Efficacy of Hand Therapy After Volar Locking Plate Fixation of Distal Radius Fracture in Middle-Aged to Elderly Women: A Randomized Controlled Trial.

PURPOSE: This study aimed to evaluate the efficacy of hand therapy after volar locking plate fixation of distal radius fractures in middle-aged to elderly women. METHODS: Fifty-seven patients diagnosed with distal radius fractures who had undergone volar plate fixation were enrolled in a prospective, randomized controlled trial. Patients were randomized into the hand therapy and independent exercise (IE) groups, in which they exercised independently under the surgeon's direction with and without hand therapy, respectively. The primary outcome was the functional outcome measured using the Disability of Arm, Shoulder, and Hand questionnaire after 6 weeks. The secondary outcomes were functional outcomes measured using the Patient-Rated Wrist Evaluation questionnaire, active and passive ranges of motion (ROMs), grip strength, key pinch strength, and pain measured on a visual analog scale. Patients were followed up in the outpatient department at 2, 4, 6, and 8 weeks and at 3 and 6 months. RESULTS: The Disability of Arm, Shoulder, and Hand scores were significantly lower in the hand therapy group at 6 weeks after surgery (12.5 vs 19.4 in the IE group). The postoperative visual analog scale pain scores were significantly lower in the hand therapy group at 2, 4, and 6 weeks (10.2 vs 17.6 in the IE group). The active ROM of the wrist flexion-extension arc at 2, 4, 6, and 8 weeks; active ROM of the pronation-supination arc at 6 and 8 weeks; and passive ROM of the wrist flexion-extension arc at 2, 4, and 8 weeks were significantly greater in the hand therapy group. CONCLUSIONS: Hand therapy improved the outcomes after volar locking plate fixation for distal radius fracture in middle-aged to elderly women at 8 weeks after surgery. No significant between-group differences were observed in any functional outcome measure at 6 months after surgery, as previously reported. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic II.

12α-Hydroxylated bile acid induces hepatic steatosis with dysbiosis in rats.

There is an increasing need to explore the mechanism of the progression of non-alcoholic fatty liver disease. Steroid metabolism is closely linked to hepatic steatosis and steroids are excreted as bile acids (BAs). Here, we demonstrated that feeding WKAH/HkmSlc inbred rats a diet supplemented with cholic acid (CA) at 0.5 g/kg for 13 weeks induced simple steatosis without obesity. Liver triglyceride and cholesterol levels were increased accompanied by mild elevation of aminotransferase activities. There were no signs of inflammation, insulin resistance, oxidative stress, or fibrosis. CA supplementation increased levels of CA and taurocholic acid (TCA) in enterohepatic circulation and deoxycholic acid (DCA) levels in cecum with an increased ratio of 12α-hydroxylated BAs to non-12α-hydroxylated BAs. Analyses of hepatic gene expression revealed no apparent feedback control of BA and cholesterol biosynthesis. CA feeding induced dysbiosis in cecal microbiota with enrichment of DCA producers, which underlines the increased cecal DCA levels. The mechanism of steatosis was increased expression of Srebp1 (positive regulator of liver lipogenesis) through activation of the liver X receptor by increased oxysterols in the CA-fed rats, especially 4ß-hydroxycholesterol (4ßOH) formed by upregulated expression of hepatic Cyp3a2, responsible for 4ßOH formation. Multiple regression analyses identified portal TCA and cecal DCA as positive predictors for liver 4ßOH levels. The possible mechanisms linking these predictors and upregulated expression of Cyp3a2 are discussed. Overall, our observations highlight the role of 12α-hydroxylated BAs in triggering liver lipogenesis and allow us to explore the mechanisms of hepatic steatosis onset, focusing on cholesterol and BA metabolism.

Activity of ERK regulates mucin 3 expression and is involved in undifferentiated Caco-2 cell death induced by 3-oxo-C12-homoserine lactone.

The signal molecule, 3-oxo-C12-homoserine lactone (3-oxo-C12-HSL), is similar to a mammalian hormone in bacteria. Although most studies have examined the effects of high 3-oxo-C12-HSL concentrations (>200 µM) on mammalian cellular functions because ~600 µM 3-oxo-C12-HSL can be secreted in biofilms of Pseudomonas aeruginosa grown in vitro, we previously showed that a low 3-oxo-C12-HSL concentration (30 µM) induces the apoptosis of undifferentiated Caco-2 cells through suppressing Akt activity. Here, we found that a low concentration of 3-oxo-C12-HSL-activated ERK1/2 in undifferentiated Caco-2 cells. Incubating cells with the ERK pathway inhibitor U0126 for 30 min alleviated the mucin 3 (MUC3) expression suppressed by 3-oxo-C12-HSL, and the upregulation of MUC3 expression induced by a 48-h incubation with U0126-reduced cell death. Thus, altered MUC3 expression caused by long-term attenuated ERK1/2 activity might correlate with the death of undifferentiated Caco-2 cells induced by 3-oxo-C12-HSL.