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Aim: Glucose fluctuations may be responsible for, or further the onset of arterial hypertension, but the exact mechanisms remain unclear. The purpose of this study was to investigate the mechanisms behind and related to aortic fibrosis and aortic stiffening induced by glucose fluctuations. Methods: Sprague-Dawley rats were injected with streptozotocin (STZ) and randomly divided into three treatment groups: controlled STZ-induced diabetes (C-STZ); uncontrolled STZ-induced diabetes (U-STZ); and STZ-induced diabetes with glucose fluctuations (STZ-GF). After 3 weeks, rat blood pressure (BP) was tested, and aortic fibrosis was detected by using the Masson trichrome staining technique. Levels of p38 mitogen-activated protein kinase (p38 MAPK), runt-related transcription factor 2 (Runx2), collagen type 1 (collagen I), and NADPH oxidases were determined by Western blot.Rat vascular smooth muscle cells in vitro were used to explore underlying mechanisms. Results: The systolic BP of diabetic rats in the C-STZ, U-STZ, and STZ-GF groups was 127.67 ± 6.53, 150.03 ± 5.24, and 171.63 ± 3.53 mm Hg, respectively (p< 0.05). The mean BP of diabetic rats in the three groups was 91.20 ± 10.07, 117.29 ± 4.28, and 140.58 ± 2.14 mm Hg, respectively (p< 0.05). The diastolic BP of diabetic rats in the three groups was 73.20 ± 12.63, 101.93 ± 5.79, and 125.37 ± 4.62 mm Hg, respectively (p< 0.05). The ratios of fibrosis areas in the aortas of the three groups were 11.85 ± 1.23, 29.00 ± 0.87, and 48.36 ± 0.55, respectively (p< 0.05). The expressions of p38 MAPK, Runx2, and collagen I were significantly increased in the STZ-GF group. In vitro, applications of inhibitors of reactive oxygen species (ROS) and p38 MAPK successfully reversed glucose fluctuations that would have possibly induced aortic fibrosis. Conclusions: Blood glucose fluctuations aggravate aortic fibrosis via affecting the ROS/p38 MAPK /Runx2 signaling pathway. [ABSTRACT FROM AUTHOR]

Aim: The objective of this study was to examine the effects of n-3 polyunsaturated fatty acids (n-3 PUFAs) on coronary arterial large conductance Ca2+ -activated K+ (BK) channel function in coronary smooth muscle cells (SMCs) of streptozotocin- induced diabetic rats. Methods: The effects of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on coronary BK channel open probabilities were determined using the patch clamp technique. The mRNA and protein expressions of BK channel subunits were measured using qRTPCR and Western blots. The coronary artery tension and coronary SMC Ca2+ concentrations were measured using a myograph system and fluorescence Ca2+ indicator. Results: Compared to nondiabetic control rats, the BK channel function was impaired with a reduced response to EPA and DHA in freshly isolated SMCs of diabetic rats. Oral administration of n-3 PUFAs had no effects on protein expressions of BK channel subunits in nondiabetic rats, but significantly enhanced those of BK-β 1 in diabetic rats without altering BK-a protein levels. Moreover, coronary ring tension induced by iberiotoxin (a specific BK channel blocker) was increased and cytosolic Ca2+ concentrations in coronary SMCs were decreased in diabetic rats, but no changes were found in nondiabetic rats. Conclusions: n-3 PUFAs protect the coronary BK channel function and coronary vasoreactivity in diabetic rats as a result of not only increasing BK-β 1 protein expressions, but also decreasing coronary artery tension and coronary smooth muscle cytosolic Ca2+ concentrations. [ABSTRACT FROM AUTHOR]

Overweight or obesity has become a serious public health problem in the world, scientists are concentrating their efforts on exploring novel ways to treat obesity. Nowadays, the availabilities of bariatric surgery and pharmacotherapy have enhanced obesity treatment, but it should has support from diet, physical exercise and lifestyle modification, especially the functional food. Resistant starch, an indigestible starch, has been studied for years for its beneficial effects on regulating blood glucose level and lipid metabolism. The aim of this review is to summarize the effect of resistant starch on weight loss and the possible mechanisms. According to numerous previous studies it could be concluded that resistant starch can reduce fat accumulation, enhance insulin sensitivity, regulate blood glucose level and lipid metabolism. Recent investigations have focused on the possible associations between resistant starch and incretins as well as gut microbiota. Resistant starch seems to be a promising dietary fiber for the prevention or treatment of obesity and its related diseases. [ABSTRACT FROM AUTHOR]

