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Biomedical subjects

Y Gao

Publications and source records attributed to Y Gao.

At least 91 records · Page 5Linked to original sources

N-terminal carboxyl and tetrazole-containing amides as adjuvants to Grb2 SH2 domain ligand binding.

High affinity binding of peptides to Src homology 2 (SH2) domains, often requires the presence of phosphotyrosyl (pTyr) or pTyr-mimicking moieties in the N-terminal position of the binding ligand. Several reports have shown that N(alpha)-acylation of the critical pTyr residue can result in increased SH2 domain binding potency. For Grb2 SH2 domains which recognize pTyr-Xxx-Asn-NH(2) motifs, significant potency enhancement can be incurred by N(alpha)-(3-amino)Z derivatization of tripeptides such as pTyr-Ile-Asn-NH(2). Using ligands based on the high affinity pY-Ac(6)c-Asn-(naphthylpropylamide) motif, (where Ac(6)c=1-aminocyclohexanecarboxylic acid), additional reports have shown moderate potentiating effects of N(alpha)-oxalyl derivatization. The current study examined variations of the N(alpha)-oxalyl theme in the context of a Xxx-Ac(6)c-Asn-(naphthylpropylamide) platform, where Xxx=the hydrolytically stable pTyr mimetics phosphonomethyl phenylalanine (Pmp) or carboxymethyl phenylalanine (Cmf). The effects of N(alpha)-(3-amino)Z derivatization were also investigated for this platform, to ascertain whether the large binding enhancement reported for tripeptides such as pTyr-Ile-Asn-NH(2) could be observed. In ELISA-based extracellular Grb2 SH2 domain binding assays, it was found for the Pmp-based series, that extending the oxalyl carboxyl out by one methylene unit or replacing carboxyl functionality with a tetrazole isostere, resulted in binding potency greater than the parent N(alpha)-acetyl-containing compound, with enhancement approximating that observed for the N(alpha)-oxalyl derivative. When Cmf was used as the pTyr mimetic, only modest differences in IC(50) values were observed for the series. Examination of the N(alpha)-(3-amino)Z derivatized Pmp-Ac(6)c-Asn-(naphthylpropylamide), showed that binding affinity was reduced relative to the parent N(alpha)-acetyl analogue, in contrast to the reported significant enhancement of affinity observed with other peptide ligands. Treatment of MDA-453 tumor cells, which are mitogenically driven through erbB-2 tyrosine kinase-dependent pathways, with Pmp-containing inhibitors resulted in growth inhibition, with the N(alpha)-oxalyl and N(alpha)-malonyl-containing compounds exhibiting IC(50) values (4.3 and 4.6 microM, respectively) approximately five-fold lower than the parent N(alpha)-acetyl-containing compound. Tetrazole and N(alpha)-(3-amino)Z-containing inhibitors were from two- to four-fold less potent than these latter analogues in the growth inhibition assays.

Adaptor Proteins, Signal Transducing↗

Distinct epitopes on formiminotransferase cyclodeaminase induce autoimmune liver cytosol antibody type 1.

Liver cytosol antibody type 1 (LC1) is regarded as a serologic marker of type 2 autoimmune hepatitis, in addition to liver kidney microsomal antibody type 1. Among 38 patients with type 2 autoimmune hepatitis, 23 were positive for LC1 antibodies. The antigen recognized by LC1 has been identified as a liver-specific 58-kd metabolic enzyme named formiminotransferase cyclodeaminase (FTCD). All 23 LC1-positive sera immunoprecipitated rat FTCD, and 22 gave an identity reaction with rat FTCD by immunodiffusion. No reaction was observed with sera from 10 patients with type 1 autoimmune hepatitis, 10 with primary biliary cirrhosis, 10 with chronic hepatitis C, and 10 healthy controls. By Western immunoblotting all 23 LC1-positive sera and all the controls tested negative, suggesting that all the antigenic epitopes were destroyed by denaturation. FTCD is a bifunctional protein composed of distinct globular FT and CD domains connected by a short linker. To identify epitopes that trigger the LC1 autoimmune response, we tested LC1 antibodies against FTCD constructs encoding the N-terminal FT domain (amino acids 1-339), or the C-terminal CD domain (amino acids 332-541). Of 20 sera positive against full-length FTCD, 8 (40%) recognized the FT domain and the CD domain, 7 (35%) recognized only the FT domain, and 5 (25%) did not recognize either construct. No sera reacted with only the CD domain. These data indicate that multiple regions of FTCD trigger the LC1 autoimmune response, and that LC1 reactivity is mainly directed to conformation-sensitive epitopes located in the FT region of FTCD.

Amino Acid Sequence↗

Primary transanal rectosigmoidectomy for Hirschsprung's disease: Preliminary results in the initial 33 cases.

