Treatment of gastrointestinal bleeding in left ventricular assist devices: A comprehensive review

Left ventricular assist devices(LVAD) are increasingly become common as life prolonging therapy in patients with advanced heart failure. Current devices are now used as definitive treatment in some patients given the improved durability of continuous flow pumps. Unfortunately, continuous flow LVADs are fraught with complications such as gastrointestinal(GI) bleeding that are primarily attributed to the formation of arteriovenous malformations. With frequent GI bleeding, antiplatelet and anticoagulation therapies are usually discontinued increasing the risk of life-threatening events. Small bowel bleeds account for 15%as the source and patients often undergo multiple endoscopic procedures.Treatment strategies include resuscitative measures and endoscopic therapies.Medical treatment is with octreotide. Novel treatment options include thalidomide, angiotensin converting enzyme inhibitors/angiotensin Ⅱ receptor blockers, estrogen-based hormonal therapies, doxycycline, desmopressin and bevacizumab. Current research has explored the mechanism of frequent GI bleeds in this population, including destruction of von Willebrand factor,upregulation of tissue factor, vascular endothelial growth factor, tumor necrosis factor-α, tumor growth factor-β, and angiopoetin-2, and downregulation of angiopoetin-1. In addition, healthcare resource utilization is only increasing in this patient population with higher admissions, readmissions, blood product utilization, and endoscopy. While some of the novel endoscopic and medical therapies for LVAD bleeds are still in their development stages, these tools will yet be crucial as the number of LVAD placements will likely only increase in the coming years.     

We Built This House; It’s Time to Move in: Leveraging Existing DICOM Structure to More Completely Utilize Readily Available Detailed Contrast Administration Information

The Digital Imaging and Communications in Medicine (DICOM) standard is the universal format for interoperability in medical imaging. In addition to imaging data, DICOM has evolved to support a wide range of imaging metadata including contrast administration data that is readily available from many modern contrast injectors. Contrast agent, route of administration, start and stop time, volume, flow rate, and duration can be recorded using DICOM attributes [1]. While this information is sparsely and inconsistently recorded in routine clinical practice, it could potentially be of significant diagnostic value. This work will describe parameters recorded by automatic contrast injectors, summarize the DICOM mechanisms available for tracking contrast injection data, and discuss the role of such data in clinical radiology.     

Thalidomide teratogenesis: evidence for a toxic arene oxide metabolite.

It was postulated that thalidomide causes birth defects by being metabolized to a toxic electrophilic intermediate. This hypothesis was tested by using an in vitro assay in which drug toxicity to human lymphocytes was assessed in the presence of a hepatic microsomal drug metabolizing system. Maternal hepatic microsomes from pregnant rabbits mediated the production of a metabolite that was toxic to lymphocytes. Toxicity was enhanced by inhibitors of epoxide hydrolase (EC 3.3.2.3) and abolished by adding the purified enzyme to the incubation medium. The metabolite thus appears to be in arene oxide, consistent with the previously reported isolation of phenolic metabolites of thalidomide from the urine of treated animals. Two teratogenic analogs of thalidomide (phthalimidophthalimide and phthalimidinoglutarimide) were also toxic in the system; two nonteratogenic analogs (phthalimide and hexahydrothalidomide) were not toxic, even in the presence of epoxide hydrolase inhibitors. The toxic metabolite of thalidomide was not produced by rat liver microsomes (the rat is not sensitive to thalidomide teratogenesis) but was produced by hepatic preparations from maternal rabbits, and rabbit, monkey, and human (all sensitive species) fetuses. A toxic arene oxide therefore may be involved in the teratogenicity of thalidomide.     

A new approach to determine solar potential using terrestrial images

Before installing Photovoltaic (PV) panels at a place it is important to estimate the solar potential of the place. Most approaches available in literature do not consider the presence of surrounding obstructions, thus leading to wrong estimates. Light Detection and Ranging (LiDAR) data or 3D (Geographic Information System) GIS based approaches consider obstructions but prove cost-effective only at city-wide scales. This paper presents a cost-effective, accurate, and scalable approach for this purpose. The proposed approach utilizes terrestrial images of surroundings and identifies obstructions present therein. Using the azimuth and elevation angles of the principal axes of the terrestrial images the azimuth and elevation angles of each pixel in these images are determined. Using thresholding and morphological closing the terrestrial images are segmented into sky and non-sky zones. Sun is considered visible at the point of interest if it lies in the sky zone. The position of the Sun is determined using the solar position algorithm and the irradiance reaching the Earth surface is computed using the modified radiative transfer model. Finally, the total irradiance over a chosen time period at a given location is estimated by integrating the irradiances for the duration when the Sun is visible.     

