scholarly journals Comparative morphometry of pial vessels in dyscirculatory-ischemic and diabetic encephalopathy

Pathologia ◽  
2019 ◽  
Vol 0 (1) ◽  
Author(s):  
V. O. Shavryn ◽  
Yu. M. Avramenko
2019 ◽  
Author(s):  
Lexiang Yu ◽  
Yao Chen ◽  
Yan Wei ◽  
Rongqiao He

2004 ◽  
pp. 477-482 ◽  
Author(s):  
Hiroki Iida ◽  
Mami Iida ◽  
Hiroto Ohata ◽  
Kiyoshi Nagase ◽  
Shuji Dohi
Keyword(s):  

1997 ◽  
Vol 2 (4) ◽  
pp. E6 ◽  
Author(s):  
Michael Bitzer ◽  
Lars Wöckel ◽  
Andreas R. Luft ◽  
Ajay K. Wakhloo ◽  
Dirk Petersen ◽  
...  

The authors studied the pial and dural blood supplies in 74 intracranial meningiomas and quantified their associated peritumoral brain edema (PTBE). The extent and localization of pial blush in relation to the total tumor volume were determined angiographically. The amount of edema and tumor size were calculated using computerized tomography. The edema-tumor volume ratio was defined as Edema Index (EI). There were 49 meningiomas with PTBE; of those tumors, 46 were supplied by pial vessels, and three were supplied exclusively by dural vessels. Tumors without PTBE showed no pial blush. The mean EI in meningiomas with pial blush was significantly larger (EI = 3.0) than in meningiomas without pial supply (EI = 1.1; p < 0.0001). Meningiomas in which 10% of the whole tumor volume was supplied by pial vessels had only a small mean EI of 2.2, whereas tumors with pial blood supply greater than or equal to 20% had a mean EI of 3.3 (p < 0.026). In 69.9% of cases with pial blood supply, major portions of the edema were located adjacent to the tumor region supplied by pial vessels. Edema index differences among tumors of different subgroups, as defined by size or histology, were significantly related to the pial supply in each subset. Thus, pial blood supply may be causative for the development of PTBE in meningiomas.


2015 ◽  
Vol 35 (1) ◽  
pp. 38-50 ◽  
Author(s):  
Shiyun Dong ◽  
Gang Li ◽  
Dan Zheng ◽  
Jichao Wu ◽  
Dianjun Sun ◽  
...  

Background: Diabetic encephalopathy is a common complication of diabetes, and it may be involved in altering intracellular calcium concentrations ([Ca2+]i) at its onset. The calcium sensing receptor (CaSR) is a G-protein coupled receptor, however, the functional involvement of CaSR in diabetic encephalopathy remains unclear. Methods: In this study, diabetic rats were modeled by STZ (50 mg/kg). At the end of 4, 8 and 12 weeks, the CaSR expression in hippocampus was analyzed by Western blot. In neonatal rat hippocampal neurons, the [Ca2+]i was detected by laser scanning confocal microscopy, the production of reactive oxygen species (ROS) in mitochondria, the level of NO and the mitochondrial transmembrane potential were measured by MitoSOX, DAF-FM and JC-1, respectively. Results: Our results showed in hippocampal neurons treated with high glucose, CaSR regulated [Ca2+]i through the PLC-IP3 pathway. CaSR expression was decreased and was involved in the changes in [Ca2+]i. Mitochondrial membrane potential, NO release and expression of p-eNOS decreased, while the production of ROS in mitochondria increased. Conclusion: Down-regulation of CaSR expression was accompanied by neuronal injury, calcium disturbance, increased ROS production and decreased release of NO. Up-regulation of CaSR expression attenuated these changes through a positive compensatory protective mechanism to inhibit and delay diabetic encephalopathy in rats.


2015 ◽  
Vol 45 (3) ◽  
pp. 276-282
Author(s):  
I. A. Volchegorskii ◽  
L. M. Rassokhina ◽  
I. Yu. Miroshnichenko

1981 ◽  
Vol 20 (6) ◽  
pp. 448-468 ◽  
Author(s):  
L.M. Auer ◽  
B. Gallhofer

2020 ◽  
Vol 24 (6) ◽  
pp. 3449-3459 ◽  
Author(s):  
Tian Hu ◽  
Xin‐Yi Lu ◽  
Jing‐Jing Shi ◽  
Xiao‐Qi Liu ◽  
Qu‐Bo Chen ◽  
...  

2003 ◽  
Vol 16 (67) ◽  
pp. 440-449 ◽  
Author(s):  
María A. García-Espinosa ◽  
María L. García-Martín ◽  
Sebastián Cerdán

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