Biomedical subjects

Ying Zhang

Publications and source records attributed to Ying Zhang.

At least 145 records · Page 8Linked to original sources

PubMed2006

Mutational analysis of the Bacillus subtilis RNA polymerase alpha C-terminal domain supports the interference model of Spx-dependent repression.

The Spx protein of Bacillus subtilis exerts both positive and negative transcriptional control in response to oxidative stress by interacting with the C-terminal domain of the RNA polymerase (RNAP) alpha subunit (alphaCTD). Thus, transcription of the srf operon at the onset of competence development, which requires the ComA response regulator of the ComPA signal transduction system, is repressed by Spx-alphaCTD interaction. Previous genetic and structural analyses have determined that an Spx-binding surface resides in and around the alpha1 region of alphaCTD. Alanine-scanning mutagenesis of B. subtilis alphaCTD uncovered residue positions required for Spx function and ComA-dependent srf transcriptional activation. Analysis of srf-lacZ fusion expression, DNase I footprinting, and solid-phase promoter retention experiments indicate that Spx interferes with ComA-alphaCTD interaction and that residues Y263, C265, and K267 of the alpha1 region lie within overlapping ComA- and Spx-binding sites for alphaCTD interaction. Evidence is also presented that oxidized Spx, while enhancing interference of activator-RNAP interaction, is not essential for negative control.

Alleles↗

PubMed2006

Phosphatidylinositol 3-kinase/protein kinase Czeta-induced phosphorylation of Sp1 and p107 repressor release have a critical role in histone deacetylase inhibitor-mediated derepression [corrected] of transcription of the luteinizing hormone receptor gene.

We have demonstrated that silencing of luteinizing hormone receptor (LHR) gene transcription is mediated via a proximal Sp1 site at its promoter. Trichostatin A (TSA) induced histone acetylation and gene activation in JAR cells that prevailed in the absence of changes in Sp1/Sp3 expression, their binding activity, disassociation of the histone deacetylase/mSin3A complex from the Sp1 site, or demethylation of the promoter. This indicated a different mechanism involved in TSA-induced derepression. The present studies have revealed that phosphatidylinositol 3-kinase/protein kinase Czeta (PI3K/PKCzeta)-mediated Sp1 phosphorylation accounts for Sp1 site-dependent LHR gene activation. TSA caused marked phosphorylation of Sp1 at serine 641 in JAR and MCF-7 cells. Blockade of PI3K or PKCzeta activity by specific inhibitors, kinase-deficient mutants, or small interfering RNA abolished the effect of TSA on the LHR gene and Sp1 phosphorylation. PKCzeta was shown to associate with Sp1, and this association was enhanced by TSA. Sp1 phosphorylation at serine 641 was required for the release of the pRb homologue p107 from the LHR gene promoter, while p107 acted as a repressor of the LHR gene. Inhibition of PKCzeta activity blocked the dissociation of p107 from the LHR gene promoter and markedly reduced Sp1 phosphorylation and transcription. These results have demonstrated that phosphorylation of Sp1 by PI3K/PKCzeta is critical for TSA-activated LHR gene expression. These studies have revealed a novel mechanism of TSA action through derecruitment of a repressor from the LHR gene promoter in a PI3K/PKCzeta-induced Sp1 phosphorylation-dependent manner.

Acetylation↗

PubMed2006

Toxicant exposure in cigarette reducers versus light smokers.

BACKGROUND: The extent of exposure to tobacco toxicants in smokers who have reduced their cigarette intake compared with smokers who are light smokers is relatively unknown. The goal of this study is to investigate the occurrence of compensatory smoking in reducers compared with light smokers by measuring toxicant exposure. METHODS: Participants in two smoking reduction intervention studies (N = 64) were selected for comparison with a group of light smokers (N = 62) who smoked the same number of cigarettes as the reducers. A compensatory smoking score was defined (biomarker level for reducer/biomarker level for light smoker) and calculated for urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronides (total NNAL), metabolites of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-I-(3-pyridyl)-1-butanone, to measure the degree of smoking compensation in reducers when compared with the light smokers. RESULTS: The mean level of creatinine-adjusted total NNAL for reducers was over twice that of light smokers even when they smoked about the same number of cigarettes per day. The difference of the mean total NNAL concentrations between light smokers and reducers was highly significant (P < 0.0001). Wide variability in total NNAL concentrations was also observed in reducers, with the extent of this variability between light smokers and reducers being significantly different (P = 0.0005). The level of individual reduction was shown to be a consistent predictor of compensatory smoking (r = 0.50; adjusted Ps = 0.002), with greater cigarette reduction associated with more compensation. CONCLUSIONS: Compensatory smoking limits the harm reduction value of decreased smoking of cigarettes.

