Background. Obesity has been considered as an important factor in the development and progression of chronic kidney diseases (CKD). Perirenal fat, which is surrounding the kidneys, has been reported to be unique in anatomy and biological functions. This study is aimed at assessing the relationship between perirenal fat thickness (PrFT) and estimated glomerular filtration rate (eGFR) in patients with type 2 diabetes (T2DM). Methods. A total of 171 patients with T2DM were recruited in the study. The basic and clinical characteristics including sex, age, diabetes duration, body mass index (BMI), waist circumference (WC), visceral fat area (VFA), glycated hemoglobin (HbA1c), serum uric acid (UA), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), and high-density lipoprotein cholesterol (HDL-c) were collected. PrFT was measured via ultrasound. eGFR was calculated using the Modification of Diet in Renal Disease (MDRD) formula. Results. Patients were divided into three groups according to PrFT, and we found patients with higher PrFT had lower eGFR. PrFT was significantly correlated with eGFR in all patients r=−0.181,P<0.05. Subgroup analysis by sex showed that PrFT still significantly and negatively related to eGFR in men r=−0.264,P<0.05, but not in women (r=−0.199, P=0.062). The association also existed in multivariate analysis after correction for the confounding factors β=−0.203,P=0.017. Conclusions. This study confirmed a negative independent relationship between PrFT and eGFR in patients with T2DM, especially in men, suggesting a possible role of perirenal fat in kidney dysfunction in T2DM patients.

Abstract. This study was conducted to investigate the biomarkers that appear to be correlated with cancer-related fatigue (CRF) and the adverse reactions (ADRs) to chemotherapy. A total of 100 lung cancer patients were selected and CRF prior to and following chemotherapy was evaluated. The plasma levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1 and the level of 17-hydroxycorticosteroid (17-OHCS) in the urine were analyzed and correlated with CRF and the ADRs associated with chemotherapy. The incidence of CRF was found to be 88.0% and ADRs following chemotherapy occurred in 15.0% of the patients. An increase in the TNF-α and IL-1 levels was detected in patients with CRF. The level of 17-OHCS in the urine was found to be elevated in cases that experienced ADRs following chemotherapy. In conclusion, CRF is closely correlated with increased plasma levels of TNF-α and IL-1. Furthermore, an abnormally elevated 17-OHCS level in the urine may be an important indicator predicting ADR development following chemotherapy.

Maternal over-nutrition may predispose offspring to obesity, type 2 diabetes and other adult diseases. The present study investigated long-term impact of prenatal high sucrose (HS) diets on cognitive capabilities in aged rat offspring. The fasting plasma glucose concentration did not differ between the control and HS groups. However, the fasting plasma insulin and insulin resistance index values were significantly increased in HS offspring that showed abnormal glucose tolerance test. HS offspring exhibited increased escape latency and swimming path length to the platform, and reduced time in the target quadrant and the number of crossing the platform, as compared with the control group. The expression of Grin2b/NR2B, Wnt2, Wnt3a and active form of β-catenin protein were decreased, and Dickkopf-related protein 1 was increased in the HS group. In addition, the levels of lipid peroxidation biomarker thiobarbituricacid reactive substance, nicotinamide adenine dinucleotide phosphate oxidases 2 and superoxide dismutase 1 were significantly increased, and the activity of catalase was decreased in the hippocampus in the HS group. The results demonstrate that prenatal HS-induced metabolic changes cause cognitive deficits in aged rat offspring, probably due to altered N-methyl-D-aspartate receptors/Wnt signaling and oxidative stress in the hippocampus.

To investigate the expression patterns of aquaporin 3 (AQP) 3 and AQP5, to evaluate their relationships with clinicopathological characteristics, and to determine their correlations with survival in esophageal squamous cell carcinoma (ESCC) patients, expression levels of AQP3 and AQP5 proteins in 126 ESCC patients were detected by immunohistochemistry. Then, paired Student's t-test, chi-square test, Spearman's rank correlation, Kaplan-Meier plots, and Cox proportional hazards regression model were used to analyze their associations with clinicopathological characteristics and survivals of ESCC patients. Both AQP3 and AQP5 proteins were localized on the cell membrane of tumor cells in ESCC tissues. The expression levels of two proteins in ESCC tissues were significantly higher than those in adjacent normal tissues (both P < 0.001). Additionally, high expression of AQP3 and AQP5 was both correlated with advanced invasion depth (both P = 0.01), aggressive lymph node status (P = 0.02 and 0.01, respectively), and positive distant metastasis (both P = 0.01). However, the overexpression of AQP3 and AQP5 alone did not influence the prognosis. Furthermore, ESCC patients with the co-expression of AQP3 and AQP5 showed the poorest prognosis in overall (P = 0.002) and disease-free survival (P < 0.001). Multivariate analysis showed that the co-expression of AQP3 and AQP5 was an independent prognostic factors of overall (P = 0.01) and disease-free survival (P = 0.01) in ESCC. Our data demonstrate for the first time that high expression of both AQP3 and AQP5, not each alone, is an independent poor prognostic factor in ESCC patients. Combined detection of the two proteins' expression may help to predict the progression and the prognosis of ESCC patients.

