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The fluorescent and confocal microscopy confirmed that the protein is localized in the mitochondria of infected macrophages and in the cells of BAL of TB patients. Together these findings indicate towards the novel function of the protein which is unlike to the earlier established mechanisms of mycobacterial physiology.

Mycophenolate mofetil (MMF), an immunosuppressive drug, exerts anti-inflammatory effects on organs during ischemia/reperfusion (I/R) injury. However, the exact function of MMF in hepatic I/R injury remains largely unknown. The purpose of this study was to explore the role and potential mechanism of MMF protection in hepatic I/R injury.

Male wild type (WT) and TLR4 knockout (KO) mice were injected intraperitoneally with MMF or normal saline. Animals underwent 90min of partial hepatic ischemia, followed by 1, 6, or 24h of reperfusion. Hepatic histology, serum amiotransferase, inflammatory cytokines, hepatocyte apoptosis, and hepatocyte autophagy were examined to assess liver injury.

Treatment with MMF significantly decreased hepatic I/R injury as indicated by a reduction in serum aminotransferase levels, Suzuki scores, and the overall degree of necrosis. MMF treatment inhibited TLR4 activation dramatically. MMF administration also significantly inhibited the activation of the NF-κB pathway and the expression of pro-inflammatory cytokines. In TLR4 KO mice, MMF still exerted protection from hepatic I/R injury. MMF treatment inhibited hepatocyte apoptosis, as indicated by reduced TUNEL staining, and reduced the accumulation of cleaved caspase-3. In addition, MMF may induce autophagy and increase autophagic flux before and after hepatic reperfusion by augmenting the expression of LC3-II, P62, and Beclin-1. The induction of autophagy by MMF treatment may be related to TLR4 activation.

Our results indicate that MMF treatment ameliorates hepatic I/R injury. The mechanism of action likely involves the ability of MMF to decrease apoptosis and the inflammatory response while inducing autophagy.

Our results indicate that MMF treatment ameliorates hepatic I/R injury. The mechanism of action likely involves the ability of MMF to decrease apoptosis and the inflammatory response while inducing autophagy.

Keratoconus is a bilateral progressive noninflammatory degenerative disease of the cornea characterized by corneal thinning, irregular astigmatism, and subsequent visual impairment. It has an aggressive course in children. This systematic review evaluates the efficacy of available corneal collagen cross-linking (CXL) protocols for stabilizing the cornea in pediatric patients with keratoconus.

We searched all peer-reviewed publications from 2000 to 2019 indexed in PubMed, Google Scholars, Web of Science, and Cochrane's Database for the terms keratoconus and cross-linking. The following data were extracted from eligible studies study design, type of intervention, number of the eyes and mean age of patients for each study, duration of follow-up period, mean pre- and postoperative uncorrected and corrected visual acuity, keratometric and aberrometric indices, were analyzed with RevMan 5.3 software. Intra-and intergroup post hoc analyses of outcome variables were performed using t tests.

A total of 28 studies, including 1,300 eyes, were reviewed. In conventional and accelerated epithelium-off techniques, there was a significant improvement in uncorrected and corrected visual acuities. Similarly, the keratometric indices improved significantly after CXL. Uncorrected visual acuity did not alter after CXL using transepithelial method.

Both conventional and accelerated collagen CXL of the cornea are effective therapeutic options in management of keratoconus in children.

Both conventional and accelerated collagen CXL of the cornea are effective therapeutic options in management of keratoconus in children.Extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) significantly suppressed hypoxia-ischemia (HI)-induced neuroinflammation in neonatal mice. However, its underlying mechanism is still unknown. Osteopontin (OPN) is one of the key molecules involved in neuroinflammation. We demonstrate here for the first time a key role of OPN in EVs-mediated neuroinflammation following HI. Epalrestat Firstly, HI exposure upregulated OPN expression in Iba-1+/ TMEM119+ microglia and Iba-1+/TMEM119- monocytes/macrophages. Blocking OPN mRNA expression with LV-shOPN attenuated edema, infarct volumes, and the levels of inflammatory cytokines following HI exposure. MSCs-EVs treatment remarkably restored synaptic reorganization and up-regulated synaptic protein expression post-HI, concomitant with reducing OPN levels. Moreover, MSCs-EVs treatment rescued microglial phagocytosis of viable neurons following HI, concomitant with decreasing OPN expression. In addition, blocking NF-κB activation with pyrrolidine dithiocarbamate (PDTC, NF-κB inhibitor) or MSCs-EVs attenuated HI-induced OPN expression in the ipsilateral cortex. This study demonstrates that upregulation of OPN expression in cerebral immune cells aggravated brain damage and inflammation following HI insult. MSCs-EVs suppressed neuroinflammation, synaptic damage and microglial phagocytosis after HI injury by preventing NF-κB-mediated OPN expression in neonate mice.

External beam radiation therapy (EBRT) with brachytherapy boost reduces cancer recurrence in patients with prostate cancer compared with EBRT monotherapy. However, randomized controlled trials or large-scale observational studies have not compared brachytherapy boost types directly.

