Need of vascular surgeon and comparison of value for anterior lumbar interbody fusion (ALIF) in lateral decubitus: Delphi consensus

European Spine Journal - Anterior lumbar approaches are recommended for clinical conditions that require interbody stability, spinal deformity corrections or a large fusion area. Anterior lumbar...     

Pivoting to Telehealth: the HSS Experience,Value Gained,and Lessons Learned

HSS Journal ® -     

Changes in serum adipokine levels during pioglitazone treatment for nonalcoholic steatohepatitis: relationship to histological improvement.

BACKGROUND & AIMS: Thiazolidinedione (TZD) therapy improves liver histology in nonalcoholic steatohepatitis (NASH) through a mechanism possibly related to its insulin-sensitizing or anti-inflammatory activity. This study was conducted to assess changes in serum levels of selected adipokines and proinflammatory cytokines and to relate these changes to the improved liver histology resulting from pioglitazone therapy for NASH. METHODS: Serum samples from 18 patients with NASH obtained at day 0 and week 48 of therapy during an open-label study of pioglitazone were tested for adiponectin, leptin, interleukin (IL)-1a, IL-6, and tumor necrosis factor (TNF)-alpha levels. Paired liver biopsy specimens were scored (0-4) for steatosis, parenchymal inflammation, cell injury, and fibrosis. RESULTS: Adiponectin levels increased from 3.7 to 10.3 mug/mL at week 48 (P < .01); the levels of the other cytokines were unchanged: TNF-alpha, 9.1 vs 8.8 pg/mL; IL-1a, 3.9 vs 3.4 pg/mL; IL-6, 19.4 vs 13.4 pg/mL; and leptin, 24.8 vs 29.6 ng/mL (P > .05 for all). Pioglitazone therapy was associated with improvements in steatosis (2.5 vs 1.0), parenchymal inflammation (3.3 vs 2.1), cell injury (2.2 vs 0.9), and fibrosis (2.0 vs 1.4). The change in adiponectin level was associated with the improvement in steatosis (P = .03) as well as in a summary NASH activity index score (P = .01). Changes in IL-1, IL-6, TNF-alpha, and leptin levels did not correlate with improvements in the histological features. CONCLUSIONS: Improvements in liver histology during TZD therapy may be modulated by an adiponectin-mediated effect on insulin sensitivity and hepatic fatty acid metabolism rather than by changes in proinflammatory cytokines.     

Hepatitis C virus JFH-1 strain infection in chimpanzees is associated with low pathogenicity and emergence of an adaptive mutation

The identification of the hepatitis C virus (HCV) strain JFH-1 enabled the successful development of infectious cell culture systems. Although this strain replicates efficiently and produces infectious virus in cell culture, the replication capacity and pathogenesis in vivo are still undefined. To assess the in vivo phenotype of the JFH-1 virus, cell culture-generated JFH-1 virus (JFH-1cc) and patient serum from which JFH-1 was isolated were inoculated into chimpanzees. Both animals became HCV RNA-positive 3 days after inoculation but showed low-level viremia and no evidence of hepatitis. HCV viremia persisted 8 and 34 weeks in JFH-1cc and patient serum-infected chimpanzees, respectively. Immunological analysis revealed that HCV-specific immune responses were similarly induced in both animals. Sequencing of HCV at various times of infection indicated more substitutions in the patient serum-inoculated chimpanzee, and the higher level of sequence variations seemed to be associated with a prolonged infection in this animal. A common mutation G838R in the NS2 region emerged early in both chimpanzees. This mutation enhances viral assembly, leading to an increase in viral production in transfected or infected cells. CONCLUSION: Our study shows that the HCV JFH-1 strain causes attenuated infection and low pathogenicity in chimpanzees and is capable of adapting in vivo with a unique mutation conferring an enhanced replicative phenotype.     

Coal power plant emission exposure and its effect on education access

Aim

We investigate the effects of exposure to coal power plant emissions on school absenteeism for children with asthma, a leading cause of health-related barriers to education.

Subject and methods

We combine responses from the 2007–2009 Behavioral Risk Factor Surveillance System survey with coal power plant emission data to estimate a zero negative binomial regression model of school absences and investigate misspecification bias associated with naive assumptions about emission dispersion and self-selection into treatment groups.

Results

The results show a robust, positive relationship (P?<?0.001) between increases in emission exposure and the likelihood of a school absence due to an asthma episode. Exposure to higher emission volumes is associated with a 1.92–4.81 % higher likelihood of missing an additional school day. Furthermore, assuming uniform emission dispersion and not controlling for self-selection underestimates the effects by 2.72–4.27 times.

Conclusion

Access to education and the ability to develop human capital through schooling are affected for children with respiratory illnesses who are exposed to emissions. Public policies for emission regulation are likely to remain relevant for lowering pediatric respiratory health risks and lowering barriers to educational opportunities.