PURPOSE: The authors describe their newly developed technique-primary transanal rectosigmoidectomy for Hirschsprung's disease (HD) and its preliminary results in neonates and infants. METHODS: Thirty-four consecutive patients (26 boys) with biopsy-proven rectosigmoid HD, aged 18 days to 4 years, underwent this new procedure. Rectal mucosectomy started 1 to 1.5 cm posteriorly and 2 to 3 cm anteriorly proximal to the dentate line. The rectal muscular sleeve below the peritoneal reflection was resected to the level of the striated muscle complex, leaving a shorter muscular cuff, into which a partial internal sphincterotomy was made posteriorly. An oblique anastomosis was constructed between the pull-through ganglionic colon and the anus canal. RESULTS: The mean time for the operation was 160 minutes, and the average length of bowel resected was 29.5 cm (range, 12.5 to 41 cm). Two children (6.06%, 2 of 33) had 2 to 5 episodes of postoperative enterocolitis (EC). One was cured by rectal irrigation and dilation, and the another by Lynn's myectomy. Eighty-four percent of patients had 1 to 6 bowel movements per day during a 6- to 18-month follow-up period. CONCLUSIONS: Primary transanal rectosigmoidectomy for HD is logical and associated with excellent early results. A long-term follow-up is required to determine bowel functions. J Pediatr Surg 36:1816-1819.

Anal Canal↗

AIDS and sex education for young people in China.

Although China has had a rich sexual culture for thousands of years, Chinese people are usually unwilling to openly discuss issues of sex. Some parents are quite ignorant of the change in their children's sexual attitude and behaviour. In China today, adolescents are becoming much more sexually liberated. Premarital sex and unplanned pregnancies among teenagers are increasing. Sexually transmitted diseases (STD) including HIV/AIDS are also spreading rapidly. However, young people lack basic information on AIDS/STD and do not know how to protect themselves from these diseases or how to avoid unintended pregnancies. Several major youth peer education programmes in China are mentioned in this paper. Among them, a four-year programme entitled the Australian-Chinese AIDS/STD/Safer Sex Peer Education Programme for Youth, is discussed in some detail. The programme has so far reached over 40000 university and school students. Evaluation results show that the programme is effective in both significantly increasing students' knowledge about AIDS/STDs and changing their attitude towards AIDS patients. In addition, the programme is highly praised by the students.

Abortion, Induced↗

Myosin light chain kinase as a multifunctional regulatory protein of smooth muscle contraction.

Myosin light chain kinase (MLCK) is a regulatory protein for smooth muscle contraction, which acts by phosphorylating 20-kDa myosin light chain (MLC20) to activate the myosin ATPase activity. Although this mode of action is well-established, there are numerous reports of smooth muscle contraction that is not associated with MLC20 phosphorylation. The kinase activity for the phosphorylation is localized at the central part of MLCK, which is also furnished with actin-binding activity at its N terminal and myosin-binding activity at its C terminal. This article overviews as to how such multifunctional properties of MLCK modify the actin-myosin interaction and presents our observations that the phosphorylation is not obligatory in induction of smooth muscle contraction.

Actins↗

Novel methodology allows simultaneous measurement of true phosphorus digestibility and the gastrointestinal endogenous phosphorus outputs in studies with pigs.

Methodology was developed for measuring the gastrointestinal endogenous phosphorus (P) outputs and true P digestibility values in studies with piglets. Four barrows, average initial body weight 6.8 kg, were fitted with a simple T-cannula at the distal ileum and fed four diets according to a 4 x 4 Latin square design. Four cornstarch-based diets containing four levels of P (1.1, 2.1, 3.2 and 4.3 g/kg diet) on a dry matter (DM) basis were formulated from soybean meal (SBM). Each experimental period comprised 8 d with a 4-d adaptation and 4-d collection of ileal digesta and feces. The apparent ileal and fecal P digestibility values in SBM were affected (P < 0.05) by P levels in the assay diets. The ileal and fecal P digestibility values increased from -24.8 to 37.1% and from 18.8 to 42.5%, respectively, as P contents increased from 1.1 to 4.3 g/kg DM diet. Linear relationships (P < 0.05), expressed as g/kg DM diet intake, between ileal and fecal outputs and dietary inputs of P, suggested that the endogenous P outputs can be determined by linear regression analysis. The endogenous P output was higher (P < 0.05) in ileal digesta than in feces (0.86 +/- 0.09 vs. 0.31 +/- 0.06 g/kg DM diet intake). There was no difference (P > 0.05) between the true ileal (50.7 +/- 7.1%) and fecal (48.5 +/- 5.4%) P digestibility values in SBM. These results suggest that differences in P contents between assay diets are primarily responsible for the large variability in apparent P digestibility values reported within the same ingredient. Apparent digestibility values underestimate the true digestive utilization of P by approximately 25%. True rather than apparent P digestibility values should be determined and used in diet formulation for pigs. In addition, this study shows that the gastrointestinal endogenous P output is important in whole-body P requirement and homeostasis.

