Role of CD34 in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is caused by a variety of pathogenic factors, including chronic recurrent inflammation of the ileum, rectum, and colon. Immune cells and adhesion molecules play an important role in the course of the disease, which is actually an autoimmune disease. During IBD, CD34 is involved in mediating the migration of a variety of immune cells (neutrophils, eosinophils, and mast cells) to the inflammatory site, and its interaction with various adhesion molecules is involved in the occurrence and development of IBD. Although the function of CD34 as a partial cell marker is well known, little is known on its role in IBD. Therefore, this article describes the structure and biological function of CD34, as well as on its potential mechanism in the development of IBD.

Apoptosis, rather than neurogenesis, induces significant hippocampal-dependent learning and memory impairment in chronic low Cd2+ exposure.

Cadmium (Cd), a ubiquitous toxic heavy metal, with the intractable trait of low degradation, can induce multiple organ damage. Whereas, far less is known about its neurotoxicity and the specific mechanism in the chronic low Cd exposure. To investigate the chronic neurotoxicity of Cd2+ , we traced its effects for up to 30 months in mice which were exposed to Cd2+ by drinking the mimicking Cd-polluted water. We found the toxicity of chronic Cd exposure was a process associated with the transition from autophagy to apoptosis, and the switch of autophagy-apoptosis was Cd dose-dependent with the threshold of [Cd2+ ] 0.04 mg/L. Furthermore, JNK was found to be a hub molecule orchestrated the switch of autophagy-apoptosis by interacting with Sirt1 and p53. At last, the hippocampus-dependent learning and memory was damaged by continuous neuron apoptosis rather than deficit of neurogenesis. Therefore, elucidation of the effect, process, and potential molecular mechanism of the chronic low Cd2+ exposure is important for controlling of the environmental-pollutant Cd.

Use of a Publicly Available Database to Determine the Impact of Diabetes on Length of Hospital Stay for Elective Orthopedic Procedures in California.

In California, 1 in 3 hospital beds are occupied by adults with diabetes. The aim of this study was to examine whether diabetes impacts length of stay (LOS) following common elective orthopedic procedures compared to nondiabetic individuals, and also the performance of hospitals across California for these procedures. Using the Public Use California Patient Discharge Data Files for 2010-2012, the authors examined LOS for elective discharges for hip, spine, or knee surgery (n = 318,861) from the total population of all discharges (n = 11,476,073) for 309 hospitals across California. In all, 16% of discharges had a codiagnosis of diabetes. Unadjusted average LOS was 3.11 days without and 3.40 days with diabetes (mean difference 0.29 [95% confidence interval (0.27, 0.31) days, P < 0.01]). After adjusting for covariates, diabetes no longer resulted in a significant difference in LOS. However, the presence of common comorbidities did significantly impact LOS. Average LOS for patients with diabetes also varied widely by hospital, ranging between -50% and +100% of the mean LOS for all hospitals. Diabetes does not prolong LOS after orthopedic procedures unless comorbidities are present. Nevertheless, across California there is significant variation in LOS between individual hospitals, which may inform the decision-making process for prospective patients and payers.