The objective of this study is to summarize the clinical and pathologic characteristics of malignant struma ovarii to facilitate the early diagnosis and treatment of this disease. All 144 patients were females from 27 countries. The mean age of the patients at diagnosis was 42.6 years. Overall, 35.71% of the patients underwent unilateral oophorectomy, 58.57% of the patients underwent bilateral oophorectomy, 5.72% of the patients were not ovariectomized, and 38.57% of the patients received radioactive iodine treatment with an average dose of 158.22 mCI each time. “Impure” types accounted for 70.19% of the cases, while pure types accounted for 29.81% of the cases. Among these cases, papillary thyroid carcinoma accounted for 50.00%, follicular thyroid carcinoma accounted for 26.47%, follicular variant of papillary thyroid carcinoma accounted for 18.63%, papillary and follicular mixed thyroid carcinoma accounted for 2.94%, anaplastic carcinoma accounted for 0.98%, and medullary carcinoma accounted for 0.98%. In total, 21 patients (51.22%) had elevated CA125. More than half of the patients (51.94%) had metastasis outside the ovary. The most common metastatic site was the pelvic cavity. The misdiagnosis rate was 17.27%. Mortality was related to metastasis and the cancer type. Gene mutations were found in the NRAS, KRAS, BRAF, and KIT genes and were similar to those in thyroid carcinoma, but some patients (37.5%) did not exhibit any gene mutations. Regardless of the treatment received, the survival rate is high. Treatment could initially include ovariectomy; however, in cases with metastasis and iodine uptake of the metastatic tumor, thyroidectomy, radioactive iodine therapy, and thyroid hormone inhibiting therapy are indicated.

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Background: Accumulating evidences indicate that the apoptosis of proximal tubular epithelial cells (PTECs) play a vital role in the progression of the diabetic kidney disease (DKD). This study aimed to explore the therapeutic potential of salidroside (SAL) in DKD and its underlying mechanism in anti-apoptosis of PTECs.Methods: Twenty-eight male Wistar rats were allocated into four groups: sham-operated, uninephrectomy (unx), diabetes with uninephrectomy (DKD) and DKD treated with SAL (DKD + SAL). SAL (70 mg/kg) was gavage administered for 8 weeks. 24-h albuminuria and serum creatinine (SCr), blood urea nitrogen (BUN), renal histological changes were examined. The silico analysis was used to identify the main therapeutic targets and pathways of SAL involved in DKD treatment. Apoptosis was determined by TUNEL and Annexin V-FITC/PI double staining in vivo and in vitro, respectively. The expression of BIM, BAX, and cleaved caspase-3 were evaluated by western blot and immunostaining.Results: Treatment with SAL significantly attenuated diabetic kidney injury via inhibiting 24-h albuminuria, SCr, BUN, glomerular mesangial dilatation and tubular injury in DKD rats. The silico analysis identified the intrinsic apoptotic pathway as an important pathway responsible for the nephroprotective properties of SAL. Our data validated that SAL effectively inhibited the apoptosis of PTECs induced by high-glucose (HG), both in vitro and in vivo. Silence of BIM by shRNA in HK-2 cells prevented HG-induced apoptosis. The up-regulated BIM and its downstream targets (BAX and cleaved caspase-3) were also inhibited by SAL.Conclusion: In summary, SAL significantly relieved DKD. And the possible mechanisms might be partially attributed to inhibiting apoptosis of proximal renal tubular cells. The apoptotic protein BIM could be an important target of SAL in this process.

The key characteristic of cardiovascular disease (CVD) is endothelial dysfunction, which is likely the consequence of inflammation. It is well demonstrated that chemokines and their receptors play a crucial role in regulating inflammatory responses, and recently, much attention has been paid to chemokine receptor 5 (CCR5) and its ligands. For example, CCR5 aggravates the inflammatory response in adipose tissue by regulating macrophage recruitment and M1/M2 phenotype switch, thus causing insulin resistance and obesity. Inhibition of CCR5 expression reduces the aggregation of pro-atherogenic cytokines to the site of arterial injury. However, targeting CCR5 is not always effective, and emerging evidence has shown that CCR5 facilitates progenitor cell recruitment and promotes vascular endothelial cell repair. In this paper, we provide recent insights into the role of CCR5 and its ligands in metabolic syndrome as related to cardiovascular disease and the opportunities and roadblocks in targeting CCR5 and its ligands.

