted soils, whereas EDTA significantly decreased growth and biomass of both plants. EDTA increased the Pb uptake (μg g^?1 dry biomass), but the total plant Pb accumulation was decreased. GA3 and IAA significantly increased both uptake and translocation, and the maximum total Pb in the entire plant of Parthenium was found with GA3 foliar spray, whereas in Z. mays the total Pb was maximum in the plant treated with GA3 in combination with EDTA, followed by the GA3 foliar spray treatment. Overall, the GA3 foliar application showed superior response compared with all other treatments. Further research is recommended to observe the role of endogenous GA3 levels in correlation with metal phytoextraction in different plants.     

Exploration of click reaction for the synthesis of modified nucleosides as chitin synthase inhibitors

Click reaction approach toward the synthesis of two sets of novel 1,2,3-triazolyl linked uridine derivatives 19a–19g and 21a–21g was achieved by Cu(I)-catalyzed 1,3-dipolar cycloaddition of 5′-azido-5′-deoxy-2′,3′-O-(1-methylethylidene)uridine (17) with propargylated ether of phenols 18a–18g and propargylated esters 20a–20g. Structure of one of the representative compound 19d was unambiguously confirmed by X-ray crystallography. Chitin synthase inhibition study of all these compounds 19a–19g and 21a–21g was carried out to develop antifungal strategy. Compounds 19d, 19e, 19f, and 21f were identified as potent chitin synthase inhibitors by comparing with nikkomycin. Compounds 19a, 19b, 19c, 19d, 21a, and 21b showed good antifungal activity against human and plant pathogens. Compounds 19a, 19b, 19f, 21c, 21f, and 21g were identified as lead chitin synthase inhibitors for further modifications by comparing results of inhibition of growth, % germ tube formation and chitin synthase activity.     

Short-term fasting attenuates the response of the HPG axis to kisspeptin challenge in the adult male rhesus monkey (Macaca mulatta)

AIMS: In primates, changes in nutritional status affect the hypothalamic-pituitary-gonadal (HPG) axis by still poorly understood mechanisms. Recently, hypothalamic kisspeptin-GPR54 signaling has emerged as a significant regulator of this neuroendocrine axis. The present study was designed to examine whether suppression of the reproductive function by acute food-restriction in a non-human primate is mediated by decreased responsiveness of the HPG axis to endogenous kisspeptin drive. MAIN METHODS: Five intact adult male rhesus monkeys habituated to chair-restraint, received intravenous boli of human kisspeptin-10 (KP10, 50 microg), hCG (50 IU), and vehicle (1 ml) in both fed and 48-h fasting conditions. Plasma concentrations of glucose, cortisol and testosterone (T) were measured by using enzymatic and specific RIAs, respectively. KEY FINDINGS: The acute 48-h fasting decreased plasma glucose (P<0.01) and T (P<0.005) levels, and increased cortisol levels (P<0.05). KP10 administration caused a robust stimulation of T secretion in both fed and fasted monkeys. However, mean T concentration and T AUC after KP10 administration were significantly (P<0.01-0.005) reduced in fasted monkeys. Likewise, the time of the first significant increase in post-KP10 T levels was also significantly (P<0.01) delayed. T response to hCG stimulation was similar in fed and fasted monkeys. SIGNIFICANCE: The present results indicate that under fasting conditions the KP10 induced T response is delayed and suppressed. These data support the notion that fasting-induced suppression of the HPG axis in the adult male rhesus monkey may involve, at least in part, a reduction in the sensitivity of the GnRH neuronal network to endogenous kisspeptin stimulation.     

