Serum IGF-1 and IGFBP-3 are useful for the diagnosis of GHD and can be utilized as auxiliary diagnosis indexes for provocative test.

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Mixed adenoneuroendocrine carcinoma (MANEC) is a malignant tumor with adenocarcinoma and neuroendocrine components, with ≥ 30% of each component required. MANEC of the ampulla is rare. To the best of our knowledge, only 15 cases of MANEC of the ampulla have been reported in the English-language literature. Here, we report two cases of MANEC of the ampulla in two women aged 43 and 60 years, which was confirmed by histology after pancreaticoduodenectomy. These tumors contained neuroendocrine and adenocarcinoma components. The neuroendocrine components were positive for chromogranin A (CgA), synaptophysin (Syn) and CD56 by immunostaining. The adenocarcinoma components were negative for CgA, Syn and CD56. Both cases were T3N0M0 (Stage ⅢA). They survived for 15 and 20 mo after surgery, respectively. A brief discussion about the histopathological features, clinical behavior and treatment of MANEC of ampulla, and review of the relevant literature are presented.

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Hemorrhagic transformation (HT) is a major complication of ischemic stroke and further deteriorates neurological outcomes. Bradykinin 1 receptor (B1R) has been proven to mediate vasculo-toxicity in various experimental models. However, its role in the development of HT after stroke remains unclear. We detected the B1R expression in brain tissues with or without HT in a rat model of cerebral ischemia/reperfusion (I/R) with type 1 diabetes, showing higher B1R expression in the hemorrhagic areas than the ischemic tissues. Then, B1R agonist or antagonist was administrated intravenously just before reperfusion to investigate its effect on HT and the underlying molecular mechanism. Administration of low (300 nmol/kg) or high (1 μmol/kg) dose of B1R antagonist mitigated hemorrhage, improved neurobehavioral deficits, and preserved blood-brain-barrier (BBB) integrity after reperfusion for 8 h whereas the 300 nmol/kg of B1R agonist aggravated these outcomes, though only the high does of B1R antagonist affected the infarction volume. Extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation was increased by B1R activation but decreased by B1R inhibition, which mediated B1R toxicity on BBB disruption and ischemia-related HT. Furthermore, B1R activation facilitated the mRNA and protein expressions of MMP-9 in the hemorrhagic tissues, and these increases were blocked by both ERK inhibitor U0126 and NF-κB inhibitor PDTC. U0126 also remarkably decreased the B1R-induced NF-κB/p65 activation. We concluded that upregulated B1R may contribute to early HT after I/R in type 1 diabetic rats via ERK1/2/NF-κB/MMP-9 pathway. B1R inhibition could be an encouraging therapeutic strategy to withstand HT after ischemic stroke in diabetic patients.

The G2385R and R1628P polymorphisms of the leucine-rich repeat kinase 2 (LRRK2) gene have been reported to be associated with Parkinson's disease (PD), but no data are available on Han-Chinese population of south-eastern China. This study aimed to investigate whether G2385R and R1628P variants are associated with sporadic PD in this population. Total 1,060 subjects were enrolled; including 550 unrelated healthy controls and 510 patients with sporadic PD. Genotyping of polymorphisms was performed by PCR-restriction fragment length polymorphism analysis. All variant samples were sequenced for further confirmation. The results showed that the A allele of the G2385R variant was significantly enriched in sporadic PD patient group (4.8%) when compared with control group [1.1%; odds ratio (OR) 4.58, 95% confidence interval (CI) 2.42-8.65, P < 0.01]. However, no significant difference in the frequency of the C allele of R1628P polymorphism variant was observed between cases and controls (2.8 vs. 1.7%, OR 1.67, 95% CI 0.93-2.99, P = 0.08). In conclusion, this study provides the first evidence that G2385R polymorphism is a risk factor for sporadic PD in Han-Chinese population of south-eastern China.

The triglyceride glucose (TyG) index is considered a simple surrogate marker for insulin resistance and has been associated with cerebrovascular diseases. However, limited information is available regarding its association with the subclinical cerebral small vessel disease (CSVD). Here, we investigated the association of TyG index with the burden and distribution of enlarged perivascular space (EPVS) in the non-diabetic population. The data of 531 non-diabetic patients from 2017 to 2020 were assessed. Participants were grouped according to the burden of EPVS. TyG index was calculated using the log scale of fasting triglycerides (mg/dl) × fasting glucose (mg/dl)/2. The association of TyG index with EPVS burden and distribution was evaluated. In the multivariable logistic regression analysis, the TyG index was associated with moderate to severe EPVS [odds ratio (OR): 2.077; 95% CI = 1.268–3.403]. The TyG index was significantly associated with an increased risk of moderate to severe EPVS in subgroups of age &lt;65 years, male, diastolic blood pressure (DBP) &lt;90 mmHg, low-density lipoprotein cholesterol (LDL-C) ≥2.85 mmol/L, serum homocysteine &lt;10 μmol/L, and estimated glomerular filtration rate (eGFR) &lt;90 ml/min/1.73 m2, as well as those without smoking. Further analysis of EPVS distribution, the TyG index was found to be associated with moderate to severe EPVS in the centrum semiovale (CSO), not in the basal ganglia (BG). Conclusively, the TyG index was independently and positively associated with moderate to severe CSO EPVS. TyG index may serve as an independent risk factor for CSVD in clinical practice.