Background: Many studies have evaluated the association between matrix metalloproteinase 9 (MMP9) gene promoter polymorphism and diabetic microvascular complications. However, the results are conflicting and inconclusive. The aim of this meta-analysis was to evaluate the association more precisely. Materials and Methods: Studies were retrieved from the PubMed, Embase, Medline, China National Knowledge Infrastructure, Web of Science, and Cochrane databases. All statistical analyses were performed using Review Manager 5.2. Results: Data were abstracted from four case-control studies that included 446 patients with diabetic microvascular complications and 496 diabetic control subjects. The MMP9-1562 C/T genotype was significantly associated with the risk of diabetic nephropathy after stratification by specific type of microvascular complication (CT + TT vs. CC: OR = 0.42, 95% CI = 0.26–0.69, p = 0.0006; TT vs. CC + CT: OR = 0.37, 95% CI = 0.19–0.76, p = 0.006). Conclusions: This study adds to the evidence that MMP9-1562 T gene mutation might reduce the risk of diabetic nephropathy.

Background: The incidence of thyroid carcinoma is increasing all over the world. Some studies have suggested that the change of adipokines expression can induce thyroid carcinoma. However, other studies have come to the opposite conclusion. Therefore, we studied the relationship between adipokines and thyroid carcinoma. Methods: Databases-PubMed, Cochrane Library, SinoMed, CNKI, Wanfang, and clinical trial registries were searched. A meta-analysis was then performed through a fixed or random-effects model to calculate I values for heterogeneity analysis. Results: Twenty-nine articles were finally included for analysis. The level of serum tumor necrosis factor-alpha (TNFα) [standardized mean difference (SMD) =1.31, 95% confidence interval (95% CI): 0.35 to 2.28, I 2 = 98%, P = 0.008] and the ratio of TNF-α immunoreactivity in tissues [odds ratios (OR) =6.36, 95% CI: 1.92 to 21.05, I 2 = 66%, P = 0.002] in thyroid carcinoma are significantly higher than those in control. The serum interleukin-6 (IL-6) in patients with thyroid carcinoma is higher than that in control (SMD = 1.04, 95% CI: 0.40 to 1.67, I 2 = 96%, P = 0.001). There is no significant difference of the ratio of IL-6 immunoreactivity in tissues between carcinoma and control (OR = 1.23, 95% CI: 0.62 to 2.43, I 2 = 86%, P = 0.55). The ratio of leptin immunoreactivity in tissues is significantly associated with the risk of thyroid carcinoma (OR = 12.21, 95% CI: 3.36 to 44.40, I 2 = 85%, P < 0.00001). However, after analyzing the expression level of serum adiponectin in three studies, no significant difference is found between thyroid carcinoma and the control (P = 0.81). Conclusions: Adipokines (TNF-α, IL-6 and leptin) show a strong relationship between elevated concentrations (in serum and/or tissue) and thyroid carcinoma. However, the association between adiponectin and thyroid carcinoma needs further research.

Background:As an important factor causing end-stage renal disease, diabetic nephropathy is correlated with low-grade chronic inflammation and immune system activation. This study aimed to investigate the protective function of puerarin on the kidneys of diabetic rats. Material/Methods:A cohort of healthy male SD rats (7 weeks old) were randomly divided into a control group, a model group, and a puerarin treatment group with high (H), moderate (M), and low (L) dosage. After streptozotocin induction, puerarin was applied via intragastric administration for 8 consecutive weeks with dosages of 0.25, 0. 5 and 1.0 mg/(kg·d) for L, M, and H groups, respectively. Fasting blood glucose (BG), creatinine (Scr), urea nitrogen (BUN), and urine albumin excretion rate (UAER) were measured, along with morphological observation of renal cells. The expression of intracellular adhesion molecule 1 (ICAM-1) and tumor necrosis factor a (TNF-a) was determined using immunohistochemical (IHC) staining, while renal cortex cell apoptosis was assayed by in situ end-labeling method. Results:Model rats had significantly elevated levels of BG, Scr, BUN, and UAER compared to controls (p<0.05). All these increases were partially but significantly suppressed by puerarin (p<0.05), which also caused marked improvement of histopathological damages. Puerarin at each dosage significantly eliminated elevations of ICAM-1 and TNF-a levels in model rats (p<0.05), and decreased apoptotic indexes of renal cortex cells (p<0.05). Conclusions:Early-stage renal damages can be significantly improved by puerarin, possibly via its suppression of ICAM-1 and TNF-a expression in diabetic rat kidneys.

An inappropriate level of TSH should always be evaluated. We found a new mutation (H435A) of the thyroid hormone receptor beta gene, which allowed for the establishment of a definitive diagnosis.