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Aim: To evaluate the therapeutic response to triamcinolone acetonide (TA) and triamcinolone hexacetonide (TH) injections in the knee of children with JIA. Material and methods: 46 joints of 42 children undergoing intra-articular injections were randomly treated with either TH or TA depending on the availability of the drug. A good response was defined as the decrease in articular score of 60% from the baseline and the ultrasound absence of synovitis. Clinical, laboratory variables were noted to examine possible predictive factors of the result. Results: Of 42 children with JIA, the most common was the oligoarticular persistent form in 24 (57.1%) children. Six-month remission was observed in 21.4 % of children, TA vs. TH: 36.8% vs. 8.7% (p=0.02). The absence of signs of knee inflammation within 12 months was found in 23.8% of children, after the application of TA vs. TH: 31.6% vs. 17.4% (p=0.28). However, long-term, a twenty-four-month remission was achieved in 52.4% of children – in twice as many children after TH (69.9%) than after TA application (31.6%) (p=0.03). A statistically significant correlation was observed between articular score values and duration of remission after TH application, (r=0.56, p=0.006; 95%CI: 0.145-0.80). Two children developed side effects in the form of subcutaneous atrophy at the site of injection, one girl developed transient crystal synovitis after TH applications. Conclusion:This study has shown that intraarticular steroid injections are safe for the treatment of joint inflammation in JIA,and TA is effective in short-term follow-up where TH is an optimum choice in long-term follow-up.

Several cardiometabolic factors such as diabetes, hypertension and dyslipidemia which are prevalent in older adults with increased body mass index (BMI) may play an important role in sarcopenia development.[[2], [7]] Excess fat mass interrupts the blood glucose pathway and triggers insulin resistance which may then further enhance the development of sarcopenia. Hospitalization rates over 5 years among individuals with BMI >= 30 kg/m SP 2 sp compared to those with normal BMI following adjustments in Model 2 and remained significant with slight attenuation after differences in diabetes status were accounted for [RR (95%CI): 1.90 (1.11-3.28), Model 3]. The direct effect of BMI categories on the risk of all outcomes (Y1, Y2, Y3) was significant for BMI >= 30 kg/m SP 2 sp but not BMI < 18.5 or BMI: 25-29.9 kg/m SP 2 sp compared to those the BMI: 18.5-25 kg/m SP 2 sp group, suggesting the potential mediating role of FBG (Figure 2A-C). [Extracted from the article]

Aims Cardiac energetic impairment is a major finding in takotsubo patients. We investigate specific metabolic adaptations to direct future therapies. Methods and results An isoprenaline-injection female rat model (vs. sham) was studied at Day 3; recovery assessed at Day 7. Substrate uptake, metabolism, inflammation, and remodelling were investigated by 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography, metabolomics, quantitative PCR, and western blot (WB). Isolated cardiomyocytes were patch-clamped during stress protocols for redox states of NAD(P)H/FAD or [Ca2+]c, [Ca2+]m, and sarcomere length. Mitochondrial respiration was assessed by seahorse/Clark electrode (glycolytic and β-oxidation substrates). Cardiac 18F-FDG metabolic rate was increased in takotsubo (P  = 0.006), as was the expression of GLUT4-RNA/GLUT1/HK2-RNA and HK activity (all P  < 0.05), with concomitant accumulation of glucose- and fructose-6-phosphates (P  > 0.0001). Both lactate and pyruvate were lower (P  < 0.05) despite increases in LDH-RNA and PDH (P  < 0.05 both). β-Oxidation enzymes CPT1b-RNA and 3-ketoacyl-CoA thiolase were increased (P  < 0.01) but malonyl-CoA (CPT-1 regulator) was upregulated (P  = 0.01) with decreased fatty acids and acyl-carnitines levels (P  = 0.0001–0.02). Krebs cycle intermediates α-ketoglutarate and succinyl-carnitine were reduced (P  < 0.05) as was cellular ATP reporter dihydroorotate (P  = 0.003). Mitochondrial Ca2+ uptake during high workload was impaired on Day 3 (P  < 0.0001), inducing the oxidation of NAD(P)H and FAD (P  = 0.03) but resolved by Day 7. There were no differences in mitochondrial respiratory function, sarcomere shortening, or [Ca2+] transients of isolated cardiomyocytes, implying preserved integrity of both mitochondria and cardiomyocyte. Inflammation and remodelling were upregulated—increased CD68-RNA, collagen RNA/protein, and skeletal actin RNA (all P  < 0.05). Conclusion Dysregulation of glucose and lipid metabolic pathways with decreases in final glycolytic and β-oxidation metabolites and reduced availability of Krebs intermediates characterizes takotsubo myocardium. The energetic deficit accompanies defective Ca2+ handling, inflammation, and upregulation of remodelling pathways, with the preservation of sarcomeric and mitochondrial integrity. [ABSTRACT FROM AUTHOR]