PAF receptor antagonist modulates neutrophil responses with thermal injury in vivo

The role of platelet-activating factor (PAF) inCa²⁺ signaling and Ca²⁺-related enhancement ofreactive oxygen intermediate (ROI) generation in neutrophils ofburn-injured rats was ascertained by evaluating the effect of treatmentof the rats with a PAF receptor antagonist. The treatment of rats withthe antagonist also allowed us to evaluate the role of PAF in thepriming of neutrophil ROI response with burn in vivo. A full skinthickness burn injury was produced in anesthetized rats by exposing30% of total body surface area to 98°C water for 10 s. Sham andburn rats were killed 1 day later, and their blood was collected toobtain neutrophils. Fluorescence-activated cell sorter analysis wasused to quantify ROI production by the neutrophils. Cytosolic-freeCa²⁺ concentration ([Ca²⁺]_i)imaging technique was employed to measure neutrophil[Ca²⁺]_i in individual cells andmicrofluorometry for the assessment of[Ca²⁺]_i responses in suspensions ofneutrophils. There was an overt enhancement of ROI generation by burnrat neutrophils. ROI release was accompanied by a marked elevation of[Ca²⁺]_i signaling. The treatment of rats withPAF receptor antagonist before burn prevented the upregulation of both[Ca²⁺]_i and ROI generation in neutrophils.These studies indicate that enhanced ROI production in neutrophils inthe early stages after burn injury results from a PAF-mediated primingof the [Ca²⁺]_i signaling pathways in vivo.

     

Rho kinase mediates serum-induced contraction in fibroblast fibers independent of myosin LC20 phosphorylation

Fibroblasts form fibers when grown inculture medium containing native type 1 collagen. The contractileforces generated can be precisely quantified and used to analyze thesignal transduction pathways regulating fibroblast contraction. Calfserum (30%) induces a sustained contraction that is accompanied by atransient increase in intracellular calcium([Ca²⁺]_i). W-7, a calmodulin inhibitor,KN-62, an inhibitor of calcium/calmodulin-dependent protein kinase, andML-7, a myosin light-chain kinase inhibitor, had no effects on eitherthe contraction or the [Ca²⁺]_i responses.Neither genistein, a tyrosine kinase inhibitor, nor calphostin C, aprotein kinase C inhibitor, had major effects on force or[Ca²⁺]_i. In contrast, the Rho kinaseinhibitors(R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide (Y-27632) and HA1077 depressed the contraction in a dose-dependent manner without affecting the [Ca²⁺]_iresponse. Stress fiber formation was also suppressed by Y-27632. Surprisingly, calf serum, Y-27632, and calf serum plus Y-27632 did notalter mono- or diphosphorylation of the myosin regulatory light chain(MRLC) compared with control untreated fibers. These results suggestthat the sustained contraction of NIH 3T3 fibroblast fibers induced bycalf serum is mediated by Rho kinase but is independent of a sustainedincrease in [Ca²⁺]_i, calcium/calmodulin- orprotein kinase C-dependent pathways, or increases in MRLC phosphorylation.

     

Neutrophil depletion prevents intestinal mucosal permeability alterations in burn-injured rats

Cutaneous thermal injury increases intestinal mucosal permeability. The mechanisms of this functional disturbance are not fully understood. We investigated whether accumulation of neutrophils in the intestine contributes to the increase in mucosal permeability. Labeled and unlabeled lactulose and mannitol were infused into a segment of rat ileum or jejunum. Blood concentrations of [(3)H]lactulose and [(14)C]mannitol were measured after 30, 60, and 90 min. On day 1 postburn, lactulose permeability increased fourfold in the ileum and twofold in the jejunum compared with sham-burned rats; mannitol permeability increased twofold in the ileum and 1. 5-fold in the jejunum. A greater increase in permeability occurred on day 3 postburn in the ileum, but not in the jejunum. The depletion of neutrophils in burned rats prevented the increase in permeability in both segments on day 1 postburn. Histological studies of intestines from burned, with or without neutrophil depletion, and sham-burned rats showed similar morphology. However, numerous neutrophils were found in the extravascular compartment in day 1 postburn, but not in neutrophil-depleted and sham-burned rats. These findings support the concept that the burn-induced increase in mucosal permeability is produced during the accumulation of neutrophils in the intestine and can be abrogated by the depletion of neutrophils.