Micturition-triggered severe headache associated with bladder paraganglioma: A case report.

BACKGROUND: Paragangliomas are rare neuroendocrine tumors, especially in the bladder. Although many paragangliomas are non-functional, functioning paragangliomas present with many non-specific signs and symptoms, such as hypertension and headache, complicating their diagnosis. Here, we report a case of micturition-induced severe headache associated with a bladder paraganglioma.Case description: This report describes a severe headache disorder triggered by micturition and associated with a bladder paraganglioma in a middle-aged woman. Her pain occurred consistently after micturition, beginning from the left side of the nose and gradually extended to the forehead and the parietal and occipital regions. The headaches lasted 5-10 min. Removal of the paraganglioma completely eliminated the patient's pain syndrome. CONCLUSION: This case elucidates the association between micturition-triggered headaches and bladder paragangliomas. The presence of a post-micturition severe headache should suggest the possibility of a bladder paraganglioma.

Effect of microstructures on temperature and stress distributions of an irradiated alumina surface.

Three types of alumina surface irradiated by laser are simulated in this study to investigate stray light ablation. Results indicate that temperature fields of triangular and rectangular microstructures exhibit the "head effect," while overall still exhibit Gaussian distributions. For the stress, there is a notable difference between the microstructure surface and the ideal surface. The most stress concentration occurs at the corners on the microstructure surface termed as the "bottom effect." The maximum tensile stress of a triangular microstructure appears below the midline of the slope. The location of the maximum tensile stress on the triangle first shifts down and then up. The inflection point is 0.9 µm in height of the triangle.

First three cases of scalp temperature change in symptomatic areas affected by nummular headache: a case report.

BACKGROUND: Nummular headache is a distinct headache disorder characterized by a rounded or elliptical symptomatic area that is typically 2 to 6 cm in diameter and does not change in shape or size with time. Although the pathomechanism is still not clear, nummular headache is thought to be a primary headache disorder. To date, more than 250 cases have been reported; the symptoms of this disease vary, but no cases with scalp temperature changes in the symptomatic areas have been reported yet. In this study, we present three patients with a new manifestation of nummular headache, in which the symptomatic areas of the scalp were colder or warmer than normal areas; we believe that our work might be helpful for medical practitioners and researchers. CASE PRESENTATION: The temperature differences between the symptomatic areas and the normal areas were tested in three patients with nummular headache accompanied by changes in scalp temperature. Three patients' symptomatic areas were either colder or warmer than the normal areas. In every case, we took measurements from the painful site and from the opposite side of the head. The margin of error was 0.01 °C, and the difference was statistically significant (P < 0.01). CONCLUSION: We firmly believe that our study will provide an enriched understanding of the variation in clinical manifestations of nummular headache. Our observations might also have clinical implications regarding the pathomechanism of this disease, which remains largely unclear at present.

Lin28a protects against diabetic cardiomyopathy via the PKA/ROCK2 pathway.

BACKGROUND: Lin28a enhances glucose uptake and insulin-sensitivity. However, the role of Lin28a on experimental diabetic cardiomyopathy (DCM) is not well understood. We investigated the potential role and mechanism ofLin28a in diabetes-induced myocardial dysfunction in mice. METHODS: Diabetes was induced by intraperitoneal (i.p.) injections of Streptozocin (STZ) in mice. Animals were randomized to be treated with lentivirus carrying Lin28a siRNA or Lin28a cDNA. Cardiac function, cardiomyocyte autophagy, apoptosis and mitochondria morphology in diabetic mice were compared between groups. The target proteins of Lin28a were examined by western blot analysis. RESULTS: Lin28a levels were markedly reduced in the cardiac tissue compared to the control mice. Lin28a overexpression significantly improved left ventricular ejection fraction (LVEF), promoted autophagy, decreased myocardial apoptotic index and alleviated mitochondria cristae destruction in diabetic mice. Lin28a knockdown exacerbated diabetic injury as evidenced by decreased LVEF, increased apoptotic index and aggravated mitochondria cristae destruction. Interestingly, pretreatment with a PKA inhibitor, N-[2-(p-Bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide], di-HCl Salt (H89) abolished the beneficial effects of Lin28a overexpression. RhoA-expression and ROCK2-expression were decreased in vivo after Lin28a overexpression, while Lin28a knockdown increased the expression of RhoA and ROCK2 in diabetic mice. CONCLUSIONS: Lin28a protects against DCM through PKA/ROCK2 dependent pathway. Lin28a might serve as a potential therapeutic target for the treatment of the patients with DCM.

MicroRNA-25 Protects Smooth Muscle Cells against Corticosterone-Induced Apoptosis.

BACKGROUND AND AIMS: Vascular smooth muscle cells (VSMCs) are central components of atherosclerotic plaque. Loss of VSMCs through apoptotic cell death can cause fibrous cap thinning, necrotic core formation, and calcification that may destabilize plaque. Elevated glucocorticoid levels caused by psychological stress promote VSMC apoptosis and can exacerbate atherosclerosis in mice and humans. Changes in the levels of antiapoptosis microRNA-25 (miR-25) have been linked with heart disease, inflammation, VSMC phenotype, oxidative stress, and apoptosis. Here, we investigated the pathways and mechanisms of glucocorticoid-induced apoptosis of mouse VSMCs and the protective role of miR-25. METHODS: Primary mouse VSMCs were cultured +/- corticosterone for 48 h. Apoptosis, ROS, apoptotic protein activities, miR-25, MOAP1, a miR-25 target, and p70S6 kinase were quantified at intervals. The roles of miR-25 were assessed by treating cells with lenti-pre-miR-25 and anti-miR-25. RESULTS: VSMC apoptosis, caspase-3 activity, and Bax were increased by corticosterone, and cell death was paralleled by marked loss of miR-25. Protection was conferred by pre-miR-25 and exacerbated by anti-miR-25. Pre-miR-25 conferred reduced expression of the proapoptotic protein MOAP1, and the protective effects of pre-miR-25 were abrogated by overexpressing MOAP1. The antiapoptotic effects of miR-25 were paralleled by inhibition of the p70S6K pathway, a convergence target for the survival signaling pathways, and protection by pre-miR-25 was abrogated by the p70S6k inhibitor rapamycin. CONCLUSIONS: MicroRNA-25 blocks corticosterone-induced VSMC apoptosis by targeting MOAP1 and the p70S6k pathway. Therapeutic manipulation of miR-25 may reduce atherosclerosis and unstable plaque formation associated with chronic stress.