Dissecting aneurysm of aorta in rats fed with cysteamine

Degeneration of elastic fibres leading to aortic aneurysm and rupture was observed in rats treated with cysteamine. The destructive changes are comparable to those of spontaneously occurring cardiovascular abnormalities in man.     

Neuroprotective Effect of CNB-001, a Novel Pyrazole Derivative of Curcumin on Biochemical and Apoptotic Markers Against Rotenone-Induced SK-N-SH Cellular Model of Parkinson’s Disease

Oxidative stress and mitochondrial dysfunction are underpinned for initiating a cascade of toxic events leading to dopaminergic neuronal death in Parkinson’s disease (PD) and identified as vital target for therapeutic intervention. Curcumin, a potent antioxidant has been reported to display diverse neuroprotective properties against various neurodegenerative diseases including PD. In this present study, we investigated the protective effect of CNB-001, a pyrazole derivative of curcumin on rotenone-induced toxicity and its possible mechanisms in neuroblastoma SK-N-SH cells. Rotenone insult significantly reduced cell viability (MTT assay) and resulted in 78 % apoptosis (dual staining) by altering Bcl-2, Bax, caspase-3, and cytochrome C expression. Moreover, rotenone enhanced ROS production and disrupts mitochondrial membrane potential. These resultant phenotypes were distinctly alleviated by CNB-001. Pretreatment with CNB-001(2 μM) 2 h before rotenone exposure (100 nM) increased cell viability, decreased ROS formation, maintained normal physiological mitochondrial membrane potential, and reduced apoptosis. Furthermore, CNB-001 inhibited downstream apoptotic cascade by increasing the expression of vital antiapoptotic protein Bcl-2 and decreased the expression of Bax, caspase-3, and cytochrome C. Collectively, the results suggest that CNB-001 protects neuronal cell against toxicity through antioxidant and antiapoptotic properties through its action on mitochondria. Therefore, it may be concluded that CNB-001 can be further developed as a promising drug for treatment of PD.     

Evaluation of an intervention for patients with alcohol‐related injuries: results of a mixed methods study

Objective: To explore the effect of education and training on the delivery of alcohol screening and brief intervention and referral to high‐risk patients in a hospital setting. Main outcome measures included; delivery of training; practice change in relation to staff performing alcohol screening, brief intervention and referrals. Methods: Observational study design using mixed methods set in a tertiary referral hospital. Pre‐post assessment of medical records and semi‐structured interviews with key informants. Results: Routine screening for substance misuse (9% pre / 71.4% post) and wellbeing concerns (6.6% pre / 15 % post) was more frequent following the introduction of resources and staff participation in educational workshops. There was no evidence of a concomitant increase in delivery of brief intervention or referrals to services. Implementation challenges, including time constraints and staff attitudes, and enablers such as collaboration and visible pathways, were identified. Conclusion: Rates of patient screening increased, however barriers to delivery of brief intervention and referrals remained. Implementation strategies targeting specific barriers and enablers to introducing interventions are both required to improve the application of secondary prevention for patients in acute settings. Implications: Educational training, formalised liaison between services, systematised early intervention protocols, and continuous quality improvement processes will progress service delivery in this area.     

Enhanced optical,magnetic and hydrogen evolution reaction properties of Mo1−xNixS2 nanoflakes

Due to exceptional electronic, optoelectronic and catalytic properties, MoS₂ has attracted extensive research interest in various applications. In the present scenario, the exploitation of noble-metal-free catalysts for hydrogen evolution is of great interest. Herein, we report the structural, optical, magnetic and electrocatalytic properties of pure and nickel-substituted MoS₂ nanostructures synthesized by the hydrothermal method. X-ray diffraction (XRD) analysis reveals that all samples exhibit the hexagonal structure of MoS₂ and the formation of NiS₂ at higher concentrations of nickel. Vibrating sample magnetometer (VSM) measurements of the Mo_1−xNi_xS₂ nanostructures show a hysteresis loop at room temperature with a higher saturation magnetization for 1% Ni-substituted MoS₂ nanostructures, confirming the ferromagnetic behaviour of the sample. The indirect-to-direct band gap transition of few-layered nanostructures was confirmed by the optical absorption spectrum showing bands in the 600–700 nm and 350–450 nm regions. This study also highlights the excitation wavelength-dependent down- and up-conversion photoluminescence of the as-synthesized samples, providing new horizons for the design of MoS₂-based optical and spintronic devices. The electrocatalytic effect of 3% Ni-substituted MoS₂ nanostructures has been found to be higher than that of other deposit concentrations as it corresponds to the efficient hydrogen evolution reaction (HER).

Hydrothermal synthesis of Mo_1–xNi_xS₂ nanostructures as efficient catalyst for hydrogen evolution reaction.     

