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1.
Chinese Journal of Pathology ; (12): 834-839, 2011.
Article in Chinese | WPRIM | ID: wpr-242017

ABSTRACT

<p><b>OBJECTIVE</b>To examine the temporal and spatial expression of vascular endothelial growth factor (VEGF) and angiopoietins (Ang) in rat brain after cerebral ischemia, and to elucidate the roles they played in angiogenesis and vascular permeability.</p><p><b>METHODS</b>Rats were subjected to either middle cerebral artery occlusion (MCAO) or sham operation. Reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemistry were used to detect the expression of VEGF, Ang-1 and Ang-2 at different time points after ischemia. CD31 was used to label endothelial cells after MCAO. Vascular permeability was determined by Evans blue.</p><p><b>RESULTS</b>VEGF was markedly increased at 2 h, had an initial peak at 12 h (0.7249 ± 0.1933, P < 0.01), and a second peak at 7 days (0.5264 ± 0.1519, P < 0.01). Ang-2 mRNA and protein significantly increased after MCAO, both of them peaked at 12 h (0.6747 ± 0.2416, P < 0.01; 1.1197 ± 0.1780, P < 0.01). In contrast, Ang-1 mRNA and protein gradually decreased after MCAO, respectively reaching a minimum at 3 d (0.3220 ± 0.1427, P < 0.01) and 1 d (0.1298 ± 0.0293, P < 0.01). Changes in the expression of these factors correlated with the progress of angiogenesis and vascular permeability. Evans blue test revealed that the vascular permeability gradually increased, and peaked at day 1 after ischemia [(6.219 ± 0.887) µg/g, P < 0.01].</p><p><b>CONCLUSION</b>Dynamic temporal changes in VEGF, Ang-1 and Ang-2 expression stimulate the cerebral angiogenesis after focal cerebral ischemia.</p>


Subject(s)
Animals , Male , Rats , Angiopoietin-1 , Genetics , Metabolism , Angiopoietin-2 , Genetics , Metabolism , Blotting, Western , Capillary Permeability , Immunohistochemistry , Infarction, Middle Cerebral Artery , Metabolism , Pathology , Neovascularization, Physiologic , RNA, Messenger , Metabolism , Random Allocation , Rats, Sprague-Dawley , Reverse Transcriptase Polymerase Chain Reaction , Vascular Endothelial Growth Factor A , Genetics , Metabolism
2.
Chinese Medical Journal ; (24): 2832-2835, 2010.
Article in English | WPRIM | ID: wpr-237406

ABSTRACT

<p><b>BACKGROUND</b>Hyalinizing trabecular tumor (HTT) is a rare thyroid neoplasm, which shares some histologic features with thyroid papillary carcinoma (TPC). Clinically, it is frequently misdiagnosed as papillary carcinoma, even for some experienced pathologists. The aim of this study was to investigate whether HTT is variant of TPC or HTT is an independent entity of thyroid neoplasm.</p><p><b>METHODS</b>The expression of CK19, galectin-3, HBME-1 and MIB-1 was detected by immunohistochemical staining in 12 cases of hyalinizing trabecular tumor and 20 cases of thyroid papillary carcinoma.</p><p><b>RESULTS</b>Two of the 12 HTT samples were positive or focally positive for CK19. Four of the 12 samples of HTT presented positive to galectin-3; 3 were stained strongly and the other one was focally positive. None of the 12 samples of HTT was positive for HBME-1. Five in 12 HTT samples were stained in nucleus for MIB-1. Almost all the 20 cases of thyroid papillary carcinoma were intensely stained for CK19, galectin-3 and HBME-1. Fifteen in 20 cases of thyroid papillary carcinoma showed nuclear staining for MIB-1.</p><p><b>CONCLUSIONS</b>HTT is an independent thyroid neoplasm, not a variant of TPC. This study could help in the differential diagnosis of HTT from TPC. CK19, galectin-3 and HBME-1 are adequate to identify HTT and TPC, but MIB-1 does not play an important role in discrimination between HTT and TPC.</p>


Subject(s)
Adolescent , Adult , Aged , Child , Female , Humans , Male , Middle Aged , Biomarkers, Tumor , Carcinoma, Papillary , Chemistry , Diagnosis , Diagnosis, Differential , Galectin 3 , Immunohistochemistry , Keratin-19 , Thyroid Neoplasms , Chemistry , Diagnosis , Ubiquitin-Protein Ligases
3.
Chinese Medical Journal ; (24): 2077-2081, 2010.
Article in English | WPRIM | ID: wpr-352509