Background: There are no reports regarding entire gastric fundic and esophageal varices evaluated with 64-row multidetector CT (MDCT). We attempt to clarify the feasibility of portal venography with this scanner in evaluation of these varices. Methods: A total of 33 patients, with clinically confirmed gastric fundic and esophageal varices secondary to posthepatitic cirrhosis, underwent thoracicoabdominal triphasic enhancement scans using 64-row MDCT along with conventional angiographic portography. CT portography and conventional portography were compared by statistical agreement to determine whether CT maximum intensity projection (CT-MIP) portography is useful in evaluation of entire gastric fundic and esophageal varices. Results: CT-MIP portography demonstrated gastric fundic and esophageal varices, and the inflowing and outflowing vessels of the varices. Gastric fundic varices were shown in 32 cases (97.0%), and esophageal varices were in 27 (81.8%). The inflowing vessels including the left gastric vein and posterior gastric vein/short gastric vein were illustrated in 31 (94.0%) and 17 (51.5%) cases, respectively. The outflowing vessels including the azygos vein, hemiazygos vein, and gastro-renal shunts were seen in 30 (90.9%), 8 (24.2%), and 12 (36.4%) cases, respectively. Findings of CT-MIP portography and conventional angiographic portography were in close agreement (Kappa value ranged from 0.621 to 1.000). Conclusion: CT-MIP venography with 64-row MDCT could be considered as a method for detecting entire gastric fundic and esophageal varices developed from posthepatitic cirrhosis. [ABSTRACT FROM AUTHOR]

Background: Mitochondrial dysfunction is linked to myocardial ischemia-reperfusion (I/R) injury. Checkpoint kinase 1 (CHK1) could facilitate cardiomyocyte proliferation, however, its role on mitochondrial function in I/R injury remains unknown., Methods: To investigate the role of CHK1 on mitochondrial function following I/R injury, cardiomyocyte-specific knockout/overexpression mouse models were generated. Adult mouse cardiomyocytes (AMCMs) were isolated for in vitro study. Mass spectrometry-proteomics analysis and protein co-immunoprecipitation assays were conducted to dissect the molecular mechanism., Results: CHK1 was downregulated in myocardium post I/R and AMCMs post oxygen-glucose deprivation/re‑oxygenation (OGD/R). In vivo, CHK1 overexpression protected against I/R induced cardiac dysfunction, while heterogenous CHK1 knockout exacerbated cardiomyopathy. In vitro, CHK1 inhibited OGD/R-induced cardiomyocyte apoptosis and bolstered cardiomyocyte survival. Mechanistically, CHK1 attenuated oxidative stress and preserved mitochondrial metabolism in cardiomyocytes under I/R. Moreover, disrupted mitochondrial homeostasis in I/R myocardium was restored by CHK1 through the promotion of mitochondrial biogenesis and mitophagy. Through mass spectrometry analysis following co-immunoprecipitation, SIRT1 was identified as a direct target of CHK1. The 266-390 domain of CHK1 interacted with the 160-583 domain of SIRT1. Importantly, CHK1 phosphorylated SIRT1 at Thr530 residue, thereby inhibiting SMURF2-mediated degradation of SIRT1. The role of CHK1 in maintaining mitochondrial dynamics control and myocardial protection is abolished by SIRT1 inhibition, while inactivated mutation of SIRT1 Thr530 fails to reverse the impaired mitochondrial dynamics following CHK1 knockdown. CHK1 Δ390 amino acids (aa) mutant functioned similarly to full-length CHK1 in scavenging ROS and maintaining mitochondrial dynamics. Consistently, cardiac-specific SIRT1 knockdown attenuated the protective role of CHK1 in I/R injury., Conclusions: Our findings revealed that CHK1 mitigates I/R injury and restores mitochondrial dynamics in cardiomyocytes through a SIRT1-dependent mechanism., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Luteolin differs as a radical scavenger dramatically from apigenin in response to Cu(II) coordination despite a minor structural difference. Coordination of Cu(II) increases the radical scavenging efficiency of luteolin, especially at low pH, while decreases the efficiency of apigenin at both low and higher pH as studied by ABTS •+ radical scavenging. Luteolin forms a 1:1 complex with Cu(II) binding to 4-carbonyl and 5-phenol for pH <6 and to 3',4'-catechol for pH >6. Apigenin forms a 1:2 complex independent of pH coordinated to 4-carbonyl and 5-hydroxylyl. Cu(II) coordinated to luteolin, as studied by pH jump stopped-flow, translocates with rate constants of 11.1 ± 0.3 s -1 from 4,5 to 3',4' sites and 1.0 ± 0.1 s -1 from 3',4' to 4,5 sites independent of Cu(II) concentration, pointing toward the dissociation of Cu(II) from an intermediate with two Cu(II) coordination as rate determining. 3',4'-Catechol is suggested to be a switch for Cu(II) translocation with deprotonation initiating 4,5 to 3',4' translocation and protonation initiating 3',4' to 4,5 translocation. For dicoordinated apigenin, the coordination symmetry balances an electron withdrawal effect of Cu(II) resulting in a decrease of phenol acidity and less radical scavenging efficiency compared to parent apigenin. Compared to that of parent luteolin, the radical scavenging rate of both 4,5 and 3',4' Cu(II)-coordinated luteolin is enhanced through increased phenol acidity by electron withdrawal by Cu(II), as confirmed by density functional theory (DFT) calculations. Coordination and translocation of Cu(II) accordingly increases the antioxidant activity of luteolin at pH approaching the physiological level and is discovered as a novel class of natural molecular machinery derived from plant polyphenols, which seems to be of importance for protection against oxidative stress.