Sonographic evaluation of intravascular volume status in the surgical intensive care unit: a prospective comparison of subclavian vein and inferior vena cava collapsibility index

Background

Traditional methods for intravascular volume status assessment are invasive and are associated significant complications. While focused bedside sonography of the inferior vena cava (IVC) has been shown to be useful in estimating intravascular volume status, it may be technically difficult and limited by patient factors such as obesity, bowel gas, or postoperative surgical dressings. The goal of this investigation is to determine the feasibility of subclavian vein (SCV) collapsibility as an adjunct to IVC collapsibility in intravascular volume status assessment.

Methods

A prospective study was conducted on a convenience sample of surgical intensive care unit patients to evaluate interchangeability of IVC collapsibility index (IVC-CI) and SCV-CI. After demographic and acuity of illness information was collected, all patients underwent serial, paired assessments of IVC-CI and SCV-CI using portable ultrasound device (M-Turbo; Sonosite, Bothell, WA). Vein collapsibility was calculated using the formula [collapsibility (%) = (max diameter – min diameter)/max diameter × 100%]. Paired measurements from each method were compared using correlation coefficient and Bland–Altman measurement bias analysis.

Results

Thirty-four patients (mean age 56 y, 38% female) underwent a total of 94 paired SCV-CI and IVC-CI sonographic measurements. Mean acute physiology and chronic health evaluation II score was 12. Paired SCV- and IVC-CI showed acceptable correlation (R² = 0.61, P < 0.01) with acceptable overall measurement bias [Bland–Altman mean collapsibility difference (IVC-CI minus SCV-CI) of −3.2%]. In addition, time needed to acquire and measure venous diameters was shorter for the SCV-CI (70 s) when compared to IVC-CI (99 s, P < 0.02).

Conclusions

SCV collapsibility assessment appears to be a reasonable adjunct to IVC-CI in the surgical intensive care unit patient population. The correlation between the two techniques is acceptable and the overall measurement bias is low. In addition, SCV-CI measurements took less time to acquire than IVC-CI measurements, although the clinical relevance of the measured time difference is unclear.     

Comparison of relapse rates and of mucosal abnormalities after healing of duodenal ulceration and after one year's maintenance with cimetidine or sucralfate: a light and electron microscopy study.

Forty six patients with endoscopically diagnosed duodenal ulceration were randomly allocated to treatment with either sucralfate 1 g qds (n = 24) or cimetidine 200 mg tds and 400 mg nocte (n = 22). When the ulcers healed, a maintenance dose of sucralfate 1 g bd or cimetidine 400 mg nocte was given for one year (or until relapse if earlier). Biopsies of duodenal mucosa adjacent to ulcer sites for light and electron microscopy were obtained before and after healing and again after one year's maintenance if the ulcer remained healed. Duodenal biopsies were also taken from 20 age and sex matched controls. Rates of healing and relapse during maintenance did not differ between the two treatments, although relapses occurred earlier with cimetidine. In the three year post-maintenance follow up period 10/13 cimetidine patients relapsed compared with four of 11 sucralfate patients (p less than 0.05), the relapses occurring significantly earlier in the cimetidine treated patients (p less than 0.05). Mucosal biopsies from both treatment groups still showed considerable abnormalities after healing. During maintenance, however, the sucralfate scores fell significantly (p less than 0.02) to near control levels unlike the cimetidine scores which remained raised at pretreatment values. The histological and ultrastructural changes were not predictive of later relapse. These findings favour the use of sucralfate in preference to cimetidine for maintenance treatment in the prevention of relapse of healed duodenal ulcers.     

Curcumin and Cancer Cells: How Many Ways Can Curry Kill Tumor Cells Selectively?

Cancer is a hyperproliferative disorder that is usually treated by chemotherapeutic agents that are toxic not only to tumor cells but also to normal cells, so these agents produce major side effects. In addition, these agents are highly expensive and thus not affordable for most. Moreover, such agents cannot be used for cancer prevention. Traditional medicines are generally free of the deleterious side effects and usually inexpensive. Curcumin, a component of turmeric (Curcuma longa), is one such agent that is safe, affordable, and efficacious. How curcumin kills tumor cells is the focus of this review. We show that curcumin modulates growth of tumor cells through regulation of multiple cell signaling pathways including cell proliferation pathway (cyclin D1, c-myc), cell survival pathway (Bcl-2, Bcl-xL, cFLIP, XIAP, c-IAP1), caspase activation pathway (caspase-8, 3, 9), tumor suppressor pathway (p53, p21) death receptor pathway (DR4, DR5), mitochondrial pathways, and protein kinase pathway (JNK, Akt, and AMPK). How curcumin selectively kills tumor cells, and not normal cells, is also described in detail.