Blood alcohol levels in road traffic accidents: Factors associated and the relationship between history of alcohol consumption and blood alcohol level detection.

INTRODUCTION: Alcohol consumption contributes to a significant number of road traffic accidents (RTAs), and data regarding the reliability of history and blood alcohol content (BAC) in RTA victims are scant. METHODOLOGY: This retrospective study was conducted in the emergency departments (EDs) over 6 weeks. All adult RTAs presenting within 12 h of the incident were included for analysis. RESULTS: The study cohort included 369 RTA patients, with the mean interval before presentation being 3 h (standard deviation: 2.22). Two-wheeler accidents (77.2%) were the predominant mode of injury. Usage of a helmet and seat belt was documented in a meager (6.4% [17/267] and 8.8% [3/34], respectively). A positive history of alcohol consumption was reported by 19.5% of cases (72/369). However, BAC was detectable in 30.1% of cases (111/369), with an alarming 19.78% (73/369) being above the legal limit for driving. Nearly 77.5% (86/111) of those who tested positive for alcohol consumption were driving the vehicle involved. Positive BAC levels showed a significant association with young age (18-39 years), male gender, two-wheeler usage, and between 5 PM and 12 AM. CONCLUSION: A history of alcohol consumption leading to an RTA is not reliable in the ED. Hence, measuring BAC levels in all RTA patients provides an objective and reliable form of documentation for medico-legal purposes.

Astaxanthin inhibits JAK/STAT-3 signaling to abrogate cell proliferation, invasion and angiogenesis in a hamster model of oral cancer.

Identifying agents that inhibit STAT-3, a cytosolic transcription factor involved in the activation of various genes implicated in tumour progression is a promising strategy for cancer chemoprevention. In the present study, we investigated the effect of dietary astaxanthin on JAK-2/STAT-3 signaling in the 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis model by examining the mRNA and protein expression of JAK/STAT-3 and its target genes. Quantitative RT-PCR, immunoblotting and immunohistochemical analyses revealed that astaxanthin supplementation inhibits key events in JAK/STAT signaling especially STAT-3 phosphorylation and subsequent nuclear translocation of STAT-3. Furthermore, astaxanthin downregulated the expression of STAT-3 target genes involved in cell proliferation, invasion and angiogenesis, and reduced microvascular density, thereby preventing tumour progression. Molecular docking analysis confirmed inhibitory effects of astaxanthin on STAT signaling and angiogenesis. Cell culture experiments with the endothelial cell line ECV304 substantiated the role of astaxanthin in suppressing angiogenesis. Taken together, our data provide substantial evidence that dietary astaxanthin prevents the development and progression of HBP carcinomas through the inhibition of JAK-2/STAT-3 signaling and its downstream events. Thus, astaxanthin that functions as a potent inhibitor of tumour development and progression by targeting JAK/STAT signaling may be an ideal candidate for cancer chemoprevention.

Astaxanthin inhibits NF-κB and Wnt/ß-catenin signaling pathways via inactivation of Erk/MAPK and PI3K/Akt to induce intrinsic apoptosis in a hamster model of oral cancer.

BACKGROUND: The oncogenic transcription factors NF-κB and ß-catenin, constitutively activated by upstream serine/threonine kinases control several cellular processes implicated in malignant transformation including apoptosis evasion. The aim of this study was to investigate the chemopreventive effects of astaxanthin, an antioxidant carotenoid, in the hamster buccal pouch (HBP) carcinogenesis model based on its ability to modulate NF-κB and Wnt signaling pathways and induce apoptosis. METHODS: We determined the effect of dietary supplementation of astaxanthin on the oncogenic signaling pathways - NF-κB and Wnt/ß-catenin, their upstream activator kinases - Erk/MAPK and PI-3K/Akt, and the downstream event - apoptosis evasion by real-time quantitative RT-PCR, western blot, and immunohistochemical analyses. RESULTS: We found that astaxanthin inhibits NF-κB and Wnt signaling by downregulating the key regulatory enzymes IKKß and GSK-3ß. Analysis of gene expression and docking interactions revealed that inhibition of these pathways may be mediated via inactivation of the upstream signaling kinases Erk/Akt by astaxanthin. Astaxanthin also induced caspase-mediated mitochondrial apoptosis by downregulating the expression of antiapoptotic Bcl-2, p-Bad, and survivin and upregulating proapoptotic Bax and Bad, accompanied by efflux of Smac/Diablo and cytochrome-c into the cytosol, and induced cleavage of poly (ADP-ribose) polymerase (PARP). CONCLUSIONS: The results provide compelling evidence that astaxanthin exerts chemopreventive effects by concurrently inhibiting phosphorylation of transcription factors and signaling kinases and inducing intrinsic apoptosis. GENERAL SIGNIFICANCE: Astaxanthin targets key molecules in oncogenic signaling pathways and induces apoptosis and is a promising candidate agent for cancer prevention and therapy.

Massive calcaneal enthesopathy in a non-healing leg ulcer: a case report.

Enthesopathy at the superior or inferior surface of a calcaneus may be seen in normal individuals having degenerative osteoarthrosis. This condition is also known to occur in patients with rheumatoid arthritis, seronegative spondyloarthropathy, trauma, as well as inflammatory and metabolic diseases. Enthesopathy may sometimes be the first manifestation of a variety of rheumatic diseases. In this report, we present a case of massive enthesopathy of the superior and inferior surface of the calcaneus giving rise to an 'axe effect'.