1213: Acetylcholinesterase Inhibitor Acting on the Brain Improves Overactive Bladder by Cerebral Infarction in Rats

2005 ◽  
Vol 173 (4S) ◽  
pp. 329-329
Author(s):  
Masaharu Nakai ◽  
Osamu Yokoyama ◽  
Hironobu Akino
Keyword(s):  
Overactive Bladder ◽  
Cerebral Infarction ◽  
Acetylcholinesterase Inhibitor ◽  
The Brain

Acetylcholinesterase inhibitor acting on the brain improves detrusor overactivity caused by cerebral infarction in rats

Neuroscience ◽  
2006 ◽  
Vol 142 (2) ◽  
pp. 475-480 ◽  
Author(s):  
M. Nakai ◽  
H. Akino ◽  
T. Kaneda ◽  
Y. Matsuta ◽  
R. Shiyama ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Detrusor Overactivity ◽  
Acetylcholinesterase Inhibitor ◽  
The Brain

Comparative changes in the blood-brain barrier and cerebral infarction of SHR and WKY rats

2007 ◽  
Vol 292 (5) ◽  
pp. R1881-R1892 ◽  
Author(s):  
Sharon Hom ◽  
Melissa A. Fleegal ◽  
Richard D. Egleton ◽  
Christopher R. Campos ◽  
Brian T. Hawkins ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Blood Brain Barrier ◽  
Infarct Volume ◽  
Brain Barrier ◽  
Ion Transporter ◽  
Transporter Proteins ◽  
Wky Rats ◽  
Blood Brain ◽  
Hypertension Development ◽  
The Brain

Hypertension is involved in the exacerbation of stroke. It is unclear how blood-brain barrier (BBB) tight-junction (TJ) and ion transporter proteins critical for maintaining brain homeostasis contribute to cerebral infarction during hypertension development. In the present study, we investigated cerebral infarct volume following permanent 4-h middle cerebral artery occlusion (MCAO) and characterized the expression of BBB TJ and ion transporter proteins in brain microvessels of spontaneously hypertensive rats (SHR) compared with age-matched Wistar-Kyoto (WKY) rats at 5 wk (prehypertension), 10 wk (early-stage hypertension), and 15 wk (later-stage hypertension) of age. Hypertensive SHR show increased infarct volume following MCAO compared with WKY control rats. BBB TJ and ion transporter proteins, known to contribute to edema and fluid volume changes in the brain, show differential protein expression patterns during hypertension development. Western blot analysis of TJ protein zonula occludens-2 (ZO-2) showed decreased expression, while ion transporter, Na+/H+ exchanger 1 (NHE-1), was markedly increased in hypertensive SHR. Expression of TJ proteins ZO-1, occludin, actin, claudin-5, and Na+-K+-2Cl− cotransporter remain unaffected in SHR compared with control. Selective inhibition of NHE-1 using dimethylamiloride significantly attenuated ischemia-induced infarct volume in hypertensive SHR following MCAO, suggesting a novel role for NHE-1 in the brain in the regulation of ischemia-induced infarct volume in SHR.

scholarly journals A case of severe acute respiratory syndrome coronavirus 2 with acute thrombotic cerebral infarction and generalized thrombosis

2021 ◽  
pp. 405-408
Author(s):  
Sylvia Nikolaeva Genova ◽  
Nikolaeva Genova ◽  
Mina Miroslavova Pencheva ◽  
Alexander Georgiev Ivanov
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Cerebral Infarction ◽  
Viral Pneumonia ◽  
Autopsy Case ◽  
Full Spectrum ◽  
Histological Changes ◽  
Large Size ◽  
Thrombotic Complications ◽  
Coronavirus Infection ◽  
The Brain

The full spectrum of coronavirus disease 2019 (COVID-19) has not been fully described yet. COVID-19 is associated with a high risk of thrombotic complications such as venous thromboembolism and cerebrovascular disease. Here, we report an autopsy case of a 55-year-old woman diagnosed with severe viral pneumonia complicated by acute cerebral infarction and venous and arterial thrombosis in different organs. The patient died due to severe acute respiratory syndrome coronavirus 2. Macroscopically and histologically, in addition to viral pneumonia and diffuse hemorrhages, fibrin clots were found in arteries and venous vessels of medium and large size in the brain, lungs, and pancreas. Propagation of cerebrovascular thrombosis has led to extensive cerebral infarction. The dating of this infarction, according to the macroscopical findings and the histological changes, was between 24 and 48 h before death. This case confirms the hypothesis on the risk of generalized arterial and venous thromboses in coronavirus infection.