Administration, Cutaneous↗

PubMed2006

The A2B adenosine receptor protects against inflammation and excessive vascular adhesion.

Adenosine has been described as playing a role in the control of inflammation, but it has not been certain which of its receptors mediate this effect. Here, we generated an A2B adenosine receptor-knockout/reporter gene-knock-in (A2BAR-knockout/reporter gene-knock-in) mouse model and showed receptor gene expression in the vasculature and macrophages, the ablation of which causes low-grade inflammation compared with age-, sex-, and strain-matched control mice. Augmentation of proinflammatory cytokines, such as TNF-alpha, and a consequent downregulation of IkappaB-alpha are the underlying mechanisms for an observed upregulation of adhesion molecules in the vasculature of these A2BAR-null mice. Intriguingly, leukocyte adhesion to the vasculature is significantly increased in the A2BAR-knockout mice. Exposure to an endotoxin results in augmented proinflammatory cytokine levels in A2BAR-null mice compared with control mice. Bone marrow transplantations indicated that bone marrow (and to a lesser extent vascular) A2BARs regulate these processes. Hence, we identify the A2BAR as a new critical regulator of inflammation and vascular adhesion primarily via signals from hematopoietic cells to the vasculature, focusing attention on the receptor as a therapeutic target.

Animals↗

PubMed2006

The role of men in chronic supervisory neglect.

This study investigates whether parents' child care demand and resources, their capacity to provide adequate supervision, and their understanding of the supervision problem predict chronic supervisory neglect. A case-comparison design was used to compare families who had one isolated incident of supervisory neglect, who were involved with child protective services (CPS) because of a persistent supervision problem (2 years or less), and who were involved with CPS because of a chronic supervision problem (more than 2 years). When the mother's partner was not the father of her children or had a drug, alcohol, or mental health challenge, and when no one understood that there was a supervision problem or took responsibility for it, the problem was more likely to persist or become chronic. Therefore, when predicting whether a family will continue to provide inadequate supervision, it is important to also assess the mother's partner.

Adolescent↗

PubMed2006

A research algorithm to improve detection of delirium in the intensive care unit.

INTRODUCTION: Delirium is a serious and prevalent problem in intensive care units (ICU). The purpose of this study was to develop a research algorithm to enhance detection of delirium in critically ill ICU patients using chart review to complement a validated clinical delirium instrument. METHODS: Prospective cohort study of 178 patients 60 years and older admitted to the Medical ICU. The Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) and a validated chart review method for delirium were performed daily. We assessed the diagnostic accuracy of the chart-based delirium method using the CAM-ICU as the gold standard. We then used an algorithm to detect delirium first using the CAM-ICU ratings, then chart review when the CAM-ICU was unavailable. RESULTS: When using both the CAM-ICU and the chart-based review the prevalence of delirium was 143/178 (80%) patients or 929/1457 (64%) of patient-days. Of these, 292 patient-days were classified as delirium by the CAM-ICU, and the remainder (n=637 patient-days) were classified as delirium by the validated chart review method when the CAM-ICU was missing due to weekends or holidays (404 patient-days), when CAM-ICU was not performed due to stupor or coma (205 patient-days), and when the CAM-ICU was negative (28 patient-days). Sensitivity of the chart-based method was 64% and specificity was 85%. Overall agreement between chart and the CAM-ICU was 72%. CONCLUSIONS: Eight of 10 patients in this cohort study developed delirium in the ICU. Although use of a validated delirium instrument with frequent direct observations is recommended for clinical care, this approach may not always be feasible, especially in a research setting. The algorithm proposed here comprises a more comprehensive method for delirium detection in a research setting taking into account the fluctuation that occurs with delirium, a key component to accurately determining delirium status. Improving delirium detection is of paramount importance first to advance delirium research and, subsequently to enhance clinical care and patient safety.

Aged↗

PubMed2006

Proliferation, viability, and metabolism of human tumor and normal cells cultured in microcapsule.