ABSTRACT

<p><b>BACKGROUND</b>Intracerebral hemorrhage (ICH) can cause brain damage through a number of pathways. The purpose of the study was to explore the effect of thrombin, protease nexin-1 (PN-1) and protease activated receptor-1 (PAR-1) in rat and human cerebellum after ICH.</p><p><b>METHODS</b>A model of ICH was produced in adult Sprague-Dawley rats by direct injection of autologous blood (50 microl) into caudate nucleus. Patients with injured hemorrhage were also enrolled in this study. Different expressions of thrombin, PAR-1, PN-1 were detected in rat and human cerebellum by immunohistochemistry and in situ hybridization.</p><p><b>RESULTS</b>In rat cerebellum, thrombin protein significantly increased at 6 hours and reached the maximum 2 days after ICH. The expression of PAR-1 protein reached the maximum at 24 - 48 hours, and then began to decrease. The expression of PN-1 protein reached the maximum at 3 hours, decreased somewhat after that and increased a little at 5 days after ICH. While in human cerebellum, the changing tendency of thrombin, PAR-1 and PN-1 was almost conform to the rat.</p><p><b>CONCLUSION</b>In cerebellum, thrombin can activate PAR-1 expression after ICH, and PN-1 appears quickly after ICH in order to control the deleterious effect of thrombin.</p>


Subject(s)
Adult , Aged , Aged, 80 and over , Animals , Female , Humans , Male , Middle Aged , Rats , Cerebellum , Metabolism , Cerebral Hemorrhage , Metabolism , Immunohistochemistry , In Situ Hybridization , Rats, Sprague-Dawley , Receptor, PAR-1 , Genetics , Metabolism , Serpin E2 , Genetics , Metabolism , Thrombin , Genetics , Metabolism
4.
Chinese Journal of Pathology ; (12): 620-622, 2006.
Article in Chinese | WPRIM | ID: wpr-268884

ABSTRACT

<p><b>OBJECTIVE</b>To study the clinical and pathologic features of ischemic intestinal disease due to mesenteric phlebitis.</p><p><b>METHOD</b>The clinical and pathologic features of the mesenteric venous lesions in 3 patients of ischemic intestinal disease admitted during the period from 2003 to 2004 were studied.</p><p><b>RESULTS</b>All 3 patients had a clinical history of acute abdominal pain accompanying with a diffuse peritonitis. During operation, an infarcted intestinal segment was identified and was resected respectively in each patient. Histologic examination showed a lymphocytic infiltration and fibrinoid necrosis of the small to medium-sized veins, associated with mural thrombosis and infarction of the corresponding intestinal wall and mesentery. The mesenteric arteries were spared. Two-year follow up of one case showed no evidence of local recurrence or systemic vasculitis.</p><p><b>CONCLUSIONS</b>Ischemic intestinal disease due to mesenteric phlebitis is a rare entity with a pathological feature of inflammation of venous wall accompanying with the development of mural thrombosis and subsequent haemorrhagic infarction of intestine. The etiology is unknown and surgical resection of the involved intestinal segment is usually recommended.</p>


Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Colitis, Ischemic , Pathology , General Surgery , Follow-Up Studies , Intestinal Diseases , Pathology , General Surgery , Intestine, Small , Pathology , General Surgery , Ischemia , Mesenteric Vascular Occlusion , Mesenteric Veins , Pathology , Phlebitis
5.
Chinese Medical Journal ; (24): 1507-1512, 2004.
Article in English | WPRIM | ID: wpr-291890