High density and intensive Litopenaeus vannamei aquaculture has increased the frequency of shrimp disease, however, it remains uncertain whether change in intestinal bacteria could be indicative of shrimp health state (healthy or diseased). Therefore, we collected water and shrimp intestine samples from ponds with or without diseased shrimps. Using bacterial 16S rRNA gene as a biomarker, the bacterial community structure and diversity were evaluated with the Illumina MiSeq sequencing technique. The results showed that the variations of bacterioplankton community were primarily shaped by the levels of NO2(-)-N, chlorophyll a and PO4(3-)-P. Bacterial diversity was signif-7 icantly lower in diseased shrimps than in healthy ones. Using a response ratio analysis, we screened 28 operational taxonomic units (OTUs), and their abundances significantly changed in the intestines between healthy and diseased shrimps. In general, the abundances of OTUs belonged to Actinobacteria, Flavobacteria and Bacilli significantly decreased in diseased shrimps compared with those in healthy shrimps., while the OTUs affiliated to Clostridia showed an opposite pattern. In addition, we obtained 61 indicator species that primarily affiliated to Bacteroidetes, Proteobacteria, Firmicutes, Planctomycetes and Actinobacteria. Notably, the identified indicator taxa exhibited clearly discriminative patterns among habitats (water or intestine) and health status. Collectively, this study provided scientific information for development of new probiotics and disease prevention.

Objective: To reconstruct three-dimensional (3D) image of posterior cruciate ligament (PCL) based on MRI and CT image fusion., Methods: CT and MRI scans were performed on 12 knees of young men. The Dicom data were extracted and unified. The outline of PCL on MRI imaging was drew and plugged into the CT data. Finally, the visible 3D image of PCL with adjacent bones was reconstructed. The imaging anatomical measurements were examined and compared with those in published literature., Results: Two cases were excluded from this study because of data deviations. The 3D visible reconstruction of PCL was proved to be feasible on the other ten cases., Conclusion: Three-dimensional visible reconstruction of PCL based on CT and MRI image fusion is feasible, which can provide support for individualized treatment of PCL injuries. Further simplification with increased accuracy may be needed.