Absorbable versus nonabsorbable sutures for the Krackow suture repair of acute Achilles tendon rupture: a prospective randomized controlled trial.

AIMS: Although absorbable sutures for the repair of acute Achilles tendon rupture (ATR) have been attracting attention, the rationale for their use remains insufficient. This study prospectively compared the outcomes of absorbable and nonabsorbable sutures for the repair of acute ATR. METHODS: A total of 40 patients were randomly assigned to either braided absorbable polyglactin suture or braided nonabsorbable polyethylene terephthalate suture groups. ATR was then repaired using the Krackow suture method. At three and six months after surgery, the isokinetic muscle strength of ankle plantar flexion was measured using a computer-based Cybex dynamometer. At six and 12 months after surgery, patient-reported outcomes were measured using the Achilles tendon Total Rupture Score (ATRS), visual analogue scale for pain (VAS pain), and EuroQoL five-dimension health questionnaire (EQ-5D). RESULTS: Overall, 37 patients completed 12 months of follow-up. No difference was observed between the two groups in terms of isokinetic plantar flexion strength, ATRS, VAS pain, or EQ-5D. No re-rupture was observed in either group. CONCLUSION: The use of absorbable sutures for the repair of acute ATR was not inferior to that of nonabsorbable sutures. This finding suggests that absorbable sutures can be considered for the repair of acute ATRs. Cite this article: Bone Joint J 2022;104-B(8):938-945.

Role of LXR alpha in regulating expression of glucose transporter 4 in adipocytes - Investigation on improvement of health of diabetic patients.

BACKGROUND: The insulin-responsive glucose transporter 4 (GLUT4) plays prominent role in insulin-mediated facilitated glucose uptake into most of the cell types, majorly muscle, liver and adipose tissue. Impaired expression of GLUT4 has been linked to insulin resistance and diabetes. In adipocytes, excess lipids that are generated from liver and by de novo lipogenesis utilizing blood sugar, are stored. There are various nuclear factors, co-factors and signaling mechanisms that directly and indirectly regulate glucose transporter activity in adipocytes. Molecular mechanism behind the regulation of GLUT4 in adipocytes has not elucidated well. OBJECTIVE: Therefore, the present study focuses to explore the role of Liver X receptor- alpha (LXRα) on GLUT4 expression and the possible co-factors involved during in vitro adipogenesis and is assessed by modulating the activity of LXRα with specific agonist and antagonist ligands in 3T3L1 differentiated cells. RESULTS: The results demonstrate that SR 9238 (300nM), a strong inhibitor of LXRα, decreased the rate of adipogenesis through reduced lipid droplet formation in adipocytes without affecting the cell morphology. The FMOC-l-Leucine (FLL), a known partial ligand of PPARγ, enhanced the expression of LXRα. Thus, it can be concluded that LXRα has a significant role in adipocyte differentiation and FLL interaction promoted the transcription of LXRα, thereby promotes GLUT4 expression. The results in this study identified the role of LXRα in regulating the expression of GLUT4 through SRC1. CONCLUSION: The study is of much relevance in treatment of diabetes and also opens the possibility of identifying new drug molecules that target LXRα.

Comparison of the quantitative CT imaging biomarkers of idiopathic pulmonary fibrosis at baseline and early change with an interval of 7 months.

RATIONALE AND OBJECTIVES: Median survival of patients with idiopathic pulmonary fibrosis (IPF) is 2-5 years. Sensitive imaging metrics can play a role in detecting early changes in therapeutic development. The aim of the present study was to compare known computed tomography (CT) histogram kurtosis and a classifier-based quantitative score to assess baseline severity and change over time in patients with IPF. MATERIALS AND METHODS: A total of 57 patients with at least baseline and paired follow-up scans were selected from an imaging database of standardized CT scans obtained from patients with IPF. CT histogram measurement of kurtosis and quantitative lung fibrosis (QLF) and quantitative interstitial lung disease (QILD) scores from a classification algorithm were calculated. Spearman rank correlations were used to assess associations between baseline severity and changes for all CT-derived measures compared to forced vital capacity (FVC) and carbon monoxide diffusion capacity (DLCO) (percent predicted). RESULTS: At baseline, mean (±SD) of kurtosis was 2.43 (±1.83). Mean (±SD) values of QLF and QILD scores were 20.7% (±13.4) and 43.3% (±20.0), respectively. All baseline histogram indices and QLF and QILD scores were correlated well with baseline FVC and DLCO. When assessing associations with changes in FVC and DLCO over time, only QLF score was statistically significant (ρ = -0.57; P < .0001 for FVC and ρ = -0.34; P = .025 for DLCO), whereas kurtosis was not. CONCLUSIONS: Classifier-model-derived scores (QLF and QILD), based on a set of texture features, are associated with baseline disease extent and are also a sensitive measure of change over time. A QLF score can be used for measuring the extent of disease severity and longitudinal changes.

Reversible MR changes in the cat brain after cerebral fat embolism induced by triolein emulsion.

BACKGROUND AND PURPOSE: Clinical cerebral-fat embolism shows both reversible and irreversible changes. We used MR imaging to investigate the reversibility of embolized lesions induced with a fat-emulsion technique and to evaluate the histologic findings. METHODS: A fat emulsion was made with 0.05 mL of triolein and 20 mL of normal saline and vigorous to-and-fro movement through a three-way stopcock. In 50 cats, the internal carotid artery was infused with the fat emulsion. Cats were divided into six groups on the basis of time delay after embolization: 1 hour; 1 and 4 days; and 1, 2, and 3 weeks. MR imaging and histologic examination were performed at these times. RESULTS: Embolized lesions were hyperintense on T2-weighted images, isointense or mildly hyperintense on diffusion-weighted images, isointense on apparent diffusion coefficient maps, and enhancing on gadolinium-enhanced T1-weighted images at 1 hour. These MR imaging findings were less evident at day 1 and reverted to normal after day 4 (isointense on all images). Electron microscopy showed minimal findings in the cortical lesion in groups 1 and 2 (group 1 at 1 hour and group 2 at 1 hour and 1 day). Light microscopic findings revealed evidence of necrosis-small focal gliosis and demyelination in the periventricular white matter-in only one cat. The number of intravascular fat globules was not significantly different between groups, as visualized by oil red O staining. CONCLUSION: Cerebral-fat embolism induced by a triolein emulsion revealed reversible MR findings and minimal histologic findings.

Hemorrhage in cerebral fat embolisms in a cat model using triolein dependent on the physical properties of triolein.

PURPOSE: Hemorrhage is a finding of clinical fat embolism syndrome. The purpose of the present study was to evaluate the occurrence of hemorrhage in the cat brain by SW MR imaging after infusion of triolein as a bolus or as an emulsion into the carotid artery. MATERIALS AND METHODS: Twenty-two cats were divided into two groups according to the type of triolein infused: group 1 (n = 11) was infused with a 0.1 ml triolein bolus, group 2 (n = 11) with triolein emulsion containing 0.1 ml triolein in 20 ml saline. SW imaging was performed before and after triolein infusion (at 2 h, 1 and 4 days). After MR imaging on day 4, cats were sacrificed and brains were immediately excised. Hemorrhage was evaluated using H&E staining. RESULTS: Hemorrhage was observed in eight cats in group 1, in no cats in group 2. Hemorrhage on SW images was found to correspond with light microscopy. CONCLUSIONS: SW images revealed hemorrhage in lesion hemispheres infused with triolein bolus. However, there was no evidence of hemorrhage infused with emulsified triolein. Thus, the occurrence of hemorrhage in cerebral fat embolism may depend on fat status.