Search

It has been reported in photodoping experiments that localized surface plasmonic resonances can be sustained with electrons as few as 3. We performed first principles calculations of density functional theory, with the Hubbard U correction, to see if localized surface plasmonic resonances can also be sustained by doping a wide bandgap ZnO with few shallow donors of Ga. We distributed 3–6 dopants approximately uniformly, due to quasi-spherical geometry of the quantum dot, in the dilute doping limit. The uniform distribution of dopants in quantum dots has been reported experimentally. Although the dopant configurations are limited due to computational cost, our findings shed light on absorption trends. Results for quantum dots of 1.4 nm, passivated with pseudo-hydrogens, show that localized surface plasmonic resonances can be generated in the near infrared range. The absorption linewidths for such small-sized quantum dots are broad. We find that the resonance linewidth depends on the orientation of surfaces and the number of secondary peaks on the concentration of dopants. The absorption coefficients, as functions of the principal values of the dielectric tensor, indicate that an electric field with orientation parallel to that of the most symmetric surface will produce localized surface plasmonic resonances with high quality factors. [ABSTRACT FROM AUTHOR]

Byline: Sumita. Danda, C. Eapen, K. Kuruvilla, S. Santhosh, G. Kurian, G. Chandy Sir, Hereditary hemochromatosis (HH) is considered to be a disease of the Caucasian population. [sup][1] C282Y mutation [...]

The morbidity and mortality rates of transplant nephrectomy are closely related to the indications of nephrectomy. This study evaluates the indications, etiology, and complications of graft nephrectomies for commercial kidney transplantation (CKT). Data were analyzed retrospectively for graft nephrectomies for CKT from January 2009 to December 2017 at the Royal Hospital, Muscat, Oman. Four hundred and three patients received CKT and 34 patients required a nephrectomy. Twenty-five patients had a nephrectomy within 10 weeks of CKT in the early group, and nine patients in the late group had the graft removed later than 10 weeks. Indications for nephrectomy in the early group were acute bleeding, infarcted kidney, and pyonephrosis in 7, 11, and 7 patients, respectively; in the late group, the indications were: pain, hematuria, fever, hypertension, and infection. Overall, seven patients had major blood loss, and those patients who had a pseudoaneurysm had tissue cultures that were positive for the fungus. Postoperative complications occurred in 26 patients. There was acute bleeding in three patients from the external iliac artery at the site of the previous anastomosis, and, in all three cases, the external iliac artery was ligated. There were 12 major wound infections, and three patients died from overwhelming sepsis and disseminated intravascular coagulation. Commercial transplants carry a high risk of immunological, vascular, and infectious complications, resulting in significant morbidity and mortality.

Ischemic heart disease (IHD) is one of the main focuses in today’s healthcare due to its implications and complications, and it is predicted to be increasing in prevalence due to the ageing population. Although the conventional pharmacological and interventional methods for the treatment of IHD presents with success in the clinical setting, the long-term complications of cardiac insufficiency are on a continual incline as a result of post-infarction remodeling of the cardiac tissue. The migration and involvement of stem cells to the cardiac muscle, followed by differentiation into cardiac myocytes, has been proven to be the natural process, though at a slow rate. SDF-1α is a novel candidate to mobilize stem cells homing to the ischemic heart. Endogenous SDF-1α levels are elevated after myocardial infarction, but their presence gradually decreases after approximately seven days. Additional administration of SDF-1α-releasing microspheres could be a tool for the extension of the time the stem cells are in the cardiac tissue after myocardial infarction. This, in turn, could constitute a novel therapy for more efficient regeneration of the heart muscle after injury. Through this practical study, it has been shown that the controlled release of SDF-1α from biodegradable microspheres into the pericardial sac fourteen days after myocardial infarction increases the concentration of exogenous SDF-1α, which persists in the tissue much longer than the level of endogenous SDF-1α. In addition, administration of SDF-1α-releasing microspheres increased the expression of the factors potentially involved in the involvement and retention of myocardial stem cells, which constitutes vascular endothelial growth factor A (VEGFA), stem cell factor (SCF), and vascular cell adhesion molecules (VCAMs) at the site of damaged tissue. This exhibits the possibility of combating the basic limitations of cell therapy, including ineffective stem cell implantation and the ability to induce the migration of endogenous stem cells to the ischemic cardiac tissue and promote heart repair.

