Genotypic diversity and immunological implications of porcine circovirus: Inspiration from PCV1 to PCV4.

Porcine circovirus (PCV) is a group of DNA viruses that cause diseases in pigs, with multiple genotypes ranging from PCV1 to PCV4. PCV1 is generally considered non-pathogenic, while PCV2 can cause severe immune system damage, especially associated with porcine multisystemic wasting syndrome (PMWS). PCV2 has a genetic homology of about 68 % but differs from PCV1 in antigenicity and phenotype.

Human podocyte injury in the early course of hypertensive renal injury.

Background: Hypertension is prevalent in the general population and is regarded as the second leading cause of renal damage and dysfunction, outnumbered only by diabetes. However, the mechanisms remain unclear.

Aim: To investigate podocyte injury induced by hypertension in the early course without massive proteinuria or renal dysfunction.

CT-707, a Novel FAK Inhibitor, Synergizes with Cabozantinib to Suppress Hepatocellular Carcinoma by Blocking Cabozantinib-Induced FAK Activation.

Hepatocellular carcinoma is among the leading causes of cancer-related deaths worldwide, and the development of new treatment regimens is urgently needed to improve therapeutic approach. In our study, we found that the combination of a Met inhibitor, cabozantinib, and a novel FAK inhibitor, CT-707, exerted synergistic antitumor effects against hepatocellular carcinoma in vitro and in vivo Interestingly, further studies showed that therapeutic concentrations of cabozantinib increased the phosphorylation of FAK, which might attenuate the antitumor activity of cabozantinib. The simultaneous exposure to CT-707 effectively inhibited the activation of FAK that was induced by cabozantinib, which contributes to the synergistic effect of the combination.

MicroRNA-23a participates in estrogen deficiency induced gap junction remodeling of rats by targeting GJA1.

Increased incidence of arrhythmias in women after menopause has been widely documented, which is considered to be related to estrogen (E2) deficiency induced cardiac electrophysiological abnormalities. However, its molecular mechanism remains incompletely clear. In the present study, we found cardiac conduction blockage in post-menopausal rats.

MicroRNA-23a mediates mitochondrial compromise in estrogen deficiency-induced concentric remodeling via targeting PGC-1α.

It is well known that menopause could worsen age-related ventricular concentric remodeling following estrogen (E2) deficiency. However the underlying mechanisms of such phenomena are not fully understood. Mitochondria, as the 'cellular power station' of hearts, play an important role in maintaining normal cardiac function and structure.

Myocardial dysfunction in early diabetes patients with microalbuminuria: a 2-dimensional speckle tracking strain study.

The aim of this study was to assess myocardial dysfunction in primary diabetes patients with microalbuminuria by 2-dimensional speckle tracking strain. Sixty-two patients with diabetes with or without hypertension and 37 matched hypertension controls were consecutively recruited from January 2011 to 2013. Routine physical examinations, laboratory tests, and echocardiography were performed in all patients.

[mTOR/p70s6k signaling pathway is involved in megakaryocyte polyploidization].

Aim: To investigate the mechanisms of megakaryocyte polyploid cell cycle control.

Methods: The expression and phosphorylation of mTOR/p70s6k pathway proteins was detected by western blot. Double-labeling techniques were used to investigate in which of the phase of the polyploid cell cycle S6K1 at Thr421/Ser424 are phosphorylated.

[Effects of ventricular demand and dual-chamber pacing models on the long-term clinical outcome and cardiac remodeling in patients with symptomatic bradycardia].

Objective: To assess the effects of VVI (ventricular demand) and DDD (dual-chamber) pacing models on cardiac remodeling and the long-term clinical outcome of patients with symptomatic bradycardia.

Methods: All patients with DDD and VVI pacing models at our hospital from January 1991 to January 2003 were retrospectively analyzed.

Results: After a follow-up period of over 8 years in DDD and VVI groups (97 ± 27, 107 ± 44 months), left atrial diameter [(45 ± 12) mm vs (39 ± 12) mm, P < 0.

The modifier protein of glyceraldehyde-3-phosphate dehydrogenase reduces free radical-mediated renal damage in a rat model of acute kidney injury.

Background: The modifier protein (MP) of glyceraldehyde-3-phosphate dehydrogenase has been shown to promote growth of renal epithelial cells in vitro. The aim of this study was to show the in vivo effects of MP in a rat model of gentamicin-induced acute kidney injury (AKI).

Method: MP was purified from monkey renal tubular epithelial cell line BSC-1 and confirmed by amino acid sequencing.

The leaf extract of Siberian Crabapple (Malus baccata (Linn.) Borkh) contains potential fatty acid synthase inhibitors.

The present work focused on the kinetics of the inhibitory effects of the leaf extract of Siberian Crabapple, named Shan jingzi in China, on chicken liver fatty acid synthase. The results showed that this extract had much stronger inhibitory ability on fatty acid synthase than that from green teas described in many previous reports. The inhibitory ability of this extract is closely related to the extracting solvent, and the time of extraction was also an important influencing factor.

The antibacterial efficacy of an aceraceous plant [Shantung maple (Acer truncatum Bunge)] may be related to inhibition of bacterial beta-oxoacyl-acyl carrier protein reductase (FabG).

Polyphenols, including flavonoids, are the major components of the extracts from aceraceous plants. They possess remarkable antibacterial and antitumour activity. Our study focused on whether the inhibition of the bacterial type II fatty acid synthesis system is the mechanism for the antibacterial effect of the related plant polyphenols.

A substitutive substrate for measurements of beta-ketoacyl reductases in two fatty acid synthase systems.

Bacterial beta-ketoacyl-ACP reductase (FabG) and the beta-ketoacyl reductase domain in mammalian fatty acid synthase (FAS) have the same function and both are rendered as the novel targets for drugs. Herein we developed a convenient method, using an available compound ethyl acetoacetate (EAA) as the substitutive substrate, to measure their activities by monitoring decrease of NADPH absorbance at 340 nm. In addition to the result, ethyl 3-hydroxybutyrate (EHB) was detected by HPLC analysis in the reaction system, indicating that EAA worked effectively as the substrate of FabG and FAS since its beta-keto group was reduced.

Inactivation mechanism of the beta-ketoacyl-[acyl carrier protein] reductase of bacterial type-II fatty acid synthase by epigallocatechin gallate.

Epigallocatechin gallate (EGCG), a major compound from green tea, reversibly inhibits beta-ketoacyl-[acyl carrier protein] reductase (FabG) from Escherichia coli. In this study, we found that EGCG exhibited an atypical time-dependent inhibition of FabG, which possibly resulted from the EGCG-induced aggregation of FabG. It was observed that FabG inactivation and aggregation occurred nearly simultaneously, with a lag time that decreased with increasing EGCG concentration.

[The proliferation, phenotype change and anti-tumor activity of cytokine induced killer cells].

Aim: To study the growth regularity, the phenotype change and the cytotoxicity of CIK cells.

Methods: The number of CIK cells was counted by living cell counting in different culturing time to observe the growth of the CIK cells, and the phenotype change of the CIK cells was detected by flow cytometry. Meanwhile cytotoxicity of CIK cells to tumor cell lines was also detected by CytoTox96 non-radiated cytotoxicity kit.