Exhumation – Nuisance to the dead,justified?

ObjectiveExhumation stands as a very significant feature of forensic investigations. The legal excavation of dead bodies for ascertainment of the cause of death has always aided the law enforcement agencies to comprehend the anonymity of any suspicious case and further convict the criminal in cases of homicides. This study analyses the different aspects of the exhumations which were carried out and were autopsied in Karachi during the study period.MethodThis was a cross-sectional study, and included all the exhumations carried out in Karachi during a period of 7 years and 7 months from 1 January 2004 to 31 July 2011.ResultsA total of 101 exhumations were carried out during the study period. Out of 101 cases, 63 were males (62.4%) and 38 females (37.6%) giving a male to female ratio of about 3:2. Causes of death were ascertained in 75 cases, thus the success rate was 74.3%. Head injury by hitting with hard blunt object was the most frequent cause of deaths (17.8%), followed by asphyxia due to strangulation (15.8%).DiscussionExhumations must be ordered by the Judiciary in suspicious cases as it aids in determining the actual causes of death and leads to convictions. It also brings a great deal of satisfaction for the relatives of the deceased and halts any doubts in their minds. As shown by our study, much attention is given to the cases in urban areas by the relatives who are determined to find the cause of death even after burial procedures.     

Early detection of pandemic (H1N1) 2009, Bangladesh

To explore Bangladesh's ability to detect novel influenza, we examined a series of laboratory-confirmed pandemic (H1N1) 2009 cases. During June-July 2009, event-based surveillance identified 30 case-patients (57% travelers); starting July 29, sentinel sites identified 252 case-patients (1% travelers). Surveillance facilitated response weeks before the spread of pandemic (H1N1) 2009 infection to the general population.     

Retinal ganglion cell and inner plexiform layer thickness measurements in regions of severe visual field sensitivity loss in patients with glaucoma

Purpose

To better understand the effects of severe glaucoma on the thickness of the retinal ganglion cell (RGC) and inner plexiform (IP) layers measured with frequency-domain optical coherence tomography.

Methods

In experiment 1, macular cube scans were obtained in 11 patients with glaucoma and the thickness of both the RGC and IP layers were measured at locations corresponding to 3, 5, and 7° eccentricity. For patients, only locations with total deviation losses of −15 dB or worse on perimetry were included. In experiment 2, higher resolution, horizontal midline scans were obtained from 30 controls in order to obtain a precise measure of the thickness of the RGC and IP layers of the healthy retina.

Results

In regions of severe field loss (experiment 1), glaucoma decreased the thickness of both layers, leaving a residual layer. The residual thickness of the IP layer was larger than the residual thickness of the RGC layer. In healthy controls (experiment 2), the RGC layer was about 57% of the RGC+IP layer thickness at 3° as compared with only 36% at 10°, in agreement with a recent histological study.

Conclusion

Glaucomatous optic neuropathy, with severe losses in visual field sensitivity, decreases the thickness of both the RGC and IP layers, but leaves a residual thickness of both. The IP layer contributes slightly more than the RGC to this residual, even just outside the center of the fovea where the RGC layer thickness exceeds the IP layer thickness in controls.     

Endothelial cells, fibroblasts and vasculitis

One of the most important questions in vasculitis research is not why inflammation of blood vessels occurs but why it persists, often in a site-specific manner. In this review we illustrate how stromal cells, such as fibroblasts and pericytes, might play an important role in regulating the site at which vasculitis occurs. Smooth muscle cells and fibroblasts directly influence the behaviour of overlying vascular cells, amplifying the response of the endothelium to proinflammatory agents such as TNF-alpha and allowing enhanced and inappropriate leucocyte recruitment. An abnormal local vascular stromal environment can therefore influence local endothelial function and drive the persistence of local vascular inflammation. However, such local vascular inflammation can have distant effects on the systemic vascular system, leading to widespread endothelial cell dysfunction. Vascular endothelial dysfunction is common in a range of immune-mediated inflammatory diseases, is seen in multiple vascular beds, and is reversible following the induction of disease remission. The mechanisms that drive such systemic vascular endothelial dysfunction are unclear but factors such as TNF-alpha and CRP may play a role. Persistence of such widespread endothelial dysfunction in systemic vasculitis appears to have long-term consequences, leading to the acceleration of atherosclerosis and premature ischaemic heart disease. It may also underlie the accelerated atherosclerosis seen in other immune-mediated rheumatic diseases, such as rheumatoid arthritis.     

