Class 3 obesity is not associated with same-day admission in obese patients undergoing parathyroidectomy.

IMPORTANCE: Rising rates of obesity and outpatient performance of parathyroidectomies are making it increasingly crucial to investigate the association of obesity with post-operative complications. OBJECTIVE: To determine whether Class 3 obesity is associated with increased same-day admission compared to lower obesity classes following outpatient parathyroidectomy. DESIGN: Retrospective cohort study. SETTING: Outpatient surgery. PATIENTS: 12,973 patients ≥18 years old who underwent outpatient parathyroidectomy between 2014 and 2016, per the American College of Surgeons National Surgical Quality Improvement Program registry. INTERVENTIONS: Primary exposure variable: body mass index (BMI), with patients assigned to one of six cohorts. MEASUREMENTS: Primary outcome measure: same-day admission. Secondary outcome measure: 30-day readmission. Logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI). MAIN RESULTS: There was a final sample size of 12,973 adult patients who underwent parathyroidectomy from 2014 to 2016. The admission rate for BMI ≥30 and < 40 kg/m2 (reference cohort) was 42.6%. The admission rates for Class 3 obesity categories were 46.2%, 56.2%, and 52.6% for those in the BMI range of ≥40 kg/m2 and < 50 kg/m2, ≥50 kg/m2 and < 60 kg/m2, and ≥ 60 kg/m2, respectively. On multivariable logistic regression, there were no difference in the odds of 30-day hospital admission or readmission rate with any of the BMI cohorts when compared to the reference group. CONCLUSIONS: There is no significant difference in rates of same-day admission or 30-day readmission between any Class 3 (BMI ≥40 kg/m2) obesity cohort and the Class 1 and 2 (BMI ≥30 and < 40 kg/m2) reference cohort following outpatient parathyroidectomy. This corroborates the notion that BMI classes cannot be used in a vacuum to determine eligibility for outpatient parathyroidectomy - a concept that can guide safe and cost-effective institutional practices.

Nerve lengthening and subsequent end-to-end repair yield more favourable outcomes compared with autograft repair of rat sciatic nerve defects.

Outcomes of end-to-end nerve repairs are more successful compared with outcomes of repairs bridged by nerve grafts. However, end-to-end repairs are not always possible for large nerve gaps, as excessive tension may cause catastrophic failure. In this study, we built on previous nerve-lengthening studies to test the hypotheses that gradual lengthening of the proximal stump across a large nerve gap enables an end-to-end repair and such a repair results in more favourable regenerative outcomes than autografts, which represent the gold standard in bridging nerve gaps. To test these, we compared structural and functional outcomes in Lewis rats after repair of sciatic nerve gaps using either autografts or a novel compact internal fixator device, which was used to lengthen proximal nerve stumps towards the distal stump over 2 weeks, prior to end-to-end repair. Twelve weeks after the initial injury, outcomes following nerve lengthening/end-to-end repair were either comparable or superior in every measure compared with repair by autografting. The sciatic functional index was not significantly different between groups at 12 weeks. However, we observed a reduced rate of contracture and corresponding significant increase in paw length in the lengthening group. This functional improvement was consistent with structural regeneration; axonal growth distal to the injury was denser and more evenly distributed compared with the autograft group, suggesting substantial regeneration into both tibial and peroneal branches of the sciatic nerve. Our findings show that end-to-end repairs following nerve lengthening are possible for large gaps and that this strategy may be superior to graft-based repairs.

The Effects of Playing Multiple High School Sports on National Basketball Association Players' Propensity for Injury and Athletic Performance.

BACKGROUND: Athletes who specialize in their sport at an early age may be at risk for burnout, overuse injury, and reduced attainment of elite status. Timing of sport specialization has not been studied in elite basketball athletes. HYPOTHESIS: National Basketball Association (NBA) players who played multiple sports during adolescence would be less likely to experience injury and would have higher participation rates in terms of games played and career length compared with single-sport athletes. STUDY DESIGN: Descriptive epidemiology study. METHODS: First-round draft picks from 2008 to 2015 in the NBA were included in the study. From publically available records from the internet, the following data were collected for each athlete: participation in high school sports, major injuries sustained in the NBA, percentage of games played in the NBA, and whether the athlete was still active in the NBA. Athletes who participated in sports in addition to basketball during high school were defined as multisport athletes and were compared with athletes who participated only in basketball in high school. RESULTS: Two hundred thirty-seven athletes were included in the study, of which 36 (15%) were multisport athletes and 201 (85%) were single-sport athletes in high school. The multisport cohort played in a statistically significantly greater percentage of total games (78.4% vs 72.8%; P < .001). Participants in the multisport cohort were less likely to sustain a major injury during their career (25% vs 43%, P = .03). Finally, a greater percentage of the multisport athletes were active in the league at time of data acquisition, indicating increased longevity in the NBA (94% vs 81.1%; P = .03). CONCLUSION: While a minority of professional basketball athletes participated in multiple sports in high school, those who were multisport athletes participated in more games, experienced fewer major injuries, and had longer careers than those who participated in a single sport. Further research is needed to determine the reasons behind these differences.

Identification of the gC1qR sites for the HIV-1 viral envelope protein gp41 and the HCV core protein: Implications in viral-specific pathogenesis and therapy.

A substantial body of evidence accumulated over the past 20 years supports the concept that gC1qR is a major pathogen-associated pattern recognition receptor (PRR). This conclusion is based on the fact that, a wide range of bacterial and viral ligands are able to exploit gC1qR to either suppress the host's immune response and thus enhance their survival, or to gain access into cells to initiate disease. Of the extensive array of viral ligands that have affinity for gC1qR, the HIV-1 envelope glycoprotein gp41, and the core protein of hepatitis C virus (HCV) are of major interest as they are known to contribute to the high morbidity and mortality caused by these pathogens. While the HCV core protein binds gC1qR and suppresses T cell proliferation resulting in a significantly diminished immune response, the gp41 employs gC1qR to induce the surface expression of the NK cell ligand, NKp44L, on uninfected CD4(+) T cells, thereby rendering them susceptible to autologous destruction by NKp44 receptor expressing NK cells. Because of the potential for the design of peptide-based or antibody-based therapeutic options, the present studies were undertaken to define the gC1qR interaction sites for these pathogen-associated molecular ligands. Employing a solid phase microplate-binding assay, we examined the binding of each viral ligand to wild type gC1qR and 11 gC1qR deletion mutants. The results obtained from these studies have identified two major HCV core protein sites on a domain of gC1qR comprising of residues 144-148 and 196-202. Domain 196-202 in turn, is located in the last half of the larger gC1qR segment encoded by exons IV-VI (residues 159-282), which was proposed previously to contain the site for HCV core protein. The major gC1qR site for gp41 on the other hand, was found to be in a highly conserved region encoded by exon IV and comprises of residues 174-180. Interestingly, gC1qR residues 174-180 also constitute the cell surface-binding site for soluble gC1qR (sgC1qR), which can bind to the cell surface in an autocrine/paracrine manner via surface expressed fibrinogen or other membrane molecules. The identification of the sites for these viral ligands should therefore provide additional targets for the design of peptide-based or antigen-based therapeutic strategies.