Mitochondria are the key players of cardiac function and their dysfunction due to oxidative stress is implicated in myocardial ischemia reperfusion injury, one of the important mediators of cardiac mortality. The present study evaluates the mitochondrial protective effect of sodium thiosulfate on isolated cardiac mitochondria (interfibrillar mitochondria and subsarcolemmal mitochondria) subjected to oxidative stress by ischemia and reperfusion. Briefly, interfibrillar mitochondria and subsarcolemmal mitochondria were treated with cobalt chloride (500 μM) for 20 min to induce oxidative stress by chemical method and nitrogen gas purging for 20 min in an ischemic buffer was used for the physiological method. The mitoprotective effect of sodium thiosulfate was evaluated with different mode of sodium thiosulfate incubation (pretreatment, cotreatment and post treatment) with the mitochondria. The mitochondria led to an increased oxidative stress (measured by malondialdehyde, reduced glutathione, superoxide dismutase and glutathione peroxidase) and decreased mitochondrial enzyme activities (measured by succinate dehydrogenase, malate dehydrogenase and NAD+ dehydrogenase) with both the models and sodium thiosulfate treated groups showed significant improvement in the above alterations. By comparing the efficiency among the different modes of sodium thiosulfate treatment, we found that pretreatment renders significant (P<0.05) mitochondrial protection against ischemia reperfusion injury by nitrogen gas. However, no such differences were observed among the treatments in cobalt chloride mediated mitochondrial dysfunction. In summary, we found that sodium thiosulfate can modulate and preserve cardiac mitochondria for the treatment of myocardial ischemia reperfusion injury. [ABSTRACT FROM AUTHOR]

Oxidative stress plays a significant role not only in cardiovascular disease but also in non-communicable diseases, where it plays a significant role the mortality rate. Hydrogen sulfide, the biological gaseous signaling molecule that preserves mitochondria in its mode of action, is an effective cardioprotective drug. However, cardiac mitochondria comprise of two distinct populations, namely interfibrillar and subsarcolemmal mitochondria, which respond distinctly in cardiovascular disease. This study was designed to determine the direct impact of cobalt chloride-induced oxidative stress in isolated mitochondrial subpopulations with an intention to examine the efficacy of hydrogen sulfide in preserving interfibrillar and subsarcolemmal mitochondria functional activities when they were incubated as pretreated, co-treated and post-treated agent. Mitochondrial subpopulations were isolated from the heart of male Wistar rats and subjected to cobalt chloride treatment (500 μM) for 20 min, followed by incubation with 10 μM sodium hydrosulfide in three different ways (Pre, Co, and Post-cobalt chloride treatment). Mitochondrial oxidative stress was measured by the concentration of thiobarbituric acid reactive species, reduced glutathione and the activities of enzymes like superoxide dismutase, catalase and glutathione peroxidase. Mitochondrial membrane potential, swelling behavior and enzyme activities were measured to assess its function. The increased level of lipid peroxidation and the decreased level of reduced glutathione in cobalt chloride-induced group confirm the induction of oxidative stress and were more predominant in the subsarcolemmal mitochondria. Hydrogen sulfide treatment to interfibrillar and subsarcolemmal mitochondria preserved their functional activities, but the effect was prominent only with co-treated group. In conclusion, the present study demonstrated that subsarcolemmal mitochondria are more prone to oxidative stress and the co-treatment of the mitochondria with hydrogen sulfide preserved the enzyme activity in the in vitro conditions. [ABSTRACT FROM AUTHOR]

Pelvi-ureteric junction (PUJ) obstruction is an enigmatic condition. While in a reasonable majority it is clear cut, the diagnosis and the need for intervention in the remainder is still a challenge. We would like to share the details of two cases, one in a transplant recipient and the other in a living kidney donor, and propose an explanation as to why PUJ obstruction becomes manifest after such a long period of time. In this presentation, we would like to propose that forced drinking of fluids by patients who have an equivocal PUJ and a single kidney could tilt the balance resulting in overt PUJ obstruction.