Oxygenated derivatives of cholesterol (oxysterols) present a remarkably diverse profile of biological activities, including effects on sphingolipid metabolism, platelet aggregation, apoptosis, and ...

Oxysterols: modulators of cholesterol metabolism and other processes.

Medical education during the past decade has witnessed a significant increase in the use of simulation technology for teaching and assessment. Contributing factors include: changes in health care delivery and academic environments that limit patient availability as educational opportunities; worldwide attention focused on the problem of medical errors and the need to improve patient safety; and the paradigm shift to outcomes-based education with its requirements for assessment and demonstration of competence. The use of simulators addresses many of these issues: they can be readily available at any time and can reproduce a wide variety of clinical conditions on demand. In lieu of the customary (and arguably unethical) system, whereby novices carry out the practice required to master various techniques—including invasive procedures—on real patients, simulation-based education allows trainees to hone their skills in a risk-free environment. Evaluators can also use simulators for reliable assessments of competence in multiple domains. For those readers less familiar with medical simulators, this article aims to provide a brief overview of these educational innovations and their uses; for decision makers in medical education, we hope to broaden awareness of the significant potential of these new technologies for improving physician training and assessment, with a resultant positive impact on patient safety and health care outcomes.

https://link.springer.com/content/pdf/10.1007%2Fs11606-007-0283-4.pdf

Simulation technology for skills training and competency assessment in medical education.

The endoplasmic reticulum (ER) in animal cells is an extensive, morphologically continuous network of membrane tubules and flattened cisternae. The ER is a multifunctional organelle; the synthesis of membrane lipids, membrane and secretory proteins, and the regulation of intracellular calcium are prominent among its array of functions. Many of these functions are not homogeneously distributed throughout the ER but rather are confined to distinct ER subregions or domains. This review describes the structural and functional organization of the ER and highlights the dynamic properties of the ER network and the mechanisms that support the positioning of ER membranes within the cell. Furthermore, we outline processes involved in the establishment and maintenance of an anisotropic distribution of ER-resident proteins and, thus, in the organization of the ER into functionally and morphologically different subregions.

Endoplasmic reticulum of animal cells and its organization into structural and functional domains.

Glycosylation . Fatty Acylation of Membrane Proteins Occurs Before They Leave the ER . . . . . . . . . . . . . . . Movement From the ER . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Regulation of protein export from the endoplasmic reticulum.

https://www.oarsijournal.com/article/S1063-4584%2803%2900028-1/pdf

Glucosamine inhibits IL-1β-induced NFκB activation in human osteoarthritic chondrocytes

P-glycoprotein (P-gp) overexpression by tumor cells imparts resistance to multiple antineoplastic chemotherapeutic agents (multiple drug resistance). Treatment of tumor cells with chemotherapeutic agents such as anthracyclines, epipodophyllotoxins, and Vinca alkaloids results in induction of P-gp expression. This study was performed to determine if clinically relevant antimicrobial drugs (i.e., drugs that are used to treat bacterial infections in cancer patients) other than antineoplastic agents can induce expression of P-gp in MCF-7 breast carcinoma cells. Expression of P-gp and MDR1 mRNA was determined in samples from MCF-7 cells that were treated in culture with doxorubicin (positive control) and the antimicrobial drugs doxycycline, piperacillin, and cefoperazone. The functional status of P-gp was assessed using laser cytometry to determine intracellular doxorubicin concentrations. The MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay was used to determine if the cytotoxicity of experimental drugs was related to their ability to induce P-gp expression. MCF-7 cells treated with doxycycline (MCF-7/doxy) were stimulated to overexpress P-gp, whereas cells treated with piperacillin and cefoperazone did not overexpress P-gp. MCF-7/doxy cells were compared to a positive-control subline, MCF-7/Adr, previously selected for doxorubicin resistance, and to MCF-7 cells treated with doxorubicin (MCF-7/doxo). All three sublines overexpressed P-gp and MDR1 mRNA and accumulated less intracellular doxorubicin than did control MCF-7 cells. P-gp expression was induced only by experimental drugs that were cytotoxic (doxorubicin and doxycycline). Doxycycline, a drug that has been used for treatment of bacterial infections in cancer patients, can induce functional P-gp expression in cancer cells, resulting in multidrug resistance.

Doxycycline induces expression of P glycoprotein in MCF-7 breast carcinoma cells.

Doxorubicin induced expression of P-glycoprotein in a canine osteosarcoma cell line

Mammalian heat shock proteins: an overview with a systems perspective.

Vascular endothelium is one of the first tissues exposed to reactive oxygen species produced during myocardial ischemia-reperfusion. Bovine coronary venular endothelial cells (CVEC) were evaluated for intracellular glutathione (GSH) levels and heat shock protein 70 (HSP 70) mRNA and protein during in vitro oxidative stress. CVEC were incubated with 0.01875 U/ml xanthine oxidase (XO) and 0.5 mM hypoxanthine (HX) for 30 min and then allowed to recover for 0, 1, 2, or 3 h. Relative GSH levels were determined by evaluation of monochlorobimane fluorescence. GSH fluorescence was significantly lower in CVEC treated with XO+HX for 30 min than in controls. GSH fluorescence was also decreased in heat-shocked CVEC. After oxidative stress, GSH levels were higher than in controls at 1 h, but by 2 or 3 h after treatment, GSH fluorescence fell below control values. HSP 70 mRNA was induced in CVEC by a 30-min treatment with XO+HX exposure. These data suggest that CVEC respond to oxidative stress by reducing intracellular GSH levels and inducing HSP 70 mRNA, although significant increases in HSP 70 protein were not detected at the time points tested.

Oxidative injury of coronary venular endothelial cells depletes intracellular glutathione and induces HSP 70 mRNA.

The critical role of outcomes assessment in veterinary medical accreditation.

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