University of Manitoba

About: University of Manitoba is a education organization based out in Winnipeg, Manitoba, Canada. It is known for research contribution in the topics: Population & Health care. The organization has 31888 authors who have published 66592 publications receiving 2095493 citations.

Allergic rhinobronchitis: The asthma–allergic rhinitis link

Abstract: Allergic rhinitis and asthma are linked by epidemiologic, histologic, physiologic, and immunopathologic characteristics and by a common therapeutic approach. Epidemiologically, the disorders often coexist. Histologically, the upper and lower airways are lined, and linked, by the respiratory epithelium. Physiologically, they may be linked by the nasobronchial reflex. Pathologically, they are linked by similar early- and late-phase allergic responses throughout the airways and by the systemic immunologic response to airborne allergens. Uncontrolled allergic rhinitis may be associated with worsening of coexisting asthma, and optimal treatment of allergic rhinitis may improve coexisting asthma. The key to managing both disorders is prevention and relief of chronic allergic inflammation in both the upper and lower airways. The similarities between allergic rhinitis and asthma outweigh the differences. To facilitate appropriate recognition and treatment of the common inflammatory process throughout the airways, consideration should be given to introducing the new term “allergic rhinobronchitis.” (J Allergy Clin Immunol 1999;104:534-40.)

Middle East respiratory syndrome coronavirus (MERS-CoV) causes transient lower respiratory tract infection in rhesus macaques

Abstract: In 2012, a novel betacoronavirus, designated Middle East respiratory syndrome coronavirus or MERS-CoV and associated with severe respiratory disease in humans, emerged in the Arabian Peninsula. To date, 108 human cases have been reported, including cases of human-to-human transmission. The availability of an animal disease model is essential for understanding pathogenesis and developing effective countermeasures. Upon a combination of intratracheal, ocular, oral, and intranasal inoculation with 7 × 106 50% tissue culture infectious dose of the MERS-CoV isolate HCoV-EMC/2012, rhesus macaques developed a transient lower respiratory tract infection. Clinical signs, virus shedding, virus replication in respiratory tissues, gene expression, and cytokine and chemokine profiles peaked early in infection and decreased over time. MERS-CoV caused a multifocal, mild to marked interstitial pneumonia, with virus replication occurring mainly in alveolar pneumocytes. This tropism of MERS-CoV for the lower respiratory tract may explain the severity of the disease observed in humans and the, up to now, limited human-to-human transmission.

Stimulation of c-myc oncogene expression associated with estrogen-induced proliferation of human breast cancer cells.

Abstract: Regulation of c-myc expression is known to be sensitive to a variety of mitogenic stimuli in various cell types. Since estrogen is a well documented mitogen of estrogen-responsive human breast cancer (HBC) cells, we studied the influence of estradiol and its antagonist tamoxifen on the expression of c-myc in HBC cell lines. Using Northern hybridization analysis, we monitored the accumulation of c-myc mRNA in a number of HBC cell lines. The cell lines studied included the estrogen-responsive, estrogen receptor positive (ER+) MCF-7, T-47D, the nonresponsive, estrogen receptor negative (ER-) MDA-MB-231, BT-20, and a nontumorous breast cell line, HBL-100. The effects of endogenous estrogen were minimized by culturing the cells in medium containing 10% (v/v) charcoal-treated fetal bovine serum and tamoxifen (10(-6) M) for 48 h prior to estradiol (10(-7) M) treatment. In the ER+ cell lines the addition of estradiol resulted in a noticeable increase in c-myc expression after 15 min with a maximal (greater than 10-fold) induction in 1-2 h. In the ER- cell lines the level of c-myc mRNA was high and was unaffected by estrogen or tamoxifen; in the ER- cancer cell lines, neither amplification nor rearrangement of the c-myc gene was observed. In contrast, the expression of another oncogene, c-H-ras, remained constant in both ER+ and ER- cell lines and was insensitive to estrogen and antiestrogen. These results suggest that regulation of c-myc expression may be an important step in estrogen-induced proliferation of HBC cells.