Homocysteine might increase the risk of recurrence in patients presenting with primary cerebral infarction.

PURPOSE: Although hyperhomocysteinemia (Hhcy) is a risk factor for cerebral infarction, its effect on recurrent cerebral infarction is less-defined. We aimed to investigate the association of Hhcy and increased risk of recurrent cerebral infarct. MATERIALS AND METHODS: From 2011 to 2013, we recruited 231 primary cerebral infarct patients that were divided to a Hhcy group (n = 105) and a control group (n = 126) according to plasma homocysteinemia (Hcy) levels exceeding 15 µmol/L. In this prospective study, risk factors such as gender, age, blood lipid and glucose levels, history of diabetes, high blood pressure, smoking habits and plasma Hhcy levels were determined. A three-year follow-up compared differences in cerebral infarction recurrence rates. Statistical analyses identified whether plasma Hhcy levels were an independent risk factor for recurrent cerebral infarction. RESULTS: Triglyceride and low-density lipoprotein (LDL) levels in the Hhcy group were significantly higher than controls, and cerebral infarct recurrence rates in the Hhcy group exceeded control subject rates through the three-year follow-up (p = .021, p = .036 and p = .025). Cox proportional hazards modeling showed that elevated Hhcy levels (hazard ratio [HR] = 3.062, p < .001), increased age (HR = 1.069, p < .01), circulating triglyceride levels (HR = 1.686, p = .048), and relative National Institutes of Health Stroke (NIHSS) score (HR = 1.068, p = .016) were risk factors for recurrent cerebral infarction. CONCLUSIONS: Level of Hhcy was a risk factor for recurrent cerebral infarction. Further, particular demographic and clinical outcomes including age, relative NIHSS scores, and circulating triglyceride levels were markedly associated with the occurrence of cerebral infarction.

Zinc finger of the cerebellum 5 promotes colorectal cancer cell proliferation and cell cycle progression through enhanced CDK1/CDC25c signaling.

INTRODUCTION: Colorectal cancer (CRC), mostly caused by external or environmental factors, is the third most common and lethal cancer worldwide. Although a large number of investigations have been carried out to reveal the evolution of CRC, the underlying mechanisms of CRC remain unclear. MATERIAL AND METHODS: Expression of zinc finger of the cerebellum 5 (ZIC5) in CRC tissues and cell models was measured by qRT-PCR and IHC. Cell transfection was carried out for ZIC5 overexpression or knockdown. The MTT assay was applied to examine the capacity of glioma cell proliferation. Wound healing assay and tumor invasion assay were used to test the capacity of glioma cell migration and invasion respectively. Cell cycle analysis and western blot were used to verify the apoptosis rates of CRC cells upon ZIC5 overexpression or downregulation. A further tumor Xenograft study was used to examine the effects of ZIC5 on tumor malignancy in vivo. RESULTS: Cell models using HCT116 and SW620 cells were established to study the ZIC5 function upon ZIC5 overexpression of knockdown. Consistently, we discovered that ZIC5 also significantly increased in Chinese CRC patients. In addition, ZIC5 promoted CRC cell proliferation through increasing the proportion of cells maintained in the S phase. ZIC5 overexpression facilitated the capacity of CRC cell migration and invasion. Inhibition of ZIC5 mitigated such malignant effects. CONCLUSIONS: Collectively, investigations of the ZIC5 in CRC provided a new insight into CRC diagnosis, treatment, prognosis and next-step translational therapeutic developments from bench to clinic.