Detection of Thyroid Nodule Prevalence and Associated Risk Factors in Southwest China: A Study of 45,023 Individuals Undergoing Physical Examinations.

Background: Thyroid nodules (TNs) are among the most common thyroid lesions, and rates of these nodules have risen over the past three decades. As the majority of TN patients remain asymptomatic when these nodules are in the early stages of development, malignant nodules may continue to develop into thyroid cancer when not detected. As such, early screening and diagnosis-based strategies represent the most promising means of preventing or treating TNs and associated cancers. The present study was thus developed to explore TN prevalence among individuals in Luzhou, China. Methods: Here, thyroid ultrasonography and metabolic-related indicators from 45,023 adults undergoing routine physical examinations in the Health Management Center of a large Grade A hospital in Luzhou over the last three years were retrospectively reviewed in an effort to identify factors associated with TN risk and the detection of these nodules through univariate and multivariate logistic regression analyses. Results: In total, 13,437 TNs were detected in these 45,023 healthy adults for an overall 29.8% detection rate. This TN detection rate rose with age, and multivariate logistic regression analyses revealed that independent risk factors associated with TNs included greater age (≥31 years old), female (OR = 2.283, 95% CI: 2.177-2.393), central obesity (OR = 1.115, 95% CI: 1.051-1.183), impaired fasting glucose (OR = 1.203, 95% CI: 1.063-1.360), overweight status (OR = 1.085, 95% CI: 1.026-1.147), and obesity (OR = 1.156, 95% CI: 1.054-1.268), while low BMI was a protective factor associated with lower rates of TN incidence (OR = 0.789, 95% CI: 0.706-0.882). When results were stratified by gender, impaired fasting glucose was not an independent predictor of TN risk among males, while high LDL levels were an independent predictor of TNs among females, and other risk factors were not significantly changed. Conclusion: TN detection rates were high among adults in Southwestern China. Female, elderly individuals, individuals exhibiting central obesity, and those with high levels of fasting plasma glucose are more likely to develop TN.

Clinicopathological significance and prognostic value of P27 expression in gastric cancer patients: a meta-analysis.

Loss of P27 expression correlates with clinical progression in a variety of human cancers. However, the correlation between P27 expression and gastric cancer remains controversial. In this meta-analysis, we performed an electronic search based on six databases to select a sufficient number of studies. Pooled hazard ratio (HR) was used as estimates to investigate the association between P27 expression and prognosis of patients with gastric cancer. We identified 19 studies with 2387 gastric cancer patients, ranging between 50 and 316 samples per study. Q and I2 tests demonstrated that the homogeneity among 19 studies (I2 = 47%, P = 0.0004), thus we applied a fixed-effects model to calculate the pooled HR of P27expression and overall survival (OS) of gastric cancer patients was 0.68, and 95% confidence interval (CI) was 0.60-0.78. Next, we conducted a subgroup meta-analysis and found that patients with low P27 expression in Asians (HR = 0.69, 95% CI: 0.58-0.82) and non-Asians (HR = 0.57, 95% CI: 0.41-0.79) had poor prognosis. In addition, we found the publication bias results of OS in the final included 19 studies showed that this funnel plot presented incomplete symmetry, and then removed three literatures with larger HRs bias, and found that the remaining 16 literatures were homogeneity (I2 = 0%, P = 0.47), the pooled HR was 0.52 with 95% CI of 0.43-0.62, and the publication bias disappeared. These results suggested a strong association between P27 underexpression and poorer prognosis of gastric cancer in patients. P27 may be a tumor suppressor for predicting survival outcome of gastric cancer patients.

TIGAR Attenuates High Glucose-Induced Neuronal Apoptosis via an Autophagy Pathway.

Hyperglycemia-induced neuronal apoptosis is one of the important reasons for diabetic neuropathy. Long-time exposure to high glucose accelerates many aberrant glucose metabolic pathways and eventually leads to neuronal injury. However, the underlying mechanisms of metabolic alterations remain unknown. TP53-inducible glycolysis and apoptosis regulator (TIGAR) is an endogenous inhibitor of glycolysis and increases the flux of pentose phosphate pathway (PPP) by regulating glucose 6-phosphate dehydrogenase (G6PD). TIGAR is highly expressed in neurons, but its role in hyperglycemia-induced neuronal injury is still unclear. In this study, we observed that TIGAR and G6PD are decreased in the hippocampus of streptozotocin (STZ)-induced diabetic mice. Correspondingly, in cultured primary neurons and Neuro-2a cell line, stimulation with high glucose induced significant neuronal apoptosis and down-regulation of TIGAR expression. Overexpression of TIGAR reduced the number of TUNEL-positive neurons and prevented the activation of Caspase-3 in cultured neurons. Furthermore, enhancing the expression of TIGAR rescued high glucose-induced autophagy impairment and the decrease of G6PD. Nitric oxide synthase 1 (NOS1), a negative regulator of autophagy, is also inhibited by overexpression of TIGAR. Inhibition of autophagy abolished the protective effect of TIGAR in neuronal apoptosis in Neuro-2a. Importantly, overexpression of TIGAR in the hippocampus ameliorated STZ-induced cognitive impairment in mice. Therefore, our data demonstrated that TIGAR may have an anti-apoptosis effect via up-regulation of autophagy in diabetic neuropathy.

Triptolide as an Alternative to IVIG Therapy for Kawasaki Disease in a Mouse Model.

BACKGROUND: Kawasaki disease is treated by immunoglobulin therapy, which has adverse side effects like renal damage. AIMS: The aim of the present study was to explore the effectiveness of triptolide, a compound derived from threewingnut that has anti-inflammatory effects, on the treatment of Kawasaki disease in a mouse model. STUDY DESIGN: Animal experiment. METHODS: A mouse model of Kawasaki disease was established through exposure to Candida albicans by intraperitoneal injection. Exposed mice were then randomly divided into several groups (each n=15): model group (saline-treated), low- or high-dose triptolide groups (0.2 mg/kg or 0.4 mg/kg, respectively), and IVIG (high-dose immunoglobulin) group (1 g/kg body weight). Unexposed mice served as an additional control group. Nine weeks from the initial exposure, mice were euthanised and coronary tissues and blood samples were harvested. The rate of apoptosis was detected by TUNEL, and ICAM-1 expression was detected by immunohistochemistry in coronary endothelial cells. Serum TNF-α levels were detected by ELISA. RESULTS: Compared to mice in the (unexposed) control group, apoptosis of endothelial cells, ICAM-1 expression, and serum TNF-α levels were significantly increased in all exposed mice (p<0.05), confirming the presence of disease. However, treatment with triptolide or IVIG significantly lowered these measures compared to untreated exposed mice (model group; p<0.05). CONCLUSIONS: Triptolide treatment reduces markers of coronary endothelial inflammation in a mouse model of Kawasaki disease, similar to IVIG treatment, and therefore may be a useful alternative therapy for this disease.