Effects of radial stretch on target lesion revascularization after percutaneous coronary intervention: an intravascular ultrasound study

OBJECTIVE: To analyze possible associations between radial stretch during coronary angioplasty and the incidence of target lesion revascularization (TLR). PATIENTS AND METHODS: Intravascular ultrasound images were obtained before and after revascularization in 182 native coronary lesions. The quantitative intravascular ultrasound parameters (external elastic membrane cross-sectional area [EEM-A], lumen areas [LA], plaque area [PA], calculated as EEM-A-LA, and changes between pre- and postinterventional LA [DLA], EEM-A [DEEM-A] and PA [DPA]) were correlated with the incidence of TLR. RESULTS: TLR was performed in 60 (33%) patients, while 122 (67%) patients remained event free. Postinterventional PA remained significantly larger in the TLR group than in the event-free group (9.2 +/- 3.3 mm2 versus 7.9 +/- 3.3 mm2; P=0.02). The radial stretch during intervention, expressed as DEEM-A, and the balloon to artery ratio was significantly larger in the TLR group (DEEM-A: 1.9 +/- 2.1 mm2 versus 1.3 +/- 2.0 mm2; P=0.03; balloon to artery ratio: 1.3 +/- 0.2 versus 1.0 +/- 0.5; P=0.04). Multivariate analysis revealed DEEM-A (P=0.01), DPA (P=0.03), diabetes (P=0.001, odds ratio 5.2, 95% CI 4.9 to 6.5) and adaptive remodelling (P<0.001, odds ratio 4.1, 95% CI 3.5 to 6.4) as independent predictors for TLR. CONCLUSION: Whereas patients in whom lumen gain is achieved primarily by plaque reduction with less wall stretch tend to remain event free, patients with significant radial stretch (ie, less reduction of the PA, but a radial outward shift of the plaque mass) experience a higher incidence of TLR.     

A missense variant of the ATP1A2 gene is associated with a novel phenotype of progressive sensorineural hearing loss associated with migraine

Hereditary sensorineural hearing loss is an extremely clinical and genetic heterogeneous disorder in humans. Especially, syndromic hearing loss is subdivided by combinations of various phenotypes, and each subtype is related to different genes. We present a new form of progressive hearing loss with migraine found to be associated with a variant in the ATP1A2 gene. The ATP1A2 gene has been reported as the major genetic cause of familial migraine by several previous studies. A Korean family presenting progressive hearing loss with migraine was ascertained. The affected members did not show any aura or other neurologic symptoms during migraine attacks, indicating on a novel phenotype of syndromic hearing loss. To identify the causative gene, linkage analysis and whole-exome sequencing were performed. A novel missense variant, c.571G>A (p.(Val191Met)), was identified in the ATP1A2 gene that showed co-segregation with the phenotype in the family. In silico studies suggest that this variant causes a change in hydrophobic interactions and thereby slightly destabilize the A-domain of Na⁺/K⁺-ATPase. However, functional studies failed to show any effect of the p.(Val191Met) substitution on the catalytic rate of this enzyme. We describe a new phenotype of progressive hearing loss with migraine associated with a variant in the ATP1A2 gene. This study suggests that a variant in Na⁺/K⁺-ATPase can be involved in both migraine and hearing loss.     

Indication of an involvement of interleukin-1 beta converting enzyme- like protease in intramedullary apoptotic cell death in the bone marrow of patients with myelodysplastic syndromes

Our previous studies using in situ end labeling (ISEL) of fragmented DNA revealed extensive apoptotic cell death in the bone marrows (BM) of patients with myelodysplastic syndromes (MDS) involving both stromal and hematopoietic cells. In the present report we show greater synthesis of interleukin-1 beta (IL-1 beta) in 4 hour cultures of density separated BM aspirate mononuclear (BMAM) cells from MDS patients as compared to the cultures of normal BM from healthy donors or lymphoma patients (1.7 +/- 0.37 pg/10(5) cells, n = 29 v 0.42 +/- 0.24 pg/10(5) cells, n = 11, respectively, P = .049). Further, these amounts of IL-1 beta in MDS showed a significant correlation with the extent of apoptosis detected by ISEL in corresponding plastic embedded BM biopsies (r = .480, n = 30, P = .007). In contrast normal BMs did not show any correlation between the two (r = .091, n = 12, P = .779). No significant correlation was found between the amounts of IL-1 beta and % S-phase cells (labeling index; LI%) in MDS determined in BM biopsies using immunohistochemistry following in vivo infusions of iodo- and/or bromodeoxyuridine. Neither anti-IL-1 beta antibody nor IL-1 receptor antagonist blocked the apoptotic death of BMAM cells in 4 hour cultures (n = 5) determined by ISEL (apoptotic index; AI%), although the latter led to a dose-dependent accumulation of active IL-1 beta in the culture supernatants. On the other hand, a specific tetrapetide- aldehyde inhibitor of ICE significantly retarded the apoptotic death of BMAM cells at 1 mumol/L in 5/6 MDS cases studied (AI% = 2.99 +/- 0.30 in controls v 1.58 +/- 0.40 with ICE-inhibitor, P = .05) and also reduced the levels of active IL-1 beta synthesized (5.59 +/- 2.63 v 2.24 +/- 0.93 pg/10(6) cells, respectively). In normal cells, neither IL-1 blockers nor the ICE inhibitor showed any effect on the marginal increase in apoptosis observed in 4 hour cultures. Our data thus suggest a possible involvement of an ICE-like protease in the intramedullary apoptotic cell death in the BMs of MDS patients.