In this study, we investigated the effect of the microenvironment provided by alginate-poly-L-lysine-alginate (APA) microcapsule with liquefied or gelled core on the proliferation, viability, and metabolism of human cells, including anchorage-dependent MCF-7 breast cancer cells and primary fibroblasts, and anchorage-independent K-562 leukemia cells; cells in conventional culture were used as control. The growth pattern of cells in microcapsule was examined by phase-contrast micrography. The cell viability, proliferation, organization, and gene expression were evaluated by 3-(4,5- dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, hematoxylin and eosin staining, live/dead staining, 5-bromo-20-deoxyuridine labeling, and immunohistochemistry, respectively. Cell metabolism was determined by measuring glucose and lactate concentrations in medium. The results demonstrate that APA microcapsule with liquefied core provides a microenvironment for both anchorage-dependent and anchorage-independent cells to grow into a large cell aggregate and maintain cell viability at a constant level for a period of time. In conclusion, cells in APA microcapsule are alive and have proliferation potential with lower metabolism rate. APA microcapsule may be a useful tool for in vitro tumor cell modeling and anticancer drug screening as well as for cancer gene therapy. In addition, it lays a solid foundation for the use of microencapsulation in cell culture in vitro and cell implantation in vivo.

Alginates↗

PubMed2006

Tritiated taurine handling by isolated rat pancreatic islets.

A gating of volume-sensitive anion channels may participate in the depolarization of the plasma membrane caused by high concentrations of D-glucose in insulin-producing B-cells of the endocrine pancreas. The efflux of tritiated taurine from prelabeled cells is currently used to assess changes in the activity of such channels. The handling of [1,2-3H]taurine by isolated rat pancreatic islets was therefore investigated. The net uptake of [1,2-3H]taurine was found to represent a concentration-, time-, and temperature-dependent process. It was progressively increased in the range of D-glucose concentrations between 2.8 and 8.3 mM, but no further increase was observed at 16.7 mM D-glucose. Over 15 min incubation, the efflux of radioactivity from prelabeled islets was inhibited by MK571 (1.0 mM). It was increased in response to hypoosmolarity both in the presence and absence of extracellular Na+. Whether in salt-balanced or Na+-deprived media, the efflux of radioactivity from prelabeled islets increased in response to a rise in D-glucose concentration from 2.8 to 5.6 or 8.3 mM, but decreased when the concentration of the hexose was further increased from 8.3 to 16.7 mM. In perifused islets, however, the radioactive efflux from prelabeled islets was inhibited, in a concentration- related manner, when islets first deprived of D-glucose for 45 min were then exposed to 2.8, 5.6, or 16.7 mM D-glucose. Likewise, in prelabeled and perifused islets first exposed for 45 min to 4.0 mM D-glucose, a later rise in hexose concentration to 8.3 mM failed to affect significantly effluent radioactivity, while an increase in hexose concentration from 4.0 to 16.7 mM inhibited the radioactive outflow. In these perifusion experiments, the rise in D-glucose concentration provoked the expected changes in insulin output. The findings obtained in islets examined immediately after preincubation in the presence of [1,2-3H]taurine are consistent with the presence of volume-sensitive anion channels in islet cells and with a gating of such channels in response to a rise in D-glucose concentration from 2.8 to 5.6-8.3 mM. However, the radioactive fractional outflow rate from prelabeled islets seems to reach its highest value at about 8.3 mM D-glucose, being unexpectedly decreased at a higher concentration (16.7 mM) of the hexose. In conclusion, the pleiotropic effects of D-glucose upon tritiated taurine outflow from prelabeled rat islets, which could conceivably be ascribed to differences in the handling of this amino sulfonic acid by distinct islet cell types, indicates that the present approach is far from optimal to characterize unambiguously the regulation by the hexose of volume-sensitive anion channel activity in insulin-producing islet cells.

Animals↗

PubMed2006

Pancreatic islet function in omega3 fatty acid-depleted rats: Glucose metabolism and nutrient-stimulated insulin release.

