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Sex refers to biological differences between men and women. Although sex is a fundamental aspect of human physiology that splits the population in two approximately equal halves, this essential biological variable is rarely considered in the design of basic physiological studies, in translating findings from basic science to clinical research, or in developing personalized medical strategies. Contrary to sex, gender refers to social and cultural factors related to being a man or a woman in a particular historical and cultural context. Unfortunately, gender is often used incorrectly by scientists and clinical investigators as synonymous with sex. This article clarifies the definition of sex and gender and reviews evidence showing how sex and gender interact with each other to influence etiology, presentation of disease, and treatment outcomes. In addition, strategies to improve the inclusion of female and male human beings in preclinical and clinical studies will be presented, and the importance of embedding concepts of sex and gender into postgraduate and medical curricula will be discussed. Also, provided is a list of resources for educators. In the history of medical concepts, physiologists have provided pivotal contributions to understanding health and disease processes. In the future, physiologists should provide the evidence for advancing personalized medicine and for reducing sex and gender disparities in health care.

Despite the emergence of glucometrics (i.e., systematic analysis of data on blood glucose levels of inpatients) as a subject of high interest, there remains a lack of standardization on how glucose parameters are measured and reported. This dilemma must be resolved before a national benchmarking process can be developed that will allow institutions to track and compare inpatient glucose control performance against established guidelines and that can also be supported by quality care organizations. In this article, we review some of the questions that need to be resolved through consensus and review of the evidence, and discuss some of the limitations in analyzing and reporting inpatient glucose data that must be addressed (or at least accepted as limitations) before hospitals can commit resources to gathering, compiling, and presenting inpatient glucose statistics as a health care quality measure. Standards must include consensus on which measures to report, the unit of analysis, definitions of targets for hyperglycemia treatment, a definition of hypoglycemia, determination of how data should be gathered (from chart review or from laboratory information systems), and which type of sample (blood or point of care) should be used for analysis of glycemic control. Hospitals and/or their representatives should be included in the discussion. For inpatient glucose control to remain a focus of interest, further dialogue and consensus on the topic are needed.

AbstractMice homozygous for the targeted disruption of the glycoprotein hormone α-subunit (αGsu) display hypertrophy and hyperplasia of the anterior pituitary thyrotropes. Thyrotrope hyperplasia results in tumors in aged αGsu−/− mice. These adenomatous pituitaries can grow independently as intrascapular transplants in hypothyroid mice, suggesting that they have progressed beyond simple hyperplasia. We used magnetic resonance imaging to follow the growth and regression of thyrotrope adenomatous hyperplasia in response to thyroid hormone treatment and discovered that the tumors retain thyroid hormone responsiveness. Somatostatin (SMST) and its diverse receptors have been implicated in cell proliferation and tumorigenesis. To test the involvement of SMST receptor 2 (SMSTR2) in pituitary tumor progression and thyroid hormone responsiveness in αGsu−/− mutants, we generated Smstr2−/−, αGsu−/− mice. Smstr2−/−, αGsu−/− mice develop hyperplasia of thyrotropes, similar to αGsu−/− mutants, demonstrating that SMSTR2 is dispensable for the development of pituitary adenomatous hyperplasia. Thyrotrope hyperplasia in Smstr2−/−, αGsu−/− mice regresses in response to T4 treatment, suggesting that SMSTR2 is not required in the T4 feedback loop regulating TSH secretion.

Objective Multiple-valve (MUV) procedures currently exhibit higher operative mortality than do single-valve procedures, but a paucity of scientific information exists to explain the observation. This topic was examined using The Society of Thoracic Surgeons Database. Methods All patients in the The Society of Thoracic Surgeons data set undergoing valve surgery (except pulmonary valve and aortic root operations) from 1993 through 2007 were identified (N = 623,039). Baseline characteristics and postoperative outcomes were contrasted between all seven combinations of single-valve and MUV procedures involving aortic, mitral, and tricuspid valves. Seven independent logistic regression analyses were performed, based on the seven procedures, and multivariable risk factors for mortality were compared, with emphasis on single-valve versus MUV procedures. Results Baseline characteristics for MUV procedures (n = 67,926) shared many similarities to those for single-valve procedures (n = 555,113), including age, ejection fraction, and comorbidities. Preoperative renal failure, New York Heart Association class III to IV, nonelective presentation, and reoperation were slightly more common in MUV subsets, and coronary bypass was less frequent. Operative mortality was almost double for MUV as compared with single-valve procedures (10.7% vs 5.7%, P = 0.0001). Categorical predictors with the largest odds ratios for mortality were emergency status, renal failure, and second reoperation. However, predictors for mortality were generally consistent in order and magnitude between the single-valve and MUV subgroups. Conclusions Despite similarities in preoperative profiles of the patients undergoing single-valve and MUV procedures, mortality for MUV surgery remains considerably higher. Determinants of operative mortality and morbidity differ little across the procedural groups, and these findings serve as a benchmark for future studies, as well as suggest a continued search for explanations of poorer MUV outcomes.

PurposeTo examine the outcomes of patients with chemotherapy-sensitive mantle-cell lymphoma (MCL) following a first hematopoietic stem-cell transplantation (HCT), comparing outcomes with autologous (auto) versus reduced-intensity conditioning allogeneic (RIC allo) HCT and with transplantation applied at different times in the disease course.Patients and MethodsIn all, 519 patients who received transplantations between 1996 and 2007 and were reported to the Center for International Blood and Marrow Transplant Research were analyzed. The early transplantation cohort was defined as those patients in first partial or complete remission with no more than two lines of chemotherapy. The late transplantation cohort was defined as all the remaining patients.ResultsAuto-HCT and RIC allo-HCT resulted in similar overall survival from transplantation for both the early (at 5 years: 61% auto-HCT v 62% RIC allo-HCT; P = .951) and late cohorts (at 5 years: 44% auto-HCT v 31% RIC allo-HCT; P = .202). In both early and late transplantation cohorts, progression/relapse was lower and nonrelapse mortality was higher in the allo-HCT group. Overall survival and progression-free survival were highest in patients who underwent auto-HCT in first complete response. Multivariate analysis of survival from diagnosis identified a survival benefit favoring early HCT for both auto-HCT and RIC allo-HCT.ConclusionFor patients with chemotherapy-sensitive MCL, the optimal timing for HCT is early in the disease course. Outcomes are particularly favorable for patients undergoing auto-HCT in first complete remission. For those unable to achieve complete remission after two lines of chemotherapy or those with relapsed disease, either auto-HCT or RIC allo-HCT may be effective, although the chance for long-term remission and survival is lower.