This observational cohort study used linked national cancer registry data, radiation therapy data, administrative hospital data, and mortality records of 54,642 patients with intermediate-risk, high-risk, and locally advanced prostate cancer in England. The records of 11,676 patients were also linked to results from a national patient survey collected at least 18 months after diagnosis. Competing risk regression analyses were used to compare gastrointestinal (GI) toxicity, genitourinary (GU) toxicity, skeletal-related events (SRE), and prostate cancer-specific mortality (PCSM) at 5 years with adjustment for patient and tumor characteristics. Linear regression was used to compare Expanded Prostate Cancer Index Composite 26-itemT monotherapy.

Compared with EBRT monotherapy, LDR-BB has worse GI and GU toxicity and HDR-BB has worse GU toxicity. HDR-BB has a lower incidence of SREs and PCSM than EBRT monotherapy.The present study examined the differences in frontal EEG asymmetry during emotion regulation between participants who had different levels of trait mindfulness. EEG recordings were taken from 23 high mindfulness adolescents (Mage = 12.34) and 22 low mindfulness adolescents (Mage = 12.53) during the Reactivity and Regulation-Image Task. The results showed that (1) high mindfulness adolescents had greater left (relative to right) asymmetry than low mindfulness adolescents in down-regulation and up-regulation conditions; however, there was no significant difference in the non-regulation condition; (2) In the up-regulating condition, adolescents showed greater right (relative to left) asymmetry for negative stimuli compared to neutral stimuli; however, there was no significant difference in down-regulation and non-regulation conditions. The results provide neurological evidence that trait mindfulness was highly related to the regulation of emotions and affects how emotions are processed.

We sought to assess and compare the prediction power of the PRECISE-DAPT and PARIS risk scores with regards to bleeding events in elderly patients suffering from acute coronary syndromes (ACS) and undergoing invasive management.

Our external validation cohort included 1883 patients older >74years admitted for ACS and treated with PCI from 3 prospective, multicenter trials.

After a median follow-up of 365days, patients in the high-risk categories according to the PRECISE-DAPT score experienced a higher rate of BARC 3-5 bleedings (p=0.002) while this was not observed for those in the high-risk category according to the PARIS risk score (p=0.3). Both scores had a moderate discriminative power (c-statistics 0.70 and 0.64, respectively) and calibration was accurate for both risk scores (all χ

>0.05), but PARIS risk score was associated to a greater overestimation of the risk (p=0.02). Decision curve analysis was in favor of the PRECISE-DAPT score up to a risk threshold of 2%.

In the setting of older adults managed invasively for ACS both the PARIS and the PRECISE-DAPT scores were moderately accurate in predicting bleeding risk. However, the use of the PRECISE-DAPT is associated with better performance.

In the setting of older adults managed invasively for ACS both the PARIS and the PRECISE-DAPT scores were moderately accurate in predicting bleeding risk. However, the use of the PRECISE-DAPT is associated with better performance.

B-type natriuretic peptide (BNP) has been widely used for the diagnosis of heart failure, its severity, and prognosis. However, little is known about factors related to disproportionately low BNP levels even during acute heart failure conditions.

Among 424 patients hospitalized for acute heart failure, we categorized the patients into the HFpEF (LVEF>50%) or HFrEF (LVEF≤50%) group and subdivided them into disproportionately low BNP (LB) group and high BNP (HB) group using a cut-off BNP level of 200pg/mL at admission. The proportion of patients with LB was higher in the HFpEF group (22.2%) than in the HFrEF group (10.9%, p=0.002). Patients with LB had a high BMI, lower blood pressure, and history of previous cardiovascular surgery in the HFpEF group, while patients in the HFrEF group had a high BMI and smaller left ventricular end-diastolic volume index. Furthermore, presence of LB in the HFrEF group was related to good prognosis, but LB in the HFpEF group was an indicator of poor prognosis as HB group.

The factors associated with LB were different between the HFpEF and HFrEF groups. LB was related to good prognosis in HFrEF, but not in HFpEF.

The factors associated with LB were different between the HFpEF and HFrEF groups. LB was related to good prognosis in HFrEF, but not in HFpEF.

This study aims to explore the possible ceRNA regulatory network of lncRNA ENST00000609755.1 in CHD patients based on the population; reveal the possible regulatory mechanism of lncRNA ENST00000609755.1.

Microarray analysis were used to identify differentially expressed miRNA, and mRNA profiles between 5 CHD and 5 healthy controls. The lncRNA ENST00000609755.1-miRNA-mRNA ceRNA regulatory network was constructed with lncRNA ENST00000609755.1 as the core based on microarray data and related prediction software (RNAhybird, miRanda, miRWalk 2.0). Furthermore, qRT-PCR was used to verify the expression levels of miRNA and mRNA. t-test and pearson correlation analysis were used to compare the expression differences and correlations of lncRNA, miRNA and mRNA. The receiver operating characteristic (ROC) curve was used to determine the discriminative ability of lncRNA ENST00000609755.1 and its downstream targets.

Totally 25 miRNAs and 953 mRNAs were differentially expressed between CHD and healthy control. The lncRNA ENST00000609755.

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