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Hantaviruses rewire the host cell and induce extensive membrane rearrangements for their replication and the morphogenesis of the virion. Transmission electron microscopy (TEM) is a powerful technique for imaging these pathological membrane changes especially when combined with large volume electron tomography. Excellent preservation of membrane structure can be obtained when chemical fixation is combined with cryofixation via high pressure freezing making the samples amenable to serial-section tomographic reconstruction. Taking advantage of this, we have optimized a hybrid method that employs aldehyde fixation, a step that is essential for virus inactivation, followed by high-pressure freezing for ultrastructural study of Hantaan (HTN) and Andes (AND) virus infected Vero E6 cells. HTNV and ANDV are two species of the Orthohantavirus, from the Old and New World, respectively, and the causative agents of hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome in humans. We applied the method for the qualitative assessment of the perturbation of the endomembrane system induced by HTNV and ANDV in infected vs. mock-infected cells. Screening of serial-sections revealed consistency of membrane preservation across large volumes indicating potential of these samples for tomographic studies. Images revealed large-scale perturbations of the endomembrane system following HTNV-infection that included the dilation of the rough endoplasmic reticulum and fragmentation of the Golgi apparatus. Infected cells exhibited a tendency to accumulate large numbers of vacuoles that were especially apparent in ANDV. In summary, our hybrid method provides a path for the study of BSL-3 pathogens using cutting edge 3D-imaging technologies.

Aim: The present study was conducted to determine the podoplanin expression in odontogenic tumors and cysts. Materials and Methods: It consisted of 12 cases of the keratocystic odontogenic tumor (KCOT), 10 cases of ameloblastoma, 8 cases of dentigerous cysts (DC), 8 cases of radicular cysts (RC) and 8 dental follicles (DF) as controls which were immunohistochemically evaluated using an antibody against podoplanin. Results: Immunostaining intensity, % of PPC and total score of ameloblastoma was higher than DC and DF but less than KCOT (t- 1.48). When DC was compared with KCOT and RC, the podoplanin expression was significantly higher with DC (P < 0.05). The podoplanin expression was comparatively higher with KCOT as compared to RC and DC. OT (t-4.40) revealed higher podoplanin expression as compared to OC and DF (t-5.54). Conclusion: There was significantly higher expression of podoplanin in cases of ameloblastoma and KCOT as compared to the RC, DC and DF. Podoplanin may be considered as a useful marker to delineate the aggressiveness of ameloblastoma and KCOT.

Group IV phospholipase A2α (cPLA2α) regulates the production of prostaglandins and leukotrienes via the formation of arachidonic acid from membrane phospholipids. The targeting and membrane binding of cPLA2α to the Golgi involves the N-terminal C2 domain, whereas the catalytic domain produces arachidonic acid. Although most studies of cPLA2α concern its catalytic activity, it is also linked to homeostatic processes involving the generation of vesicles that traffic material from the Golgi to the plasma membrane. Here we investigated how membrane curvature influences the homeostatic role of cPLA2α in vesicular trafficking. The cPLA2α C2 domain is known to induce changes in positive membrane curvature, a process which is dependent on cPLA2α membrane penetration. We showed that cPLA2α undergoes C2 domain-dependent oligomerization on membranes in vitro and in cells. We found that the association of the cPLA2α C2 domain with membranes is limited to membranes with positive curvature, and enhanced C2 domain oligomerization was observed on vesicles ~50 nm in diameter. We demonstrated that the cPLA2α C2 domain localizes to cholesterol enriched Golgi-derived vesicles independently of cPLA2α catalytic activity. Moreover, we demonstrate the C2 domain selectively localizes to lipid droplets whereas the full-length enzyme to a much lesser extent. Our results therefore provide novel insight into the molecular forces that mediate C2 domain-dependent membrane localization in vitro and in cells.

Diagnosis of arsenicosis relies on both clinical and laboratory criteria, but principally it can be diagnosed on the basis of its cutaneous manifestations. Cutaneous manifestations (melanosis, keratosis, and cutaneous cancers) are essential clues in the diagnosis, and trained dermatologists or arsenic experts are able to clinically confirm a case even without laboratory backup. Although systemic manifestations are not considered as diagnostic hallmarks, yet their presence serves as important telltale signs in arriving at the diagnosis. In countries where laboratory facilities are available, measuring the level of arsenic in drinking water (consumed in the last 6 months), urine, hair, and nails is of immense value. Newer biomarkers of arsenic exposure are being explored to provide early information about arsenic intoxication, of which urinary porphyrin level, blood metallothionein have shown promising results. Controlling the problem of arsenicosis depends on various factors, of which the most important is cessation of intake of arsenic-contaminated water. Deep wells, traditional dug wells, treatment of surface water, rainwater harvesting, and removing arsenic from the contaminated water by arsenic removal plant or arsenic treatment unit are the available options for providing arsenic-free drinking water. The role of nutrition and antioxidants in preventing the onset of symptoms of arsenicosis is also of importance. Nonspecific therapies (e.g., keratolytics for hyperkeratosis) cannot also be ignored and serve as palliative measures. The persons affected need to be followed up at regular intervals to detect the onset of cancers (if any) at the earliest. Role of counseling and education should never be underestimated since absence of public awareness can undermine all efforts of mitigation measures. [ABSTRACT FROM AUTHOR]

