Association between the remnant cholesterol to high-density lipoprotein cholesterol ratio and the risk of coronary artery disease.

BACKGROUND: The purpose of this study was to evaluate the relationship between remnant cholesterol (RC) to high-density lipoprotein cholesterol (HDL-C) ratio and the risk of coronary artery disease (CAD). We also investigated the clinical value of RC/HDL-C ratio in evaluating the severity of CAD and in predicting the short-term prognosis of CAD patients. METHODS: In total, 615 patients were enrolled and they were classified into a CAD group (418 cases) and a normal group (197 cases) according to the results of coronary angiography. Serum RC/HDL-C ratio and Gensini score were calculated. Multivariate logistic regression and receiver operating characteristic (ROC) curves were employed to evaluate the association between RC/HDL-C ratio and CAD. The effect of RC/HDL-C ratio on the progression of major adverse cardiovascular events (MACEs) was also explored. RESULTS: Increased RC/HDL-C ratio was associated with an increased risk of CAD (OR: 11.122; 95% CI: 5.903-20.954; P  < 0.001). When stratified by CAD subtypes, increased RC/HDL-C ratio was correlated with a greater risk of acute coronary syndrome (ACS) (OR:1.549; 95% CI: 1.014-2.364; P  < 0.05). Compared with the first quartile, the 4th quartile of RC/HDL-C ratio had a 9.774-fold ( P  = 0.000) increase in the odds ratio for CAD, and a 2.241-fold ( P  = 0.017) increase in the odds ratio for ACS. RC/HDL-C ratio was an independent determinant of Gensini score ≥32 (OR: 2.138, 95% CI:1.389-3.292, P  < 0.01), and multi-branch (MVD) (OR: 2.245; 95% CI: 1.468-3.443; P  < 0.001). The prevalence of Gensini score ≥32 and MVD in the 4th quartile of RC/HDL-C ratio group were much higher than that of other quartile groups ( P  < 0.01). Moreover, the areas under the ROC for the predictive value of RC/HDL-C ratio for CAD, ACS, Gensini score ≥32, and MVD were 0.702, 0.563, 0.602, and 0.669, respectively. Furthermore, the incidence of MACEs was significantly increased in CAD patients with levels of RC/HDL-C ratio ( P  < 0.05). CONCLUSION: RC/HDL-C ratio plays an important role in the progression and severity of CAD.

Active film preparation using pectin and polyphenols of watermelon peel and its applications for super-chilled storage of chilled mutton.

We investigated the effect of active packaging films prepared by pectin (WMP) and polyphenols (WME) obtained from watermelon peel on the quality of chilled mutton during super-chilled storage. The addition of WME created new chemical and hydrogen bonds in film. Furthermore, an appropriate amount of WME (≤1.5%) was evenly distributed throughout the film matrix, improving barrier properties, mechanical properties, thermal stability, and light transmittance of the film. An assessment of the meat quality showed that the pH, L*, b*, thiobarbituric acid reactive substances (TBARs), total volatile basic nitrogen (TVB-N), and total bacterial count (TCA) of super-chilled + film group were significantly lower, whereas shear force and a* value were significantly higher (P < 0.05) than other groups. The WMP/WME film has dense microstructure and excellent mechanical properties after storage. Pectin and polyphenols obtained from watermelon peel have good potential as a novel packaging material for chilled mutton during super-chilled storage.

DRG-Derived Neural Progenitors Differentiate into Functional Enteric Neurons Following Transplantation in the Postnatal Colon.

Cell therapy has great promise for treating gastrointestinal motility disorders caused by intestinal nervous system (ENS) diseases. However, appropriate sources, other than enteric neural stem cells and human embryonic stem cells, are seldom reported. Here, we show that neural progenitors derived from the dorsal root ganglion (DRG) of EGFP mice survived, differentiated into enteric neurons and glia cells, migrated widely from the site of injection, and established neuron-muscle connections following transplantation into the distal colon of postnatal mice. The exogenous EGFP+ neurons were physiologically functional as shown by the activity of calcium imaging. This study shows that that other tissues besides the postnatal bowel harbor neural crest stem cells or neural progenitors that have the potential to differentiate into functional enteric neurons in vivo and can potentially be used for intestinal nerve regeneration. These DRG-derived neural progenitor cells may be a choice for cell therapy of ENS disease as an allograft. The new knowledge provided by our study is important for the development of neural crest stem cell and cell therapy for the treatment of intestinal neuropathy.

[Regulation of gacA, dsbA and phoP/phoQ genes on the transcription of small RNA gene RsmZ in Pseudomonas fluorescens].

OBJECTIVE: Pseudomonas fluorescens 2P24 is a plant disease-suppressive bacterium isolated from wheat rhizosphere. Small RNA gene rsmZ in strain 2P24 plays an important role in the production of antibiotic 2,4-diacetylphloroglucinol (2,4-DAPG), a key factor in disease suppression. OBJECTIVE: The aim of this study was to determine the influence of upstream regulators on the transcription of rsmZ. METHODS: A reporting vector was constructed by fusing the promoter region of rsmZ gene with a promoterless lacZ gene on plasmid pRK970Km. The resulting plasmid was introduced into several regulatory gene mutants and the corresponding effects on RsmZ transcription were investigated. RESULTS: The results indicated that a response regulator gene gacA from GacS/GacA two-component system positively regulated the transcription of RsmZ, whereas the oxidoreductase gene dsbA negatively regulated RsmZ expression. Furthermore, mutation on PhoP/PhoQ two-component system resulted in the delay of RsmZ transcription. CONCLUSION: Our study suggests that the rsmZ gene in strain 2P24 transcripts under the pleiotropic regulation of a number of upstream genes, and may be involved in a more complex signal transduction cascade than that we have known.

