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OBJECTIVES The aim of this study was to investigate the influences of accumulated experience on rotational atherectomy (RA) operation regarding to in-hospital outcomes in the drug-eluting stent (DES) era. METHODS Between 2015 and 2019, 540 de novo lesions with calcified coronary lesions treated by RA and DES implantation at our center were retrospectively assessed. In-hospital major adverse cardiac events (MACE) were defined as all cause death, cardiac death, target vessel revascularization, and stroke. RESULTS From 2015 to 2019, RA operations were 22, 60, 102, 157, and 199 cases, respectively. Rates of procedural complications were 4.5, 3.3, 11.8, 8.3, and 7.5%, respectively. Rates of in-hospital MACE were 0, 0, 3.9, 2.5, and 2.0%, respectively. Compared with planned RA, bailout RA was associated with more contrast use (207.5 ± 82.8 ml vs. 189.2 ± 70.0 ml, p = .008). As for procedural complications and in-hospital outcomes, no differences were observed between two strategies. Logistic regression revealed that hypertension was independently associated with complications (OR 5.830, 95% CI 1.382-24.591, p = .016). For MACE, independent risk factors were heart failure (OR 17.593, 95% CI 1.475-209.816, p = .023) and procedural complications (OR 127.629, 95% CI 15.135-1,076.258, p

Almost all living organisms have evolved autoregulatory transcriptional-translational feedback loops that produce oscillations with a period of approximately 24-h. These endogenous time keeping mechanisms are called circadian clocks. The main function of these circadian clocks is to drive overt circadian rhythms in the physiology of the organisms to ensure that main physiological functions are in synchrony with the external environment. Disruption of circadian rhythms caused by genetic or environmental factors has long-term consequences for metabolic health. Of relevance, host circadian rhythmicity and lipid metabolism are increasingly recognized to cross-regulate and the circadian clock-lipid metabolism interplay may involve in the development of obesity. Multiple systemic and molecular mechanisms, such as hormones (ie, melatonin, leptin, and glucocorticoid), the gut microbiome, and energy metabolism, link the circadian clock and lipid metabolism, and predictably, the deregulation of circadian clock-lipid metabolism interplay can increase the risk of obesity, which in turn may exacerbate circadian disorganization. Feeding time and dietary nutrients are two of key environmental Zeitgebers affecting the circadian rhythm-lipid metabolism interplay, and the influencing mechanisms in obesity development are highlighted in this review. Together, the characterization of the clock machinery in lipid metabolism aimed at producing a healthy circadian lifestyle may improve obesity care.

This study was conducted to investigate the effects of dietary supplementation with Sangrovit® (SAG; minimum of 1.5% sanguinarine, a quaternary benzo[c]phenanthridine alkaloid extracted from Macleaya cordata) on growth performance, intestinal morphology, intestinal microflora and its metabolites of early-weaned piglets. A total of 20 healthy weaned piglets (Duroc× [Large White×Landrace]), weaned at 21 days of age with an average body weight (BW) of 6.52 ± 0.23 kg, were randomly assigned to receive either a corn-soybean meal basal diet (CTR) or a basal diet supplemented with 50 mg/kg SAG (SAG). During the 21-days trial, we collected and analysed intestinal tissues and the luminal digesta for their morphology and populations of gut microbiota, as well as for measuring the concentrations of short-chain fatty acids (SCFAs) and ammonia. Compared with the CTR group, supplementation with SAG improved average daily gains (p = 0.011) and average daily feed intake (p = 0.037). Piglets fed the SAG diet had an average lower value for crypt depth of the jejunum (p = 0.011) and greater values for villus height in the ileum (p = 0.015) and ratios of villus height to crypt depth in the jejunum (p < 0.01) and in the ileum (p = 0.027) than did animals receiving the CTR diet. The addition of SAG increased the amounts of Lactobacillus in the ileum (p = 0.033) and caecum (p < 0.01), and tended to increase the amounts of Bifidobacterium (p = 0.058) in the caecum, while decreasing the amounts of Escherichia coli (p = 0.046) and Salmonella spp. (p = 0.035) in the ileum, as well as Salmonella spp. (p = 0.029) in the caecum. Dietary supplementation with SAG enhanced (p < 0.05) the concentrations of acetate, propionate, butyrate and total SCFAs, and also tended to increase the level of valerate (p = 0.055 and p = 0.052) in the ileal and caecal contents when compared with the CTR group. Concentrations of ammonia also declined in the caecal (p = 0.037) and ileal (p = 0.046) digesta in response to SAG. These results indicate that feeding early-weaned piglets a SAG-supplemented diet can potentially improve their growth performance and intestinal morphology, and can modify the intestinal luminal environment in a beneficial manner.