Arsenicosis is a multisystem disorder, with virtually no system spared from its vicious claw; though its predominant manifestations are linked to cutaneous involvement. Cutaneous effects take the form of pigmentary changes, hyperkeratosis, and skin cancers (Bowen.s disease, squamous cell carcinoma, and basal cell epithelioma). Peripheral vascular disease (blackfoot disease), hypertension, ischemic heart disease, noncirrhotic portal hypertension, hepatomegaly, peripheral neuropathy, respiratory and renal involvement, bad obstetrical outcome, hematological disturbances, and diabetes mellitus are among the other clinical features linked to arsenic toxicity. The effects are mediated principally by the trivalent form of arsenic (arsenite), which by its ability to bind with sulfhydryl groups present in various essential compounds leads to inactivation and derangement of body function. Though the toxicities are mostly linked to the trivalent state, arsenic is consumed mainly in its pentavalent form (arsenate), and reduction of arsenate to arsenite is mediated through glutathione. Body attempts to detoxify the agent via repeated oxidative methylation and reduction reaction, leading to the generation of methylated metabolites, which are excreted in the urine. Understandably the detoxification/bio-inactivation process is not a complete defense against the vicious metalloid, and it can cause chromosomal aberration, impairment of DNA repair process, alteration in the activity of tumor suppressor gene, etc., leading to genotoxicity and carcinogenicity. Arsenic causes apoptosis via free radical generation, and the cutaneous toxicity is linked to its effect on various cytokines (e.g., IL-8, TGF-β, TNF-α, GM-CSF), growth factors, and transcription factors. Increased expression of cytokeratins, keratin-16 (marker for hyperproliferation) and keratin-8 and -18 (marker for less differentiated epithelial cells), can be related to the histopathological findings of hyperkeratosis and dysplastic cells in the arsenicosis skin lesion. [ABSTRACT FROM AUTHOR]

Arsenicosis is a global problem but the recent data reveals that Asian countries, India and Bangladesh in particular, are the worst sufferers. In India, the state of West Bengal bears the major brunt of the problem, with almost 12 districts presently in the grip of this deadly disease. Recent reports suggest that other states in the Ganga/Brahmaputra plains are also showing alarming levels of arsenic in ground water. In West Bengal, the majority of registered cases are from the district of Nadia, and the maximum number of deaths due to arsenicosis is from the district of South 24 Paraganas. The reason behind the problem in India is thought to be mainly geogenic, though there are instances of reported anthropogenic contamination of arsenic from industrial sources. The reason for leaching of arsenic in ground water is attributed to various factors, including excessive withdrawal of ground water for the purpose of irrigation, use of bio-control agents and phosphate fertilizers. It remains a mystery why all those who are exposed to arsenic-contaminated water do not develop the full-blown disease. Various host factors, such as nutritional status, socioeconomic status, and genetic polymorphism, are thought to make a person vulnerable to the disease. The approach to arsenicosis mitigation needs be holistic, sustainable, and multidisciplinary, with the 2 main pillars being health education and provision of .arsenic-free water.. In the state of West Bengal, the drive for arsenic mitigation has been divided into 3 phases using various methods, including new hand pumps/tube wells at alternative deep aquifers, dug wells, arsenic removal plants, arsenic treatment units, as well as piped and surface water supply schemes. The methods have their own limitations, so it is intended that a pragmatic approach be followed in the arsenicosis prevention drive. It is also intended that the preventive measures be operationally and economically feasible for the people living in the affected areas. [ABSTRACT FROM AUTHOR]

In India, Silk industry plays an important part in textile industry. Muga silk, the golden yellow silk is quite unique to Assam, North-east India where its production is regarded as an important tool for economic development. But, outdated manufacturing technology is followed during the silk production in Assam. The existing cooking process of silk cocoons consists of boiling of silk cocoons in a stainless steel vessel along with water and soda in an open fireplace which is highly energy inefficient. Therefore, two modified systems have been designed; one having cylindrical boiling chamber (vessel) and the other having spherical boiling chamber (vessel). Both the chambers are having a cocoon heating chamber associated with them for cooking and drying of silk cocoons simultaneously. These designs are further classified into two types of designs based on channel and nozzle type combustion chambers. Therefore, the main objective of this paper is to improve the existing designs to maximize the utilization of heat carried by the combustion gases. These modified systems are analysed by using Computational Fluid Dynamics (CFD) selecting standard k–є model. From the analysis, it is seen that these new systems having nozzle type combustion chambers are more efficient than the systems having cylindrical combustion chambers and if these systems are used in silk production, it will be very beneficial for the silk industry as well as for our society.

Background: Lupus erythematosus (LE) is an autoimmune disorder with diverse clinical manifestation ranging from mild cutaneous disorder to life-threatening systemic illness (SLE). In some patients, it remains to persist in the skin-limited form while in others it evolves into SLE. Here comes the role of identifying the markers of systemic involvement, which could determine the course and prognosis of the disease. Aim: To identify those manifestations that could be used to identify the activity of the disease SLE. Materials and Methods: An institution based, descriptive, cross-sectional study carried out over 1 year period. Sixty patients (male : female 1 : 4) with cutaneous LE were recruited for the study. The patients were classified in two groups depending on the presence or absence of ARA criteria of SLE. Detailed account of LE-specific and nonspecific lesions were noted. Statistical significance of the results was compared between the two groups using the chi-square test. Results: Among the different cutaneous manifestations, highly significant (P value