Probability Mapping to Determine the Spatial Risk Pattern of Acute Gastroenteritis in Coimbatore District,India, Using Geographic Information Systems (GIS)

Background:

Maps show well the spatial configuration of information. Considerable effort is devoted to the development of geographical information systems (GIS) that increase understanding of public health problems and in particular to collaborate efforts among clinicians, epidemiologists, ecologists, and geographers to map and forecast disease risk.

Objectives:

Small populations tend to give rise to the most extreme disease rates, even if the actual rates are similar across the areas. Such situations will follow the decision-maker''s attention on these areas when they scrutinize the map for decision making or resource allocation. As an alternative, maps can be prepared using P-values (probabilistic values).

Materials and Methods:

The statistical significance of rates rather than the rates themselves are used to map the results. The incidence rates calculated for each village from 2000 to 2009 is used to estimate λ, the expected number of cases in the study area. The obtained results are mapped using Arc GIS 10.0.

Results:

The likelihood of infections from low to high is depicted in the map and it is observed that five villages namely, Odanthurai, Coimbatore Corporation, Ikkaraiboluvampatti, Puliakulam, and Pollachi Corporation are more likely to have significantly high incidences.

Conclusion:

In the probability map, some of the areas with exceptionally high or low rates disappear. These are typically small unpopulated areas, whose rates are unstable due to the small numbers problem. The probability map shows more specific regions of relative risks and expected outcomes.     

Health-related outcomes of critically ill patients with and without sepsis

Purpose

To determine differences in health-related quality of life (HRQoL), survival and healthcare resource use of critically ill adults with and without sepsis.

Methods

We conducted a primary propensity score matched analysis of patients with and without sepsis enrolled in a large multicentre clinical trial. Outcomes included HRQoL at 6 months, survival to 2 years, length of ICU and hospital admission and cost of ICU and hospital treatment to 2 years.

Results

We obtained linked data for 3442 (97.3%) of 3537 eligible patients and matched 806/905 (89.0%) patients with sepsis with 806/2537 (31.7%) without. After matching, there were no significant differences in the proportion of survivors with and without sepsis reporting problems with mobility (37.8% vs. 38.7%, p?=?0.86), self-care (24.7% vs. 26.0%, p?=?0.44), usual activities (44.5% vs. 46.8%, p?=?0.28), pain/discomfort (42.4% vs. 41.6%, p?=?0.54) and anxiety/depression (36.9% vs. 37.7%, p?=?0.68). There was no significant difference in survival at 2 years: 482/792 (60.9%) vs. 485/799 (60.7%) (HR 1.01, 95% CI 0.86–1.18, p?=?0.94). The initial ICU and hospital admission were longer for patients with sepsis: 10.1?±?11.9 vs. 8.0?±?9.8 days (p?<?0.0001) and 22.8?±?21.2 vs. 19.1?±?19.0 days, (p?=?0.0003) respectively. The cost of ICU admissions was higher for patients with sepsis: A$43,345?±?46,263 (€35,109?±?35,043) versus 34,844?±?38,281 (€28,223?±?31,007), mean difference $8501 (€6885), 95% CI $4342–12,660 (€3517?±?10,254), p?<?0.001 as was the total cost of hospital treatment to 2 years: A$74,120?±?60,750 (€60,037?±?49,207) versus A$65,806?±?59,856 (€53,302?±?48,483), p?=?0.005.

Conclusions

Critically ill patients with sepsis have higher healthcare resource use and costs but similar survival and HRQoL compared to matched patients without sepsis.

     

Differential effect of corticosterone deficiency on the expression of LH, prolactin and insulin receptors on rat Leydig cells

The adverse effects of glucocorticoid deficiency on the expression of genes encoding Leydig cell surface receptors and the response to LH/prolactin/insulin to produce testosterone production are yet to be recognized. Following metyrapone-induced corticosterone deficiency, serum corticosterone, testosterone and insulin levels decrease, whereas serum prolactin exhibits a significant increase and serum LH remains unaltered. LH binding and LH receptor mRNA expression were not altered, but a significant decrease in PRL and insulin binding and in the mRNA expressions of their receptors were observed in corticosterone-deficient rats in vivo. Corticosterone deficiency significantly decreases the Leydig cellular basal as well as hormone-stimulated testosterone production in vitro. Simultaneous administration of corticosterone prevented its deficiency-induced changes in Leydig cells both in vivo and in vitro. Our results show that metyrapone-induced corticosterone deficiency impairs Leydig cell insulin and prolactin receptors, and their mRNA expression and the response of Leydig cells to LH/PRL/insulin on testosterone production.