Abnormal resting-state brain activity and connectivity of brain-bladder control network in overactive bladder syndrome

2021 ◽  
pp. 028418512110572
Author(s):  
Wang Biao ◽  
Zuo Long ◽  
Zhou Yang ◽  
Gu Hua ◽  
Wang Shuangkun
Keyword(s):  
Overactive Bladder ◽  
Resting State ◽  
Clinical Symptoms ◽  
Pearson Correlation ◽  
Functional Integration ◽  
Anterior Cingulate ◽  
Control Network ◽  
Bladder Control ◽  
The Brain ◽  
Left Insula

Background Neuroimaging studies have shown that the brain is involved in the mechanism of overactive bladder disease (OAB). Purpose To explorer spatial patterns of spontaneous neural activities and functional integration in patients with OAB. Material and Methods In total, 28 patients with OAB and 28 matched healthy controls (HC) underwent resting-state functional magnetic resonance imaging and completed questionnaires to assess clinical symptoms. The amplitude of low-frequency fluctuation (ALFF) and ROI-based functional connectivity (FC) within the brain-bladder control network (BBCN) were calculated and compared between the two groups using a two-sample t-test. Pearson correlation analysis was performed to investigate the relationship between ALFF and the clinical score of patients with OAB. Results Compared with HCs, patients with OAB exhibited significantly decreased ALFF in the left superior medial middle gyrus (SFGmed) and superior dorsal frontal gyrus (SFGdor), and increased ALFF in the right hippocampus. Furthermore, ALFF values in the left SFGmed were negatively correlated with OABSS scores. FC in patients with OAB was significantly increased between the bilateral caudate nucleus (CAU) and bilateral SFGdor, the bilateral CAU and bilateral supplementary motor area (SMA), the bilateral thalamus and SMA; the left CAU and bilateral SFGmed, the left CAU and bilateral anterior cingulate gyrus, and the left CAU and left insula. Additionally, decreased FC was found between the bilateral amygdala and bilateral SFGmed and the left SMA and left insula. Conclusion These abnormal activities and connectivities of BBCN may indicate impaired cortical control of micturition in OAB, suggesting a possible neural mechanism of OAB.

scholarly journals Glutathione Suppresses Cerebral Infarct Volume and Cell Death after Ischemic Injury: Involvement of FOXO3 Inactivation and Bcl2 Expression

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Juhyun Song ◽  
Joohyun Park ◽  
Yumi Oh ◽  
Jong Eun Lee
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Cerebral Infarction ◽  
Infarct Size ◽  
Cell Survival ◽  
Ischemia Reperfusion ◽  
Ischemic Injury ◽  
Cerebral Infarct ◽  
Ros Scavenging ◽  
The Brain

Ischemic stroke interrupts the flow of blood to the brain and subsequently results in cerebral infarction and neuronal cell death, leading to severe pathophysiology. Glutathione (GSH) is an antioxidant with cellular protective functions, including reactive oxygen species (ROS) scavenging in the brain. In addition, GSH is involved in various cellular survival pathways in response to oxidative stress. In the present study, we examined whether GSH reduces cerebral infarct size after middle cerebral artery occlusionin vivoand the signaling mechanisms involved in the promotion of cell survival after GSH treatment under ischemia/reperfusion conditionsin vitro. To determine whether GSH reduces the extent of cerebral infarction, cell death after ischemia, and reperfusion injury, we measured infarct size in ischemic brain tissue and the expression of claudin-5 associated with brain infarct formation. We also examined activation of the PI3K/Akt pathway, inactivation of FOXO3, and expression of Bcl2 to assess the role of GSH in promoting cell survival in response to ischemic injury. Based on our results, we suggest that GSH might improve the pathogenesis of ischemic stroke by attenuating cerebral infarction and cell death.

scholarly journals The protective role of proton-sensing TDAG8 in the brain injury in a mouse ischemia reperfusion model

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Koichi Sato ◽  
Ayaka Tobo ◽  
Chihiro Mogi ◽  
Masayuki Tobo ◽  
Nobuhiro Yamane ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
G Protein ◽  
Morphological Changes ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Cerebral Injury ◽  
G Protein Coupled Receptor ◽  
Dysfunctional Behavior ◽  
G Protein Coupled ◽  
The Brain

Abstract Extracellular acidification in the brain has been observed in ischemia; however, the physiological and pathophysiological implications of the pH reduction remain largely unknown. Here, we analyzed the roles of proton-sensing G protein-coupled receptors, including T-cell death-associated gene 8 (TDAG8), ovarian cancer G protein-coupled receptor 1 (OGR1), and G protein-coupled receptor 4 (GPR4) in a mouse ischemia reperfusion model. Cerebral infarction and dysfunctional behavior with transient middle cerebral artery occlusion (tMCAO) and subsequent reperfusion were exacerbated by the deficiency of TDAG8, whereas no significant effect was observed with the deficiency of OGR1 or GPR4. We confirmed that the pH of the predicted infarction region was 6.5. TDAG8 mRNA was observed in Iba1-positive microglia in the mouse brain. The tMCAO increased the mRNA expression of tumor necrosis factor-α in the ipsilateral cerebral hemisphere and evoked morphological changes in microglia in an evolving cerebral injury. These tMCAO-induced actions were significantly enhanced by the TDAG8 deficiency. Administration of minocycline, which is known to inhibit microglial activation, improved the cerebral infarction and dysfunctional behavior induced by tMCAO in the TDAG8-deficient mouse. Thus, acidic pH/TDAG8 protects against cerebral infarction caused by tMCAO, at least due to the mechanism involving the inhibition of microglial functions.

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