Protective effects of noradrenaline on benzo[a]pyrene-induced oxidative stress responses in brain tumor cell lines.

Benzo[a]pyrene (B[a]P) is an ubiquitous environmental pollutant that is generated during combustion of fossil fuels. We examine the effect of noradrenaline (NA) on B[a]P-induced neurotoxicity in brain tumor cell lines like neuroblastoma (Neuro2a) and glioma (C6). We pre-treated tumor cells with NA for 6 h, followed by addition of B[a]P for additional 24 h. Cell viability was measured using trypan blue dye-exclusion assay and comet assay was performed to measure DNA damage. Cell cycle status was analyzed using flow cytometry and oxidative DNA damage (8-oxodG) production was examined by immunostaining. The intracellular Ca2+ concentration was analyzed using Fura-2AM. Our results showed viability of Neuro2a and C6 cells declined (24% and 20%) in B[a]P-treated groups. However, pre-treating with NA increased viability of cells by reducing percentage of cell death in both. Furthermore, B[a]P-induced deregulation of cell cycle (G2/M and S phase cell arrest) was significantly restored by pre-treatment with NA in Neuro2a cells as compared to C6 cells. We further observed increased 8-oxodG production in B[a]P-treated cells; however, NA pre-treatment significantly (p < 0.05) reduced the 8-oxodG production in Neuro2a, while C6 cells were less affected possibly due to better protective machinery. B[a]P-induced intracellular Ca2+ influx was significantly reduced in both the cell lines due to co-treatment of NA possibly by reducing Ca2+ influx. NA protects brain tumor cells against B[a]P-induced neurotoxicity may be by decreasing percentage of G2 cell arrest, oxidative DNA damage, and reducing intracellular Ca2+ influx. These findings suggested that NA may be considered as a natural potential protective agent against B[a]P-induced neurotoxicity. Graphical abstract Graphical abstract showing differential protective mechanism of NA against B[a]P-induced toxicity through antioxidant mechanism maintaining homeostasis for oxidative stress in Neuro2a and C6 cell lines. The schematic graph showed the biological significance of the NA that regulates the induction of metabolic processes of cell cycle after exposure to the environmental pollutants. B[a]P increases the intracellular levels of Ca2+, but also induces damage to cellular molecules including DNA causing cell cycle arrest. The B[a]P-induced DNA damage due to base lesions generated in the genome, 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) is one of the most abundant because of guanine's lowest redox potential among DNA bases through intracellular calcium homoeostasis.

Metal Immiscibility Route to Synthesis of Ultrathin Carbides, Borides, and Nitrides.

Ultrathin ceramic coatings are of high interest as protective coatings from aviation to biomedical applications. Here, a generic approach of making scalable ultrathin transition metal-carbide/boride/nitride using immiscibility of two metals is demonstrated. Ultrathin tantalum carbide, nitride, and boride are grown using chemical vapor deposition by heating a tantalum-copper bilayer with corresponding precursor (C2 H2 , B powder, and NH3 ). The ultrathin crystals are found on the copper surface (opposite of the metal-metal junction). A detailed microscopy analysis followed by density functional theory based calculation demonstrates the migration mechanism, where Ta atoms prefer to stay in clusters in the Cu matrix. These ultrathin materials have good interface attachment with Cu, improving the scratch resistance and oxidation resistance of Cu. This metal-metal immiscibility system can be extended to other metals to synthesize metal carbide, boride, and nitride coatings.

Mycotic keratitis in India: a five-year retrospective study.

BACKGROUND: Mycotic keratitis is a fungal infection of the cornea. This infection is difficult to treat and it can lead to severe visual impairment or blindness. It is worldwide in distribution, but is more common in the tropics and subtropical regions. Trauma is the major predisposing factor, followed by ocular and systemic defects, prior application of corticosteroids, and prolonged use of antibiotic eye-drops. The objective of this study was to determine causative agents and to identify the predisposing factors of mycotic keratitis. METHODOLOGY: Corneal scrapings from 90 corneal ulcer patients with suspected fungal etiology were subjected to direct examination by 10% KOH mount, Gram stain and culture. RESULTS: This study included 90 subjects with corneal ulcers, based on clinical suspicion, of whom 41 cases were diagnosed with mycotic keratitis in the laboratory. Among these 41 cases, culture showed fungal growth only in 36 cases whereas the remaining five cases were positive only by potassium hydroxide (KOH) preparation. Males were more commonly affected and were mostly in the age group of 31-40 years. Aspergillus flavus was the most common fungus isolated followed by fusarium solani. CONCLUSION: Rapid diagnosis and early institution of antifungal therapy is necessary to prevent ocular morbidity and blindness. Although culture helps in definite diagnosis and identification, direct microscopic detection of fungal structures in corneal scrapes or biopsies permits a rapid presumptive diagnosis.

Risk assessment for pressure ulcer: a hospital-based study.

AIM: To identify patients at risk for developing pressure ulcer among hospitalized patients and the prevalence of pressure ulcer in this group. PATIENTS AND METHOD: A prospective study included 100 patients from medical and surgical wards. Data were collected on admission, and subjects were followed up at regular intervals. The Waterlow pressure ulcer risk assessment tool was completed and patients were stratified "as not at risk," "at risk", "high risk", and "very high risk". Subjects were then monitored for 2 weeks and the actual incidence of pressure ulcer formation was analyzed in the various risk groups. RESULTS: Of 100 patients studied, 20% were at risk, 10% were assessed at high risk, and 7% were classified as at very high risk for developing a pressure ulcer. Necessary preventive measures were taken (posture change, specialized beds/mattresses, nursing care, nutritional input, etc) for those patients at risk of development of pressure ulcer. Four of 7 patients (57.1%) who were at very high-risk developed pressure ulcer as compared with 2 of 10 patients (20%) categorized in the high-risk category within a period of 2 weeks. No patient who was classified as not at risk on the Waterlow pressure ulcer risk assessment tool developed a pressure ulcer within the observation period. CONCLUSION: Pressure ulcers developed in identified risk groups despite adequate available preventive measure being taken to prevent their development. It is of extreme importance to identify patients at risk for the development of pressure ulcers so that preventive measures can be instituted to reduce the incidence of hospital-acquired pressure ulcers.