The search for substitutes for antibiotics has recently become urgent. In our previous work, dietary α-ketoglutarate (AKG) combined with allicin improved growth performance and enhanced immunity in growing pigs, whereas the effects on them of intestinal microbiota were unclear. Here, we further investigate the effects of dietary AKG and allicin supplementation on the composition and diversity of intestinal microbiota in growing pigs.; Results: Treatment with a combination of AKG and allicin enhanced cecal bacteria richness and diversity, as evidenced by changes in Chao 1, ACE, Shannon, and Simpson values when compared to the control group and antibiotics group. At the phylum level, Bacteroidetes and Firmicutes were the two most abundant phyla. Treatment with a combination of AKG and allicin increased the numbers of Firmicutes and reduced the numbers of Bacteroidetes. Prevotella was the most abundant genus; it was increased by treatment with a combination of AKG and allicin. Furthermore, compared with the antibiotic group, the level of acetate was increased in the AKG group with or without allicin. Treatment with a combination of AKG and allicin increased the levels of cecal butyrate and total volatile fatty acids (VFA) when compared with the control group in growing pigs.; Conclusion: Dietary 1.0% AKG combined with 0.5% allicin improved cecal microbial composition and diversity, which might further promote VFA metabolism in growing pigs. © 2018 Society of Chemical Industry.; © 2018 Society of Chemical Industry.

Mammalian skeletal muscles are composed of two major fibre types (I and II) that differ in terms of size, metabolism and contractile properties. In general, slow-twitch type I fibres are rich in mitochondria and have a greater insulin sensitivity than fast-twitch type II skeletal muscles. Although not widely appreciated, a forced induction of the slow skeletal muscle phenotype may inhibit the progress of obesity and diabetes. This potentially forms the basis for targeting slow/oxidative myofibers in the treatment of obesity. In this context, a better understanding of the molecular basis of fibre-type specification and plasticity may help to identify potential therapeutic targets for obesity and diabetes.

Objective We aimed to investigate short-term outcomes of the XINSORB bioresorbable sirolimus-eluting scaffold in human coronary artery. Background Bioresorbable scaffolds are considered to be the fourth milestone in percutaneous coronary intervention. Methods Thirty patients with symptomatic ischemic coronary disease were enrolled and treated with the XINSORB scaffolds that were 3.0 × 12, 15, and 18 mm in size. The primary angiographic endpoint was late luminal loss (LLL), whereas the primary clinical endpoint was major adverse cardiac events (MACEs) at the 6 month follow-up. In a subset of 19 patients, intravascular ultrasound (IVUS) and optical coherence tomography (OCT) were performed at follow-up. Results The success rates of the procedure and the device were both 100%. Twenty-seven patients received angiographic follow-up. All patients were clinically assessed. Neither MACEs nor stent thrombus-related events were recorded. The percentage of diameter stenosis at follow-up was similar to that at postprocedure. In-scaffold and periscaffold LLL were 0.17 ± 0.12 and 0.13 ± 0.24 mm, respectively. No in-stent restenosis was detected. IVUS showed that the mean areas of the lumen, scaffold, and neointima at follow-up were 6.27 ± 0.69, 6.48 ± 0.70, and 0.20 ± 0.09 mm2, while in-device stenosis was 3.1 ± 1.3%. OCT showed that 97.9% of the struts presented a preserved box, while 2.1% had an open box after 6 months. A total of 95.9% of the struts were covered by neointima. Conclusions This first-in-human study demonstrates the effectiveness and safety of the XINSORB scaffold in treating single de novo coronary lesions. © 2016 Wiley Periodicals, Inc.