The principal findings demonstrated that down-regulation of HOTAIR elicits an inhibitory effect on proliferation, invasion, and migration, while promoting the apoptosis of CRC cells through the up-regulation of p21. We believe that HOTAIR could represent a novel target for the treatment of CRC.

The present study tested the hypothesis that angiotensin II plays a role in the regulation of placental vascular tone, which contributes to hypertension in preeclampsia. Functional and molecular assays were performed in large and micro placental and non-placental vessels from humans and animals. In human placental vessels, angiotensin II induced vasoconstrictions in 78.7% vessels in 155 tests, as referenced to KCl-induced contractions. In contrast, phenylephrine only produced contractions in 3.0% of 133 tests. In non-placental vessels, phenylephrine induced contractions in 76.0% of 67 tests, whereas angiotensin II failed to produce contractions in 75 tests. Similar results were obtained in animal placental and non-placental vessels. Compared with non-placental vessels, angiotensin II receptors and β -adrenoceptors were significantly increased in placental vessels. Compared to the vessels from normal pregnancy, angiotensin II-induced vasoconstrictions were significantly reduced in preeclamptic placentas, which was associated with a decrease in angiotensin II receptors. In addition, angiotensin II and angiotensin converting enzyme in the maternal-placenta circulation in preeclampsia were increased, whereas angiotensin I and angiotensin1-7 concentrations were unchanged. The study demonstrates a selective effect of angiotensin II in maintaining placental vessel tension, which may play an important role in development of hypertension in preeclampsia.

Fluorouracil (5-FU) has been wildly used as a primary medication in the treatment of solid tumors including colorectal cancer. The treatment efficacy and toxicity of 5-FU varies greatly among individuals, suggesting a need for individualized regimen for cancer patients. The present study analyzed the blood concentration of 5-FU and its therapeutic efficacy and toxicity, evaluated the relationship of AUC (area under the plasma concentration-time curve), and the protein expression of DPD (dihydropyrimidine dehydrogenase) and TS (thymidylate synthetase), and therapeutic efficacy and toxicity. It was found that the AUC of 5-FU was 34.16±14.83mg·h/L in this cohort of study. The immunohistochemical analysis revealed 38.96% and 81.82% positive staining for DPD and TS in colorectal cancer tissues, respectively. We demonstrated that the expression of TS is positively correlated with the expression of DPD. There was a positive correlation between AUC and therapeutic efficacy, and gastrointestinal tract and neural toxicity. The expression of neither DPD nor TS had significant correlations with therapeutic efficacy and toxicity. Based on the blood 5-FU concentration and its relationship with treatment efficacy and toxicity, we determined an optimal therapeutic dosage of 5-FU to be equivalent to an AUC=28.03-38.94mg·h/L. Our study will be helpful in providing an individualized medical regimen for the treatment of colorectal cancer patients.

BackgroundApolipoprotein E (ApoE) is a multifunctional protein that plays an important role in lipoprotein metabolism. However, the relationship between APOE gene polymorphisms and cerebral infarction in the Chinese population remains unclear. Therefore, we studied the role of APOE gene polymorphisms in patients with cerebral infarction in a Chinese population.Material/MethodsThis study involved 906 patients with cerebral infarction and 1,141 individuals without cerebral infarction who served as controls. APOE genotypes were identified in all participants who participated in the study. Factors influencing cerebral infarction were also analyzed.ResultsStatistically significant variances in the distribution and frequencies of the APOE genotypes in the patients were observed (ɛ2/ɛ3 versus ɛ2/ɛ4 versus ɛ3/ɛ3=22.85% versus 7.62% versus 56.95%) and controls (ɛ2/ɛ3 versus ɛ2/ɛ4 versus ɛ3/ɛ3=17.27% versus 2.72% versus 66.87%; p<0.001). Univariate analysis showed that the APOE ɛ3/ɛ3 genotype [OR, 0.393 (95% CI, 0.237–0.653); p<0.001] and ɛ3/ɛ4 genotype [OR, 0.376 (95% CI 0.221–0.637); p<0.001] played a protective role against cerebral infarction in Chinese men.ConclusionsStatistically significant variances in the distribution and frequencies of the APOE genotypes of the patients and controls were observed. The study demonstrated that the APOE ɛ3/ɛ3 and ɛ3/ɛ4 genotypes played a protective role against cerebral infarction in Chinese men, but not women. Additionally, the ɛ2/ɛ4 genotype may be a potential risk factor in men, whereas ɛ3/ɛ4 genotype may play a potential protective role against this disease in women.