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An objective of EHRAP was to evaluate the HIV risk factor information reported to CDC through routine surveillance. HIV/AIDS surveillance programmes used medical and ancillary records to determine if information on HIV risk factors can be found for surveillance. Surveillance staff from Mississippi, South Carolina, and Virginia collected data on risk factors for HIV infection on a sample of cases diagnosed during 1998 and 1999. Overall percent agreement and Cohen kappa statistics were calculated for initially reported compared to EHRAP-identified risk factors. Of 160 cases reported without an identified risk factor, 86% were reclassified with a known risk factor. A risk factor was identified for 96% of all cases of HIV infection. Overall, agreement was good (kappa = 0.89) between initially reported and verified HIV risk factor. All three states met the national goal of at least 85% of reported cases with a risk factor for HIV infection. The completeness of collection and reporting of HIV risk factors for national HIV/AIDS surveillance can be improved. The current method of risk factor redistribution at the national level should be evaluated. [ABSTRACT FROM AUTHOR]

The NRG Oncology/NSABP B-47 menstrual history (MH) study examined trastuzumab effects on menstrual status and associated circulating reproductive hormones. MH was evaluated by questions related to hysterectomy, oophorectomy, and reported menstrual changes. Pre/perimenopausal women were assessed at entry, 3, 6, 12, 18, 24, 30, and 36 months. Consenting women had estradiol and FSH measurement at entry, 3, 6, 12, 18, and 24 months. Logistic regression determined predictors of amenorrhea and hormone levels at 12, 24, and 36 months. Between 2/8/2011 and 2/10/2015, 3270 women with node-positive/high-risk node-negative HER2-low breast cancer were enrolled. There were 1,458 women enrolled in the MH study; 1231 consented to baseline blood samples. Trastuzumab did not contribute to a higher amenorrhea rate. Amenorrhea predictors were consistent with earlier studies; however, to our knowledge, this is the largest prospective study to include serial reproductive hormone measurements to 24 months and clinical amenorrhea reports to 36 months. These data can help to counsel patients regarding premature menopause risk.

Objectives: This phase II, open-label study was designed to evaluate the response rate to the polo-like kinase 1 (Plk-1) inhibitor BI 2536 in patients with sensitive-relapsed small cell lung cancer (SCLC). Secondary endpoints included progression-free survival (PFS), overall survival (OS), duration of response, and safety., Materials and Methods: Patients were treated with the recommended phase II dose of 200mg of BI 2536 intravenously every 21days. This was a two-stage design with an early stopping rule in place if responses were not seen in at least 2 of the first 18 enrolled patients., Results and Conclusion: Twenty-three patients were enrolled in the study and 21 patients were evaluable for response. No responses were observed and all 23 patients have progressed. The median PFS was 1.4 months. Treatment was generally well tolerated and the most frequent adverse events were neutropenia, fatigue, nausea, vomiting, and constipation. BI 2536 is not effective in the treatment of sensitive relapsed SCLC. The criteria for expanding the trial to the second stage were not achieved, and the study was terminated for a lack of efficacy., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

To evaluate the feasibility of using a monoclonal anti-Fc receptor antibody to alter Fc receptor function in vivo, the disappearance of radiolabeled human serum albumin-rabbit anti-human serum albumin (HSA-anti-HSA) complexes was studied in mice before and after the infusion of 2.4G2, a monoclonal antibody (developed by J. Unkeless). 2.4G2 specifically binds to Fc receptors on mouse macrophages. Under standardized conditions, 6.1% of an i.v. administered dose of anti-HSA was sequestered in the liver of B6/D2J mice. When HSA-anti-HSA complexes were administered, 53.4% were sequestered. If 8 micrograms/g body weight of 2.4G2 was infused i.p. 1.5 hr before HSA-anti-HSA, only 13.7% of the infused complexes were sequestered in the liver. The inhibition in Fc receptor-mediated sequestration produced by this dose of antibody persisted for at least 24 hr. A dose of 1 to 2 micrograms/g was sufficient to inhibit sequestration by 50%. Animals receiving daily injections of 2.4G2 cleared immune complexes from their blood much more slowly than untreated animals. Because 2.4G2 was not cytotoxic to peritoneal macrophages in vitro in the presence of serum, and because comparable inhibition of Fc receptor function was observed in vivo in C5-deficient mice, blockade of function does not depend upon complement-mediated lysis of macrophages. The maximal degree of inhibition of Fc receptor function obtained by using intact 2.4G2 was about twice that observed by using Fab fragments of 2.4G2 to block receptors. In addition to its effect on Fc receptor function, 2.4G2 also had a small but significant inhibitory effect upon the clearance of 125I-labeled heat-aggregated HSA by the mononuclear phagocyte system both in intact and C5-deficient mice. We conclude that 2.4G2 is a potent inhibitor of IgG Fc receptor-mediated immune clearance in vivo.

In response to norepinephrine or isoproterenol, dogs with pressure overload cardiac hypertrophy showed depressed contractility and myocardial lactic acid production when compared to normal dogs. In these dogs with hypertrophy the inotropic response to ouabain remained normal and myocardial lactate production was not induced. This finding is compatible with the idea that the increased oxygen demand induced by beta-agonists exceeds the limited coronary blood flow reserve of the hypertrophied heart leading to myocardial anaerobic metabolism and reduced inotropic responsiveness. Ouabain, on the other hand, did not induce anaerobic metabolism and the inotropic response was not depressed.