In order to gain information on the determinism of the perturbation of fuel homeostasis in situations characterized by a depletion in long-chain polyunsaturated omega3 fatty acids (omega3), the metabolic and hormonal status of omega3-depleted rats (second generation) was examined. When required, these rats were injected intravenously 120 min before sacrifice with a novel medium-chain triglyceride-fish oil emulsion able to provoke a rapid and sustained increase of the omega3 content in cell phospholipids. The measurement of plasma glucose, insulin, phospholipid, triglyceride, and unesterified fatty acid concentration indicated modest insulin resistance in the omega3-depleted rats. The plasma triglyceride and phospholipid concentrations were decreased in the omega3-depleted rats with abnormally low contribution of omega3 in both circulating and pancreatic islet lipids. The protein, insulin, and lipid content of the islets, as well as their intracellular and extracellular spaces, were little affected in the omega3-depleted rats. The metabolism of D-glucose in the islets of omega3-depleted rats was characterized by a lesser increase in D-[5-3H]glucose utilization and D-[U-14C]glucose oxidation in response to a given rise in hexose concentration and an abnormally low ratio between D-glucose oxidation and utilization. These abnormalities could be linked to an increased metabolism of endogenous fatty acids with resulting alteration of glucokinase kinetics. The release of insulin evoked by D-glucose, at a close-to-physiological concentration (8.3 mM), was increased in the omega3-depleted rats, this being considered as consistent with their insulin resistance. Relative to such a release, that evoked by a further rise in D-glucose concentration or by non-glucidic nutrients was abnormally high in omega3-depleted rats, and restored to a normal level after of the intravenous injection of the omega3-rich medium-chain triglyceride-fish oil emulsion. Because the latter procedure failed to correct the perturbation of D-glucose metabolism in the islets of omega3-depleted rats, it is proposed that the anomalies in the secretory behaviour of islets in terms of their response to an increase in hexose concentration or non-nutrient secretagogues is mainly attributable to alteration in K+ and Ca2+ handling, as indeed recently documented in separate experiments.

Animals↗

PubMed2006

Human kallikrein 10, a predictive marker for breast cancer.

Our laboratory is involved in identifying genes that can be used as early diagnostic or prognostic markers in breast cancer. We previously identified a gene (NES1) that is expressed in normal but not in transformed mammary epithelial cells (MECs). NES1 is located on chromosome 19q13.4 within the kallikrein locus and thus was designated as human kallikrein 10 (hK10), although we have been unable to detect any protease activity. Importantly, hK10 expression is decreased in a majority of breast cancer cell lines. Transfection of hK10 into hK10-negative breast cancer cells reduces the tumorigenicity. Using methylation-specific PCR and subsequent sequencing, we demonstrate a strong correlation between hypermethylation of hK10 and loss of mRNA expression. Further analysis showed that essentially 100% of normal breast specimens had hK10 expression, whereas 46% of ductal carcinoma in situ (DCIS) and the majority of infiltrating ductal carcinoma (IDC) samples lacked the hK10 mRNA. Importantly, hK10-negative DCIS diagnosed at the time of biopsy were subsequently diagnosed as IDC at the time of definitive surgery. It has been shown that hK10 protein expression is regulated by steroids. In addition to breast cancers, hK10 is downregulated in cervical cancer, prostate cancer and acute lymphocytic leukemia, whereas it is upregulated in ovarian cancers. These results point to the paradoxical role of hK10 in human cancers and underscore the importance of further studies of this kallikrein.

Biomarkers, Tumor↗

PubMed2006

The human kallikrein 10 promoter contains a functional retinoid response element.

Human kallikrein 10 (hK10) protein is expressed in normal breast but is significantly downregulated in a majority of invasive breast cancers. Thus, understanding how hK10 expression is regulated is of substantial significance. In this study, we analyzed the promoter region of hK10 using a website software (TRANSFAC 3.0), which predicted three possible retinoic acid response elements (RAREs), RARE1 at -1041 (TGACCTCGTGATCC), RARE2 at -859 (TGACCTCCTATGA) and RARE3 at -765 (TGACCTCCTGTGA), each with a half-site of a canonical sequence (TGACCT; reverse complement AGGTCA). Using electrophoretic mobility shift assays and nucleotide competition analysis, as well as chromatin immunoprecipitation of the native hK10 promoter, we demonstrated specific binding of RXR only to RARE1. The functional importance of RARE in the hK10 promoter was demonstrated by retinoid induction of hk10 promoter-reporters; furthermore, mutation of RARE1 but not of RARE2 or RARE3 abolished the induction of the reporter. Finally, we demonstrated the induction of hK10 mRNA and protein expression upon retinoid treatment of cells. In view of the correlation of the downregulation of hK10 mRNA and protein with breast cancer progression, these findings suggest a potential approach to restore hK10 expression in cancer patients.