ABSTRACT

<p><b>BACKGROUND</b>Cerebral ischemia is a significant clinical problem, and cerebral ischemia usually causes neuron injury such as apoptosis in various brain areas, including hippocampus. Cysteinyl aspartate-specific protease (Caspases) are fundamental factors of apoptotic mechanism. Caspase-3 inhibitors show effect in attenuating brain injury after ischemia. But all the results were from animal models in research laboratories. This study aimed at investigating the correlation between the change of ischemic neuronal injury and Caspase-3 post-ischemia in human hippocampus.</p><p><b>METHODS</b>We selected and systematized 48 post-mortem specimens from 48 patients, who died of cerebral infarction. Morphological change was firstly analyzed by observing hematoxyline/eosin-staining hippocampal sections. The expression of Caspase-3 was investigated using the methods of in situ hybridization and immunohistochemistry. Terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick-end labeling (TUNEL) method was used to clarify the involvement of Caspase-3 in neuron death. The loss of MAP 2 (MAP-2) was applied to judging the damaged area and degree of neuronal injury caused by ischemia.</p><p><b>RESULTS</b>In the CA1 sector of hippocampus, Caspase-3 immunostaining modestly increased at 8 hours [8.05/high-power field (hpf)], dramatically increased at 24 hours (24.85/hpf), decreased somewhat after 72 hours. Caspase-3 mRNA was detectable at 4 hours (6.75/hpf), reached a maximum at 16 hours (17.60/hpf), faded at 72 hours. TUNEL-positive cells were detectable at 24 hours (10.76/hpf), markedly increased at 48 - 72 hours. The loss of MAP-2 was obviously detected at 4 hours, progressed significantly between 24 and 72 hours; MAP-2 immunoreactivity was barely detectable at 72 hours. Before 72 hours, the Caspase-3 evolution was related with the upregulation of TUNEL and the loss of MAP-2. The positive correlation between Caspase-3 mRNA and TUNEL was significant at the 0.05 level (correlation coefficient was 0.721); the negative correlation between Caspase-3 mRNA and MAP-2 was significant at the 0.05 level (correlation coefficient is 0.857). In the early stage (before 72 hours), the staining of Caspase-3 mRNA and immunohistochemistry was predominantly present in cytoplasm; the staining of TUNEL was predominantly localized in nucleus. At 4 - 16 hours, most neurons in hippocampal CA1 areas had relatively normal morphology; at 24 - 48 hours, neurons showed apoptotic morphology; at 72 hours, most cells showed significantly pathological morphology.</p><p><b>CONCLUSIONS</b>There exist a time-dependent evolution of neuronal damage after hippocampal ischemia in human brain, which was characterized by its close correspondence to Caspase-3.</p>


Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Brain Ischemia , Pathology , Caspase 3 , Caspases , Genetics , Physiology , Hippocampus , Pathology , Immunohistochemistry , In Situ Hybridization , In Situ Nick-End Labeling , Microtubule-Associated Proteins
6.
Chinese Journal of Geriatrics ; (12)2001.
Article in Chinese | WPRIM | ID: wpr-675949

ABSTRACT

Objective To observe the time-dependent changes of astrocytes and microvessels in the ischemic core and surrounding areas.Methods Glial fibrillary acidic protein (GFAP)was measured by HE,and CD31 by immunohistochemistry as markers in post-mortem specimens from ten patients,who died of cerebral infarction.Results Each section of the infarcted brains was divided into four areas (the area 0-3).GFAP expressed a little in area 0 and 1,increased in a time-dependent manner in area 2 and 3;CD31 die not expressed in area 0,expressed a little in the area 1,and increased in area 2 and 3 continuously.Conclusions The proliferation of astrocytes and microvessels may play a significant role in the process of restoration after cerebral infarction.

7.
Chinese Journal of Neurology ; (12)1999.
Article in Chinese | WPRIM | ID: wpr-676426

ABSTRACT

Objective To investigate the relationship between the expression of matrix metalloproteinase-9 (MMP-9) and intercellular adhesion molecule-1 (ICAM-1) in the perihematomal tissues in human hypertensive,intracerebral hemorrhage (ICH) and brain edema formation following ICH.Methods Paraffin-embedded brain tissues of 39 human fatal cases of ICH from the perihematomal tissues,1—3 cm away from the margin of the hemorrhagic lesion,as well as tissues from the corresponding area at the opposite side as controls,were stained with HE and immunohistochemistry staining.The expressions of MMP-9 and ICAM-1 in the pefihematomal tissues were analyzed with the SPSS 11.5 system.Results ①With MMP-9 immunohistochemical staining positive capillaries in the perihematomal tissues were identified at 2 h ((1.2? 0.8)/HP).The number of MMP-9 positive capillaries began to rise at 5—10 h ((4.1?0.8)/HP) reaching the peak at 45—48 h ((10.6?1.4)/HP,P

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