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Craniocerebral and spinal penetrating trauma, which may be either missile (most typically gun-related) or non-missile (most typically knife-related), is becoming an increasingly common presentation to the urban general and specialized radiology service in the UK. These injuries carry significant morbidity and mortality with a number of criteria for prognosis identifiable on cross-sectional imaging. Potential complications can also be pre-empted by awareness of certain neuroradiological features. Not all of these injuries are criminal in origin, however, a significant proportion will be, requiring, on occasion, provision of both ante-mortem and post-mortem radiological opinion to the criminal investigative procedure. This review aims to highlight certain imaging features of penetrating craniocerebral and spinal trauma including important prognostic, therapeutic, and forensic considerations. [Copyright &y& Elsevier]

Tranilast (N-[3,4-dimethoxycinnamoyl]anthranilic acid) is a synthetic compound that we have recently reported to inhibit transforming growth factor-β1 (TGF-β1)-induced tubulointerstitial fibrosis in the kidney. Connective tissue growth factor (CTGF) is recognized as a potent downstream mediator of TGF-β1. Both proximal tubule cells (PTCs) and cortical fibroblasts (CFs) are considered to be responsible for the production of tubulointerstitial extracellular matrix (ECM). These studies were undertaken to assess the profibrotic effects of CTGF in an in vitro model of the human PTCs and CFs, and to determine whether tranilast is effective in limiting the in vitro matrix responses induced by CTGF. Primary cultures of PTCs and CFs were exposed to CTGF (20 ng/ml)±tranilast (100 μM). Cell hypertrophy and the secretion of the ECM proteins fibronectin and collagen IV were determined. The effects of tranilast on TGF-β1-induced CTGF mRNA expression and on phosphorylation of Smad2 were determined. CTGF significantly induced cell hypertrophy, increased fibronectin, and collagen IV secretion in PTCs and CFs. In all cases, the CTGF-induced increase in ECM protein was inhibited in the presence of tranilast. Tranilast reduced CTGF mRNA and phosphorylation of Smad2, which were induced by TGF-β1 in PTCs and CFs. These results suggest that tranilast is a potential effective antifibrotic compound in the kidney, exerting its effects via inhibition of TGF-β1-induced CTGF expression and downstream activation of the Smad2 pathway in both PTCs and CFs.Kidney International (2006) 69, 989–995. doi:10.1038/sj.ki.5000189; published online 22 February 2006 [ABSTRACT FROM AUTHOR]

Aims: This retrospective study aimed to investigate both established and less well-explored factors as potential predictive variables for failed and delayed ulcer healing. Methods: Patients with type 1 or 2 diabetes with foot ulceration presenting consecutively to, and then subsequently managed at, a multidisciplinary, high-risk foot clinic were followed until ulcer healing, amputation or death. Data comprised prospective standardised documentation at each visit and retrospective collection from hospital records, and included patient demographics, comorbidities, laboratory variables, and ulcer infection, depth and area at each presentation. Multiple regression analysis was used to determine independent predictors of failure to heal and delayed healing. Results: Of the 107 consecutive patients studied, 95 (89%) healed overall, 50 (47%) had healed in 12 weeks and the mean healing rate was a 10% decrease in ulcer area per week. Amongst all variables examined, comorbid congestive heart failure (CHF) was the only factor independently predictive of all measured outcomes of failure to heal overall, delayed healing at 12 weeks, and reduced healing rate. Ulcer infection at presentation, longer duration of antibiotic use, and liver enzyme abnormalities of raised ALT and AST:ALT < 1 (each suggestive of non-alcoholic fatty liver disease), were also predictive of poor ulcer outcomes. Conclusions: Comorbid congestive cardiac failure is predictive of delayed foot ulcer healing rate as well as a lower probability of healing overall. Liver enzyme abnormalities also predicted delayed ulcer healing outcomes. The mechanisms underlying these associations with foot ulcer outcomes in diabetes are unclear. Further studies are needed to determine the role of systematic routine documentation of heart failure and its severity, and then targeting of heart failure to potentially aid the management of foot ulcers in diabetes. [ABSTRACT FROM AUTHOR]