Upregulation of AKIP1 contributes to metastasis and progression and predicts poor prognosis of patients with colorectal cancer.

BACKGROUND: A kinase-interacting protein 1 (AKIP1) has been reported to play an important role in the development and progression of cancer. However, the clinicopathological and biological roles of AKIP1 in colorectal cancer (CRC) remain largely unknown. The aim of this study was to investigate AKIP1 protein expression in CRC and determine the correlation between AKIP1 protein expression and clinicopathological features, as well as prognosis in CRC patients. MATERIALS AND METHODS: AKIP1 protein expression was determined by immunohistochemical analysis using tissue microarrays of CRC. We also used an siRNA approach to knock down AKIP1 expression and determine the effect of AKIP1 on CRC cell migration by transwell analysis. RESULTS: AKIP1 expression in CRC tissue was significantly higher compared with that of noncancerous colorectal mucosa (P<0.001). Further analysis showed that AKIP1 expression was significantly associated with tumor diameter, TNM stage, and lymph node metastasis (P<0.05). Kaplan-Meier survival analysis demonstrated that patients with a positive AKIP1 expression had significantly poorer overall survival rates when compared with those with negative AKIP1 expression (P=0.031). Multivariate analysis using the Cox proportional hazard model, however, revealed that AKIP1 expression was not a significant independent prognostic factor for CRC. Transwell assay showed that the migration potential of si-AKIP1-transfected cells was significantly reduced when compared with control cells. CONCLUSION: Elevated AKIP1 expression may contribute to metastasis and progression of CRC. Moreover, high AKIP1 expression in CRC significantly correlated with a patient's shorter survival time. Therefore, AKIP1 may be a useful prognostic marker for CRC and a promising novel target for the treatment of CRC.

Neurovascular recovery via co-transplanted neural and vascular progenitors leads to improved functional restoration after ischemic stroke in rats.

The concept of the "neurovascular unit," emphasizing the interactions between neural and vascular components in the brain, raised the notion that neural progenitor cell (NPC) transplantation therapy aimed at neural repair may be insufficient for the treatment of ischemic stroke. Here, we demonstrate that enhanced neurovascular recovery via cotransplantation of NPCs and embryonic stem cell-derived vascular progenitor cells (VPCs) in a rat stroke model is correlated with improved functional recovery after stroke. We found that cotransplantation promoted the survival, migration, differentiation, and maturation of neuronal and vascular cells derived from the cotransplanted progenitors. Furthermore, it triggered an increased generation of VEGF-, BDNF-, and IGF1-expressing neural cells derived from the grafted NPCs. Consistently, compared with transplantation of NPCs alone, cotransplantation more effectively improved the neurobehavioral deficits and attenuated the infarct volume. Thus, cotransplantation of NPCs and VPCs represents a more effective therapeutic strategy for the treatment of stroke than transplantation of NPCs alone.

Characterization of interstitial Cajal progenitors cells and their changes in Hirschsprung's disease.

Interstitial cells of Cajal (ICC) are critical to gastrointestinal motility. The phenotypes of ICC progenitors have been observed in the mouse gut, but whether they exist in the human colon and what abnormal changes in their quantity and ultrastructure are present in Hirschsprung's disease (HSCR) colon remains uncertain. In this study, we collected the surgical resection of colons, both proximal and narrow segments, from HSCR patients and normal controls. First, we identified the progenitor of ICC in normal adult colon using immunofluorescent localization techniques with laser confocal microscopy. Next, the progenitors were sorted to observe their morphology. We further applied flow cytometry to examine the content of ICC progenitors in these fresh samples. The ultrastructural changes in the narrow and proximal parts of the HSCR colon were observed using transmission electron microscopy (TEM) and were compared with the normal adult colon. The presumed early progenitor (c-Kit(low)CD34(+)Igf1r(+)) and committed progenitor (c-Kit(+)CD34(+)Igf1r(+)) of ICC exist in adult normal colon as well as in the narrow and proximal parts of the HSCR colon. However, the proportions of mature, early and committed progenitors of ICC were dramatically reduced in the narrow segment of the HSCR colon. The proportions of mature and committed progenitors of ICC in the proximal segment of the HSCR colon were lower than in the adult normal colon. Ultrastructurally, ICC, enteric nerves, and smooth muscle in the narrow segment of the HSCR colon showed severe injury, including swollen vacuola or ted mitochondria, disappearance of mitochondrial cristae, dilated rough endoplasmic reticulum, vesiculation and degranulation, and disappearance of the caveolae on the ICC membrane surface. The contents of ICC and its progenitors in the narrow part of the HSCR colon were significantly decreased than those of adult colon, which may be associated with HSCR pathogenesis.

SNX13 reduction mediates heart failure through degradative sorting of apoptosis repressor with caspase recruitment domain.

Heart failure (HF) is associated with complicated molecular remodelling within cardiomyocytes; however, the mechanisms underlying this process remain unclear. Here we show that sorting nexin-13 (SNX13), a member of both the sorting nexin and the regulator of G protein signalling (RGS) protein families, is a potent mediator of HF. Decreased levels of SNX13 are observed in failing hearts of humans and of experimental animals. SNX13-deficient zebrafish recapitulate HF with striking cardiomyocyte apoptosis. Mechanistically, a reduction in SNX13 expression facilitates the degradative sorting of apoptosis repressor with caspase recruitment domain (ARC), which is a multifunctional inhibitor of apoptosis. Consequently, the apoptotic pathway is activated, resulting in the loss of cardiac cells and the dampening of cardiac function. The N-terminal PXA structure of SNX13 is responsible for mediating the endosomal trafficking of ARC. Thus, this study reveals that SNX13 profoundly affects cardiac performance through the SNX13-PXA-ARC-caspase signalling pathway.