Expression and intracellular localization of FKHRL1 in mammary gland neoplasms.

FKHRL1 (FOXO3a), a member of the Forkhead family of genes, has been considered to be involved in the development of breast tumors; however, the in vivo expression and activation status of FKHRL1 in breast tumors still remains unclear. We immunohistochemically demonstrated the expression and intracellular localization of FKHRL1 in human breast tumors by the novel anti-FKHRL1 antibody which is available for formalin-fixed paraffin-embedded specimens. In a total of 51 cases of benign tumors, FKHRL1 was diffusely expressed in all cases, and its intracellular localization was revealed to be cytoplasmic (inactive form) in 94% of cases of intraductal papillomas (16/17) and 91% cases of fibroadenomas (31/34), with a similar pattern to normal glandular epithelium. In invasive ductal carcinomas, 83% of the cases (93/112) diffusely expressed FKHRL1; however, unlike benign tumors, 71% of the cases (66/93) showed the nuclear-targeted, active form of FKHRL1. Moreover, activated FKHRL1 was predominantly observed in scirrhous (29/36, 81% of the cases) and papillotubular (30/38, 79% of the cases) subtypes, compared to the solid-tubular subtype (7/19, 37% of the cases). Furthermore, the cases with nuclear-targeted FKHRL1 showed a tendency to have lymph nodal metastasis with statistical significance (P < 0.0001). Thus, the activation of FKHRL1 seems to be recognized as one of the specific features of invasive ductal carcinoma of the breast.</p

The Driving Force for 2014 Dengue Outbreak in Guangdong, China.

Dengue fever has rapidly spread in recent decades to become the most globally expansive viral vector-borne disease. In mainland China, a number of dengue outbreaks have been reported since 1978, but the worst epidemic in decades, involving 45230 cases and 76 imported cases, resulting in six deaths in Guangdong province, emerged in 2014. Reasons for this ongoing surge in dengue, both imported and autochthonous, are currently unclear and demand urgent investigation. Here, a seasonally-driven dynamic epidemiological model was used to simulate dengue transmission data recorded from the unprecedented outbreak. Sensitivity analysis demonstrate that delayed mosquito control, the continuous importations between the end of April to the early of July, the transmission of asymptomatic dengue infections, and the abnormally high precipitation from May to August might be the causal factors for the unprecedented outbreak. Our results suggested that the earlier and more frequent control measures in targeting immature and adult mosquitoes were effective in preventing larger outbreaks, and enhanced frontier health and quarantine from the end of April to the early of July for international communications and travelers

The Chinese (Cantonese) Montreal Cognitive Assessment in Patients with Subcortical Ischemic Vascular Dementia

Background: Subcortical ischemic vascular dementia (SIVD) has been proposed as the most frequent subtype of vascular cognitive impairment. The aim of this study was to evaluate the psychometric properties of the Chinese (Cantonese) Montreal Cognitive Assessment (CC- MoCA) in patients with SIVD in the Guangdong Province of China. Methods: 71 SIVD patients and 60 matched controls were recruited for the CC-MoCA, Mini Mental State Examination and executive clock drawing tasks. Receiver-operating characteristic curve analyses were performed to determine optimal sensitivity and specificity of the CC-MoCA total score in differentiating mild vascular dementia (VaD) patients from moderate VaD patients and controls. Results: The mean CC-MoCA scores of the controls, and mild and moderate VaD patients were 25.2 ± 3.8, 16.4 ± 3.7, and 10.0 ± 5.1, respectively. In our study, the optimal cutoff value for the CC-MoCA to be able to differentiate patients with mild VaD from controls is 21/22, and 13/14 to differentiate mild VaD from moderate VaD. Conclusion: The CC-MoCA is a useful cognitive screening instrument in SIVD patients

Menin prevents liver steatosis through co-activation of peroxisome proliferator-activated receptor alpha

AbstractFatty liver is strongly associated with metabolic syndrome. Here, we show that the impaired hepatic expression of menin, the product of the MEN1 (multiple endocrine neoplasia type 1) tumor suppressor gene, represents a common feature of several fatty liver mouse models. The liver specific ablation of MEN1 gene expression in healthy mice induced hepatic steatosis under high-fat dietary conditions. Moreover, overexpression of menin in livers of steatotic db/db mice reduced liver triglyceride accumulation. At the molecular level, we found that menin acts synergistically with the nuclear receptor PPARα to control gene expression of fatty acid oxidation. Collectively, these data suggest a crucial role for menin as an integrator of the complex transcriptional network controlling hepatic steatosis.Structured summary of protein interactionsMenin physically interacts with PPAR alpha by anti tag coimmunoprecipitation (View Interaction: 1, 2)