Applying Haddon Matrix for Evaluation of Road Crash Victims in Delhi,India

Road traffic injuries are placing an increasing and disproportionate global health burden upon developing countries. An understanding of region specific epidemiological risk factors is imperative in order to plan appropriate prevention and control strategies. The objective of the study was to evaluate epidemiological risk factors of road traffic injury victims in Delhi, India with the help of Haddon injury analysis framework. The current study was conducted among crash victims admitted to the government hospital. Data obtained from the hospital, police records and crash victims was triangulated with geospatial analysis. Haddon matrix was utilized to understand the interplay of human, vehicle and environmental factors in pre-crash, crash and post-crash phases of an accident. A total of 544 victims were included as study participants with mean age of 30.8 years for males and 31.81 years for females and were from lower socio-economic groups. Pedestrians (36.2%) and two-wheeler riders, especially those on pillion vehicles (21.5%), were worst affected victims. The crude odds ratio for motorized road users for experiencing a crash was higher on slippery roads [p < 0.05; OR = 0.197 (0.082–0.474)]. Moderate to heavy traffic flow (p = 0.001; OR = 0.469 (0.317–0.696) was found to be a protective factor for accidents. Geospatial analysis revealed clustering of crashes near traffic lights, markets and schools. Integrated approaches addressing engineering, technological and environmental factors along with behavioural modifications is needed to produce definitive changes in road crash trends.     

Cavernous sinus haemangioma: systematic review and pooled analysis relating to a rare skull base pathology

Neurosurgical Review - Cavernous sinus haemangiomas (CSHs) are rare malformations of the microcirculation arising from the cavernous sinus. A systematic review and pooled data analysis of the...     

Letter to the editor concerning “A systematic review and meta-analysis on the management of accidental dural tears in spinal surgery: drowning in information but thirsty for a clear message” by Alshameeri ZAF,et al. [Eur Spine J (2020); DOI 10.1007/s00586-020-06401-y]

European Spine Journal -     

The role of RAS in the pathogenesis of preeclampsia

Preeclampsia is a hypertensive disorder that is unique to pregnancy, with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression in human preeclampsia and in transgenic mouse models with a human preeclampsia-like syndrome shows that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. Vascular maladaptation in preeclampsia with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms through angiotensin receptor type I (AT1) activation. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT1 and bradykinin B2 receptor heterodimerization and the production of autoantibody against AT1. Various organ systems with predilection for involvement in preeclampsia are sites of tissue-based RAS. Angiotensin II-mediated mechanisms may explain the primary clinicopathologic features of preeclampsia. In this review, these various aspects are critically examined and an integrated concept on the role of RAS in preeclampsia is presented.     

Discordant intracellular and plasma D-2-hydroxyglutarate levels in a patient with IDH2 mutated angioimmunoblastic T-cell lymphoma

Objectives: Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive peripheral T-cell lymphoma with mutations in genes encoding isocitrate dehydrogenase1 and 2 (IDH1 and IDH2). Mutant IDH generates the oncometabolite D-2-hydroxyglutarate (D-2HG). We report the first case of discordant intracellular and plasma D-2HG levels in a patient with IDH2 R172S mutated AITL. Methods: An 87-year-old woman was diagnosed with AITL in the groin lymph node by morphologic and immunophenotypic analyses, and molecular studies by DNA sequencing. D-2HG was measured in both tumoral tissue and in pre-treatment plasma by liquid chromatography-tandem mass spectrometry. Results: While D-2HG was markedly elevated in the tissue sample, its level in plasma was normal. We discuss this discordant D-2HG result within the context of previously reported discordant 2HG results in other IDH mutated tumors, and its implication for using circulating D-2HG as a biomarker of IDH mutation. In addition, this case also harbored mutations in RHOA, TET2, and TP53. The molecular pathogenesis is briefly discussed. Conclusion: While our case suggests that circulating D-2HG is not a reliable marker of IDH mutation in AITL, more cases need to be studied to arrive at a definite conclusion.