Comparison of volumetric bone mineral density in the operated and contralateral knee after anterior cruciate ligament and reconstruction: A 1‐year follow‐up study using peripheral quantitative computed tomography

The purpose of this study was to quantify changes in volumetric bone mineral density (vBMD) in the tibial plateau of the operated and contralateral leg measured using peripheral quantitative computed tomography (pQCT) before and 3, 6, and 12 months after anterior cruciate ligament (ACL) reconstruction. The ACL was reconstructed with a hamstring tendon autograft using press‐fit fixation. pQCT measurements of the proximal tibia were obtained in 61 patients after ACL reconstruction, and total, cortical, and trabecular vBMD were calculated. vBMD in the operated leg decreased from baseline to 3 months (?12% [total], ?11% [cortical], and ?12.6% [trabecular]; p < 0.001) and remained below baseline for 12 months after surgery (6 months: ?9.5%, ?9.4%, and ?9.6%, p < 0.001; 12 months: ?8%, ?5%, and ?11%, p < 0.001). vBMD in the contralateral leg was slightly reduced only 6 months after surgery. Including age and sex as covariates into the analysis did not affect the results. ACL reconstruction contributed to loss in bone mineral density within the first year after surgery. The role of factors such as time of weight‐bearing, joint mechanics, post‐traumatic inflammatory reactions, or genetic predisposition in modulating the development of posttraumatic knee osteoarthritis after ACL injury should be further elucidated. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1804–1810, 2015.

     

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Extracellular vesicles (EV) are secreted signaling entities that enhance various pathological processes when released in response to cellular stresses. Respiratory exposures such as cigarette smoke and air pollution exert cellular stresses and are associated with an increased risk of several chronic diseases. The aim of this review was to examine the evidence that modifications in EV contribute to respiratory exposure-associated diseases. Publications were searched using PubMed and Google Scholar with the search terms (cigarette smoke OR tobacco smoke OR air pollution OR particulate matter) AND (extracellular vesicles OR exosomes OR microvesicles OR microparticles OR ectosomes). All original research articles were included and reviewed. Fifty articles were identified, most of which investigated the effect of respiratory exposures on EV release in vitro (25) and/or on circulating EV in human plasma (24). The majority of studies based their main observations on the relatively insensitive scatter-based flow cytometry of EV (29). EV induced by respiratory exposures were found to modulate inflammation (19), thrombosis (13), endothelial dysfunction (11), tissue remodeling (6), and angiogenesis (3). By influencing these processes, EV may play a key role in the development of cardiovascular diseases and chronic obstructive pulmonary disease and possibly lung cancer and allergic asthma. The current findings warrant additional research with improved methodologies to evaluate the contribution of respiratory exposure-induced EV to disease etiology, as well as their potential as biomarkers of exposure or risk and as novel targets for preventive or therapeutic strategies.     

In situ investigation of the kinetics and microstructure during photopolymerization by positron annihilation technique and NIR-photorheology

The microstructural free volume evolution during a photopolymerization process was studied on a commercial photopolymer (SPOT LV) in situ by positron annihilation lifetime spectroscopy (PALS) and concomitant NIR-photorheology. Analysis of the positron lifetime spectra revealed a high sensitivity of the PALS technique to the different phases of photopolymerization associated with different reaction rates as well as to the evolution of microstructural free-volume shrinkage, which was described at the molecular level by the Kohlrausch–Williams–Watts equation. The in situ PALS study of microstructural changes in photopolymerization was related to the vitrification (gel point) accompanied by shrinkage stress registered via NIR-photorheology. The simultaneous NIR measurements yield information on the monomer conversion of SPOT LV, which can be correlated to the occurrence of the gel point and the evolution of the microstructural free volume. This combined study allows us to see deeper into the crosslinking process and its influence on the resulting material characteristics.

Positron annihilation lifetime spectroscopy is a sensitive tool for the in situ study of the microstructural evolution during photopolymerization.     

Sudden hearing loss in patients with chronic hepatitis C treated with pegylated interferon/ribavirin

BACKGROUND: Sudden hearing loss has been reported on standard interferon (IFN)-alpha2 therapy. This is the first report on the occurrence of sudden hearing loss in six cases of chronic hepatitis C in temporal relation to treatment with pegylated (PEG)-IFN alfa2a or b/ribavirin combination therapy. Three patients were treated in an ongoing randomized placebo-controlled trial comparing the addition of 200 mg amantadine or placebo to the combination of 180 microg PEG-IFN alpha2a (PEGASYS, Roche, Basel, CH)/wk and 1-1.2 g ribavirin/d (COPEGUS, Roche, Nutley, USA) in de novo patients infected with HCV genotype 1. Sudden hearing loss and tinnitus developed on day 1 and after 4, 23, 25, 36, and 40 wk of treatment, respectively. CONCLUSIONS: Sudden hearing loss may occur in about 1% of patients on PEG-IFN/ribavirin combination therapy. This rate was not different to that observed in an untreated population. Possible mechanisms involved include direct ototoxicity of IFN, autoimmunity, and hematological changes. In contrast to published cases on auditory disability due to standard IFN, hearing loss did not fully resolve after discontinuation of therapy with PEG-IFN. On the other hand, symptoms did not worsen on continued treatment. Therefore, the decision whether to continue or to stop the treatment when signs of ototoxicity appear is based on the clinical judgment of the treating physician.