Gene Expression Regulation, Neoplastic↗

PubMed2006

Association study between fibronectin and coronary heart disease.

Fibronectin is a known chemoattractant for several cell types that play a role in the wound healing process, including fibroblasts, endothelial cells and macrophages. It also generates a scaffold that allows attachment of other extracellular matrix components. Large amounts of fibronectin have been detected in atherosclerotic plaques, suggesting that it may play a role in the pathogenesis of atherosclerosis. To examine the possible involvement of fibronectin in the etiology of atherosclerotic coronary heart disease, we analyzed four polymorphisms in the human fibronectin gene and determined the plasma fibronectin levels in patients with coronary heart disease (n = 109) and age- and gender-matched controls (n = 123) in Chinese Han people. No significant positive association was observed between these polymorphisms and coronary heart disease. The levels of circulating plasma fibronectin, however, were significantly lower in patients with coronary heart disease (mean +/- SD 245 +/- 87 mg/L) compared with controls (354 +/- 88 mg/L) (p < 0.001). The odds ratio (OR) for plasma fibronectin was 0.94 in a multivariate unconditional logistic regression model (OR = 0.94, 95% CI 0.91-0.96, p < 0.001). We conclude that, in our population, the four fibronectin gene polymorphisms detected are not associated with clinical coronary heart disease. Our data suggest that low circulating fibronectin levels might be a new marker of coronary heart disease.

Alleles↗

PubMed2006

Characteristics of transgenic tomatoes antisensed for the ethylene receptor genes LeETR1 [corrected] and LeETR2 [corrected].

Two stable transformed lines containing antisense LeETR1 [corrected] or LeETR2 [corrected] sequences and their hybridized line were investigated to determine the effect of LeETR1 [corrected] and LeETR2 [corrected] specificity in the ethylene receptor family in tomato (Lycopersicon esculentum Mill.) on ethylene signaling. The transgenic line ale1 containing antisense LeETR1 [corrected] displayed shorter length of seedling grown in the dark and adult plant in the light, severe epinastic petiole, and accelerated abscission of petiole explant and senescence of flower explant, compared with its wild type B1. The transgenic line ale2 containing antisense LeETR2 [corrected] also exhibited shorter hypocotyls and slightly accelerated abscission. The phenotypes of cross line dale of LeETR1 [corrected] and LeETR2 [corrected] were close to ale1 in many aspects. These results suggested that LeETR1 [corrected] probably plays a relatively important role in ethylene signaling of tomato growth and development.

Ethylenes↗

PubMed2006

Expression, purification, crystallization and preliminary crystallographic analysis of the human intracellular chloride channel protein CLIC4.

The human chloride intracellular channel protein CLIC4 has been crystallized by the hanging-drop vapour-diffusion technique using trisodium citrate as the precipitant. The best crystals were obtained by the microseeding method. The crystals diffracted to 2.2 A resolution and were found to belong to space group P121, with unit-cell parameters a = 73.19, b =86.05, c = 73.38 A, beta = 112.99 degrees and three molecule per asymmetric unit.

Chloride Channels↗

PubMed2006

[Genotypes of aminoglycoside-modifying enzyme and clinical study of high-level gentamycin resistant enterococcus].

OBJECTIVE: To determine the antibiotics resistance, aminoglycoside-modifying enzymes and homology of high-level gentamycin resistant enterococcus in clinical specimens. METHODS: The high-level gentamicin resistant (HLGR) isolates were screened by the agar method and the resistance of 14 antimicrobial agents was determined by K-B method. The aminoglycoside-modifying enzyme genes were detected by polymerase chain reaction (PCR). Pulsed-field gel electrophoresis (PFGE) was used to analyze the homology of HLGR isolates. RESULTS: The ratio of HLGR was 64.2% (68/106). Among the HLGR,there were no isolates resistant to linezolid, vancomycin and tecoplanin, and Enterococcus faecium was more resistant to beta-lactam antibiotics and quinolone than Enterococcus faecalis. The positive rate of aac(6')-Ie-aph(2')-Ia was 92.6% and 3 isolates had the resistance gene mostly similar to aph(2')-Id. And among 51 HLGR isolates from the hospitalized patients, PFGE grouped 17 E. faecalis isolates into 4 clusters (A-D), and 33 E. faecium isolates into 8 clusters (A-H) with A cluster as predominant. CONCLUSION: HLGR has become the important antibiotic resistance bacteria which results in nosocomial infection; and aac(6')-Ie-aph(2')-Ia is the main aminoglycoside-modifying enzyme gene which causes HLGR.

