Lung injury by amiodarone, an antiarrhythmic drug, in male rats.

Administration of single dose (175 mg/kg body wt) of amiodarone dissolved in water through gavage for 3 weeks damaged the lung and changed the content of lung lavage. Activities of bronchoalveolar lavage (BAL) angiotensin converting enzyme (ACE) and lactate dehydrogenase (LDH) increased significantly. Also, the protein and lactate content of the lavage fluid increased significantly over the control. The drug also produced marked changes in morphology of the lung of experimental animals.     

Monocytes treated with ciprofloxacin and oxyLDL express myristate,priming atherosclerosis

Antibiotics are essential in many life‐threatening diseases. On the other hand, improper use of antibiotics can be disastrous. Cell morphological changes were observed in the ciprofloxacin‐treated cells starting at 48 hours. Changes in cell morphology were continuously observed up to 14 days, which showed gradual morphological changes from monocyte to plaque‐like cells at day 12, and foam cell, which is an intermediate stage in atherosclerosis was observed at day 8, which was confirmed with Oil Red O staining. Flow cytometry data revealed that oxidized LDL (oxyLDL)‐induced cells showed 60.16% of CD64 (proinflammatory macrophage markers) and no expression of CD23 (anti‐inflammatory macrophage markers), whereas ciprofloxacin‐treated cells expressed 67.97% of CD64 and 13.78% of CD23. Chemokine antibody array analysis revealed that ciprofloxacin exposed cells showed a proinflammatory role (ENA78, Eotaxin1, Eotaxin2, IP‐10, MIG, MIP‐3β, SDF‐1β, TECK, CXCL16, and Fractalkine). Liquid chromatography with tandem mass spectrometry (LC‐MS/MS) revealed that myristic acid was incorporated into a protein with 68 kDa molecular mass in exposing oxyLDL‐induced monocytes with ciprofloxacin, which could be a reason for the observed foam cells and in vitro plaque formation. As myristic acid primes atherosclerosis, it is better to limit the intake of antibiotics like ciprofloxacin for common illness, specifically the high‐risk patients, which may contribute to atherosclerosis.     

Influence of upwelling on the chaetognath community along the Southeastern Arabian Sea

Community structure and distribution of chaetognaths were investigated along the upwelled and non-upwelled waters of Southeastern Arabian Sea (SEAS) from the coastal, shelf and open ocean regions. With the onset of monsoon, intense upwelling along the southern part of SEAS (8° 28′ N) and a weak coastal upwelling along the northern counterpart (15° 30′ N) was evident. Zooplankton biomass was observed to be high in the upwelled waters with the dominance of copepods. Chaetognaths were also observed in significant numbers all along the SEAS, however maximum numerical abundance was observed in the southern upwelled waters. Chaetognaths belonging to 10 genera were identified of which genus Flaccisagitta (54%) made the most dominant group along the entire study area followed, in order of abundance, by Serratosagitta (20%), Mesosagitta (18.2%), Sagitta (12.3%), Ferosagitta (11%) and Krohnitta (6.4%). Flaccisagitta were observed to be abundant in the upwelled waters along with Pterosagitta, Serratosagitta, Sagitta, Krohnitta and Ferosagitta whereas genus Mesosagitta dominated the non-upwelled waters of northern transects.

     

Oxidative Stress,Inflammation, and Diabetic Vasculopathies: The Role of Alpha Tocopherol Therapy

The diabetic state confers an increased propensity to accelerated atherogenesis. In addition to the established risk factors, there is evidence for increased oxidative stress and inflammation in diabetes. Increased oxidative stress is manifested by increased lipid peroxidation (e.g. increased F 2 -isoprostanes) and increased DNA damage. Evidence for increased inflammation includes increased monocyte superoxide and pro-inflammatory cytokine release (IL-1, IL-6, and TNF- &#102 ), increased monocyte adhesion to endothelium and increased levels of plasma C-reactive protein, the prototypic marker of inflammation. Most importantly, alpha tocopherol therapy, especially at high doses, clearly shows a benefit with regards to LDL oxidation, isoprostanes and a decrease in inflammatory markers such as C-reactive protein, pro-inflammatory cytokines and PAI-1 levels. Thus, it appears that, in diabetes, alpha tocopherol therapy could emerge as an additional therapeutic modality.     

Inhibition of Megakaryocyte Development in the Bone Marrow Underlies Dengue Virus-Induced Thrombocytopenia in Humanized Mice

A characteristic clinical feature of dengue virus infection is thrombocytopenia, though its underlying mechanism is not definitively determined. By adoptive transfer of human CD34⁺ fetal liver cells into immunodeficient mice, we have constructed humanized mice with significant levels of human platelets, monocytes/macrophages, and hepatocytes. Infection of these mice with both lab-adapted and clinical strains of dengue virus induces characteristic human hematological changes, including transient leukopenia and thrombocytopenia. We show that the specific depletion of human platelets is not mediated by antibodies in the periphery or reduced production of human thrombopoietin in the liver but reduction of human megakaryocytes and megakaryocyte progenitors in the bone marrow of the infected mice. These findings identify inhibition of platelet production in the bone marrow as a key mechanism underlying dengue-induced thrombocytopenia and suggest the utility of the improved humanized mouse model in studying dengue virus infection and pathogenesis in a human cell context.     

Molecular mechanism of molt-inhibiting hormone (MIH) induced suppression of ecdysteroidogenesis in the Y-organ of mud crab: Scylla serrata

The present study was focused on the regulation of ecdysteroidogenesis in the Y-organ of Scylla serrata during molting cycle. A strong expression of molt-inhibiting hormone (MIH) and phosphorylation of ERK was predominantly observed in the postmolt and intermolt stages of Y-organs, whereas protein kinase C, steroidogenic acute regulatory protein (StAR) and cytochrome P450(scc) activity were exclusively seen in the premolt stages. Interestingly, inhibition of ERK phosphorylation by PD98059 in the early postmolt (A), middle postmolt (B) and intermolt (C) stages resulted in the prominent expression of PKC and StAR in the postmolt stages. This result indicates that phosphorylation of ERK is required for suppression of ecdysteroid biosynthesis with the involvement of protein kinase C, and StAR protein.     

Antioxidant effect of eugenol in rat intestine

The effect of eugenol on the antioxidant status of the rat intestine after short and long term (15 days and 90 days respectively) oral administration of 1000 mg/kg.b.wt (a dosage which has been reported to be highly hepatoprotective) was studied. The level of lipid peroxidation products (TBARS) and the activities of glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) were found to be near normal on eugenol treatment. The level of glutathione (GSH) did not show any change on 15 days of eugenol treatment, but it was increased significantly on 90 day eugenol treatment. The activity of glutathione-S-transferases (GSTs) was increased significantly in both 15 day eugenol treated and 90-day eugenol treated groups. The results suggest that eugenol is nontoxic, protective and induces glutathione-S-transferases (GSTs) and thereby it may facilitate the removal of toxic substances from the intestine.