Male Zucker diabetic fatty (ZDF) rats were used to study effects of oral administration of interferon tau (IFNT) in reducing obesity. Eighteen ZDF rats (28 days of age) were assigned randomly to receive 0, 4 or 8 μg IFNT/kg body weight (BW) per day (n=6/group) for 8 weeks. Water consumption was measured every two days. Food intake and BW were recorded weekly. Energy expenditure in 4-, 6-, 8-, and 10-week-old rats was determined using indirect calorimetry. Starting at 7 weeks of age, urinary glucose and ketone bodies were tested daily. Rates of glucose and oleate oxidation in liver, brown adipose tissue, and abdominal adipose tissue, leucine catabolism in skeletal muscle, and lipolysis in white and brown adipose tissues were greater for rats treated with 8 μg IFNT/kg BW/day in comparison with control rats. Treatment with 8 μg IFNT/kg BW/day increased heat production, reduced BW gain and adiposity, ameliorated fatty liver syndrome, delayed the onset of diabetes, and decreased concentrations of glucose, free fatty acids, triacylglycerol, cholesterol, and branched-chain amino acids in plasma, compared to control rats. Oral administration of 8 μg IFNT/kg BW/day ameliorated oxidative stress in skeletal muscle, liver and adipose tissue, as indicated by decreased ratios of oxidized glutathione to reduced glutathione and increased concentrations of the antioxidant tetrahydrobiopterin. These results indicate that IFNT stimulates oxidation of energy substrates and reduces obesity in ZDF rats and may have broad important implications for preventing and treating obesity-related diseases in mammals.

Optimal timing of cell therapy for myocardial infarction (MI) appears during 5 to 14 days after the infarction. However, the potential mechanism requires further investigation. This work aimed to verify the hypothesis that myocardial stiffness within a propitious time frame might provide a most beneficial physical condition for cell lineage specification in favour of cardiac repair. Serum vascular endothelial growth factor (VEGF) levels and myocardial stiffness of MI mice were consecutively detected. Isolated bone marrow mononuclear cells (BMMNCs) were injected into infarction zone at distinct time-points and cardiac function were measured 2 months after infarction. Polyacrylamide gel substrates with varied stiffness were used to mechanically mimic the infarcted myocardium. BMMNCs were plated on the flexible culture substrates under different concentrations of VEGF. Endothelial progenitor lineage commitment of BMMNCs was verified by immunofluorescent technique and flow cytometry. Our results demonstrated that the optimal timing in terms of improvement of cardiac function occurred during 7 to 14 days after MI, which was consistent with maximized capillary density at this time domains, but not with peak VEGF concentration. Percentage of double-positive cells for DiI-labelled acetylated low-density lipoprotein uptake and fluorescein isothiocyanate (FITC)-UEA-1 (ulex europaeus agglutinin I lectin) binding had no significant differences among the tissue-like stiffness in high concentration VEGF. With the decrease of VEGF concentration, the benefit of 42 kPa stiffness, corresponding to infarcted myocardium at days 7 to 14, gradually occurred and peaked when it was removed from culture medium. Likewise, combined expressions of VEGFR2(+) , CD133(+) and CD45(-) remained the highest level on 42 kPa substrate in conditions of lower concentration VEGF. In conclusion, the optimal efficacy of BMMNCs therapy at 7 to 14 days after MI might result from non-VEGF dependent angiogenesis, and myocardial stiffness at this time domains was more suitable for endothelial progenitor lineage specification of BMMNCs. The results here highlight the need for greater attention to mechanical microenvironments in cell culture and cell therapy.

Detection of the optimal cell transplantation strategy for myocardial infarction (MI) has attracted a great deal of attention. Commitment of engrafted cells to angiogenesis within damaged myocardium is regarded as one of the major targets in cell-based cardiac repair. Bone marrow–derived CD34-positive cells, a well-characterized population of stem cells, might represent highly functional endothelial progenitor cells and result in the formation of new blood vessels. Recently, physical microenvironment (extracellular matrix stiffness) around the engrafted cells was found to exert an essential impact on their fate. Stem cells are able to feel and respond to the tissue-like matrix stiffness to commit to a relevant lineage. Notably, the infarct area after MI experiences a time-dependent stiffness change from flexible to rigid. Our previous observations demonstrated myocardial stiffness-dependent differentiation of the unselected bone marrow–derived mononuclear cells (BMMNCs) along endothelial lineage cells. Myocardial stiffness (∽42 kPa) within the optimal time domain of cell engraftment (at week 1 to 2) after MI provided a more favourable physical microenvironment for cell specification and cell-based cardiac repair. However, the difference in tissue stiffness-dependent cell differentiation between the specific cell subsets expressing and no expressing CD34 phenotype remains uncertain. We presumed that CD34-positive cell subsets facilitated angiogenesis and subsequently resulted in cardiac repair under induction of infarcted myocardium-like matrix stiffness compared with CD34-negative cells. If the hypothesis were true, it would contribute greatly to detect the optimal cell subsets for cell therapy and to establish an optimized therapy strategy for cell-based cardiac repair.