Drug Resistance, Bacterial↗

PubMed2006

Fructokinase activity in rat liver, ileum, parotid gland, pancreas, pancreatic islet, B and non-B islet cell homogenates.

The presence of fructokinase (ketohexokinase) in rat pancreatic islet homogenates was previously documented. However, no information was so far available on the activity of this enzyme in islets relative to that in other tissues and on the respective contribution of insulin-producing B cells and non-B islet cells. The present study provides such an information. The activity of fructokinase, as assessed by the phosphorylation of 1.0 mM D-fructose, was compared to that of hexokinase isoenzyme(s), as measured in the presence of 1.0 mM D-glucose, and further characterized by its heat-resistance, K+ dependency and resistance to the inhibitory action of D-mannoheptulose. As judged from the results obtained in heated homogenates, the activity of fructokinase, expressed relative to protein content (nmol/min per mg protein) was highest in liver (21.5 +/- 2.5; n = 11) and lowest in parotid gland (0.16 +/- 0.09; n = 3), with in-between values in ileum (2.45 +/- 0.53; n = 3), pancreas (0.82 +/- 0.11; n = 11) and pancreatic islets (0.46 +/- 0.07; n = 6). The paired ratio between fructokinase and hexokinase isoenzyme activity was also highest in liver (548 +/- 45%; n = 8) and lowest in parotid gland (0.93 +/- 0.52%; n = 3). Such a ratio was not significantly different in pancreas, islets and purified B or non-B islet cells, with an overall mean value of 2.57 +/- 0.46% (n = 12). The present findings thus unambiguously document the presence of fructokinase activity in all cell types under consideration, except possibly parotid cells, with the following hierarchy: liver > ileum > pancreas. Relative to paired hexokinase activity, no obvious difference was found for fructokinase activity in B versus non-B islet cells.

Animals↗

PubMed2006

[The application of the magnetic resonance hydrography of inner ear in diagnosing large vestibular aqueduct syndrome].

OBJECTIVE: To study the effect of the magnetic resonance hydrography of inner ear technique in diagnosing large vestibular aqueduct syndrome. METHOD: 3D-Fast Advanced Spin Echo MR imaging was performed on the petrosal bone of the patient who suffered from large vestibular aqueduct syndrome(LVAS). Then all the original images were transferred to an online workstation and underwent image postprocessing. The 3D images of the inner ears were obtained after 3D reconstruction. RESULT: The MR hydrography of inner ear of the patient displayed that there was an extradural high-signal intumescence which was like silver shape and the edge of it was smooth and neat between the sigmoid sinus of the posterior cranial fossa and the inner acoustic meatus. The maximum width of the mid position of endolymphatic sac in the temporal bone of the patient was 2.470 mm. This was much bigger than the diagnosis standard of the large vestibular aqueduct syndrome with ordinary MR imaging. CONCLUSION: The MR hydrography technique is an effective method to diagnose large vestibular aqueduct syndrome. The final diagnosis in clinic could be made with the assistance of this technique.

Adult↗

PubMed2006

[Protective effects of hirudin on acute experimental intracerebral hemorrhage].

OBJECTIVE: To explore the protective effects of hirudin on acute experimental intracerebral hemorrhage (ICH) by observing the changes of histologic pathology and brain water content as well as GFAP-positive cells in the perihematomal brain regions. METHOD: The models of rat ICH were made with infusion of autologous blood into the right neucleus caudatus. The rats were divided randomly into control group, intracerebral hemorrhage group and treating group with hirudin. Brain water content was measured, and pathological and GFAP changes were observed. RESULT: The pathological impairation after ICH were gradually deteriorated and peaked at the third day. Brain water content after ICH was gradually increased and obviously after one day(P < 0.05) and peaked at the third day. GFAP-positive cells were gradually increased and peaked at the seventh day after ICH. In the treating groups, the pathological impairation and brain water content as well as the GFAP-positive cells were decreased as compared to those in the intracerebral hemorrhage group and the control group. And the positive correlation between GFAP-positive cell numbers and brain water content were shown by linear regression. CONCLUSION: The local administration of hirudin, a special inhibitor of thrombin, has protective effects within the first week after ICH.

Acute Disease↗