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Introduction Statin intensification is required in patients who have high-risk for cardiovascular events. However, it is unclear if this is needed in whom plasma LDL-C target was achieved with low-dose statin for primary prevention. We investigated the efficacy and safety of switching from low-dose statin to high-intensity statin among type 2 diabetes (T2D) who had achieved plasma LDL-C less then 100 mg/dl with low-dose statin treatment. Methods T2D patients with no atherosclerotic cardiovascular disease who had plasma LDL-C level less then 100 mg/dl while taking simvastatin ≤20 mg/day were randomized to continue using the same dosage of simvastatin (low-dose statin group; LS) for 12 weeks, or to switch to atorvastatin 40 mg/day for 6 weeks, and then, if tolerated, to atorvastatin 80 mg/day for 6 weeks (high-intensity statin group; HS). Biochemical test and adverse events were evaluated at baseline, 6 weeks, and 12 weeks. Results One hundred and fifty patients (76 LS, 74 HS, mean age 58.9±8.9 years, 72% female) were included. The mean baseline plasma LDL-C level on statin was slightly higher in the HS group (71.9±13.6 vs. 68.1±14.2 mg/dl, p=0.09). The HS group had a significantly lower plasma LDL-C level at both 6 and 12 weeks (both p less then 0.001). Plasma LDL-C less then 40 mg/dl was found more frequently in the HS group (23.0% vs. 3.9%, p less then 0.001). Discontinuation of statin due to adverse effects was more frequent in the HS group (5.4% vs. 1.3%, p=0.38 for atorvastatin 40 mg/day, 12.2% vs. 1.3%, p=0.03 for atorvastatin 80 mg/day). No serious adverse events were observed in either group. Conclusion Switching from low-dose statins to high-intensity statins resulted in a significant reduction in plasma LDL-C levels, and was fairly well tolerated during a 12-week study period. © 2020 Thongtang et al.Background Long non-coding RNAs (lncRNAs), as competing endogenous RNAs (ceRNAs), can regulate various pathophysiological processes by binding competitively to microRNAs at the post-transcription level. Our previous work demonstrated that miR-146a-5p was lowly expressed in diabetic peripheral neuropathy (DPN) rats. However, the ceRNA network in DPN mediated by lncRNAs and miR-146a-5p remains to be explored. Methods Two groups of rats (n=4 per group), a type 2 diabetes (T2DM) group and a DPN group, were used in this study. Sciatic nerve conduction velocity (NCV) of each rat was determined at the 6th and the 12th week. HDM201 concentration LncRNA microarray analysis was performed in the sciatic nerve of DPN and T2DM rats. Based on the TargetScan algorithm and the miRanda database, we determined the differentially expressed (DE) lncRNAs bound to miR-146a-5p. Furthermore, we verified the DE lncRNAs potentially bound to miR-146a-5p by qRT-PCR. The genes targeted by miR-146a-5p were identified by bioinformatics prediction and experimental techniques. Results We found 413 DE lncRNAs between DPN and T2DM rats (|log2FC| ≥ 2 and adjust P ≤ 0.05). Eight DE lncRNAs were predicted to bind to miR-146a-5p by both algorithms, of which four were verified by qRT-PCR. TRAF6, IRAK1, and SMAD4 were identified as miR-146a-5p targeted genes and were predominantly enriched in the inflammatory signaling pathway. Conclusion LncRNAs may contribute to the pathogenesis of DPN by regulating inflammation through functioning as ceRNAs of miR-146a-5p. © 2020 Feng et al.Objective To analyse the clinical features of pneumomediastinum associated with DKA (diabetic ketoacidosis) to improve clinicians' understanding of the disease. Methods A total of 78 patients with pneumomediastinum associated with DKA were identified in the literature search, and one patient treated in our hospital was included. The clinical features of the 79 patients were retrospectively analysed, and the pathogenesis, clinical symptoms, diagnostic methods, treatment strategies and prognoses were explored. Results All cases were confirmed by chest CT (computed tomography), and Kussmaul respiration, severe vomiting, chest pain were common symptoms. The main treatment principle was to correct acidosis and treat the primary disease. The majority of patients recovered within 1-2 weeks, and only 2 patients died. Conclusion Pneumomediastinum associated with DKA is a rare disease, and it has a benign course when an early diagnosis is made and aetiological treatment is administered. © 2020 Zhang et al.Purpose Methicillin-resistant S. aureus (MRSA) belonging to clonal complex 15 (CC15-MRSA) is rare among clinical isolates with few reports from retail camel meat and human patients. This study investigated the genetic relatedness of CC15-MRSA isolated for the first time from patients in Kuwait hospitals. Methods Antibiotic susceptibility was tested by the disk diffusion method. Minimum inhibitory concentration was determined using Etest strips. Molecular typing was performed using spa tying, multilocus sequence tying and DNA microarray. Results Of 1327 MRSA isolates, 42 (3.1%) were identified as CC15-MRSA. The 42 isolates belonged to sequence type ST1535-harbored SCCmec type V and spa types t084 (36 isolates), t346 (3 isolates) and one of t114, t228 and t7583. All 42 isolates were resistant to gentamicin, kanamycin, fusidic acid and cadmium acetate; 38 isolates were resistant to tetracycline. The isolates harbored aacA-aphD and fusC that codes for gentamicin and fusidic acid resistance, respectively. Tet(K) was present in the tetracycline-resistant isolates. In addition, the 42 isolates carried inu(A) (lincosamide nucleotidyltransferase) that confers resistance to lincomycin and clindamycin although phenotypically susceptible to these antibiotics. The isolates belonged to accessory gene regulator type II and capsular polysaccharide group 8 but lacked genes for Staphylococcus enterotoxins, toxic shock syndrome toxin, collagen-binding adhesins and Panton-Valentine leukocidin. Conclusion This study revealed the emergence and transmission of a previously rare MRSA clone among human patients in Kuwait hospitals and highlights the increasing infiltration of rare MRSA into the human population. © 2020 Udo et al.
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