Absorption↗

Interchain disulfide bonds promote protein cross-linking during protein folding.

We provide evidence that in vitro protein cross-linking can be accomplished in three concerted steps: (i) a change in protein conformation; (ii) formation of interchain disulfide bonds; and (iii) formation of interchain isopeptide cross-links. Oxidative refolding and thermal unfolding of ribonuclease A, lysozyme, and protein disulfide isomerase led to the formation of cross-linked dimers/oligomers as revealed by SDS-polyacrylamide gel electrophoresis. Chemical modification of free amino groups in these proteins or unfolding at pH < 7.0 resulted in a loss of interchain isopeptide cross-linking without affecting interchain disulfide bond cross-linking. Furthermore, preformed interchain disulfide bonds were pivotal for promoting subsequent interchain isopeptide cross-links; no dimers/oligomers were detected when the refolding and unfolding solution contained the reducing agent dithiothreitol. Similarly, the Cys326Ser point mutation in protein disulfide isomerase abrogated its ability to cross-link into homodimers. Heterogeneous proteins become cross-linked following the formation of heteromolecular interchain disulfide bonds during thermal unfolding of a mixture of of ribonuclease A and lysozyme. The absence of glutathione and glutathione disulfide during the unfolding process attenuated both the interchain disulfide bond cross-links and interchain isopeptide cross-links. No dimers/oligomers were detected when the thermal unfolding temperature was lower than the midpoint of thermal denaturation temperature.

Animals↗

Fast kappa-space sample selection in MRSI with a limited region of support.

One of the primary drawbacks in the application of magnetic resonance spectroscopic imaging is the long acquisition times required to obtained the desired resolution. When region of support information is available, the number of phase-encoding steps and thus time can be reduced without loss of information if the kappa-space locations are chosen well. We propose to select locations using a rectangular sampling array that is shifted to various positions in kappa-space to obtain the necessary sampling density. This method allows multiple samples to be selected simultaneously and reduces the computation required to evaluate the selection criterion. We present an efficient forward selection algorithm for optimizing the shift pattern so that the image can be reconstructed as reliably as possible from a periodic nonuniform set of samples. The proposed algorithm has important practical potential in that it can finish the selection in less than half a minute for typical image sizes and can reconstruct the image with fewer samples than regular sampling. With appropriate imaging hardware, this new algorithm makes selective sampling possible in a real-time image acquisition setting.

Algorithms↗

Fv-4: identification of the defect in Env and the mechanism of resistance to ecotropic murine leukemia virus.

Mice expressing the Fv-4 gene are resistant to infection by ecotropic murine leukemia viruses (MuLVs). The Fv-4 gene encodes an envelope (Env) protein whose putative receptor-binding domain resembles that of ecotropic MuLV Env protein. Resistance to ecotropic MuLVs appears to result from viral interference involving binding of the endogenously expressed Fv-4 env-encoded protein to the ecotropic receptor, although the immune system also plays a role in resistance. The Fv-4 env-encoded protein is processed normally and can be incorporated into virus particles but is unable to promote viral entry. Among the many sequence variations between the transmembrane (TM) subunit of the Fv-4 env-encoded protein and the TM subunits of other MuLV Env proteins, there is a substitution of an arginine residue in the Fv-4 env-encoded protein for a glycine residue (gly-491 in Moloney MuLV Env) that is otherwise conserved in all of the other MuLVs. This residue is present in the MuLV TM fusion peptide sequence. In this study, gly-491 of Moloney MuLV Env has been replaced with other residues and a mutant Env bearing a substitution for gly-487 was also created. G491R recapitulates the Fv-4 Env phenotype in cell culture, indicating that this substitution is sufficient for creation of an Env protein that can establish the interference-mediated resistance to ecotropic viruses produced by the Fv-4 gene. Analysis of the mutant MuLV Env proteins also has implications for an understanding of the role of conserved glycine residues in fusion peptides and for the engineering of organismal resistance to retroviruses.

Amino Acid Sequence↗

PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated I kappa B alpha degradation.

PR-39 inhibits proteasome-mediated I kappa B alpha degradation and might protect against ischemia-reperfusion injury. We studied PR-39, its truncated form PR-11, and a mutant PR-11AAA, which lacks the ability to prevent I kappa B alpha degradation, in a rat heart ischemia-reperfusion model. After 30 min of ischemia and 24 h of reperfusion, cardiac function, infarct size, neutrophil infiltration, and myeloperoxidase activity were measured. Intramyocardial injection of 10 nmol/kg PR-39 or PR-11 at the time of reperfusion reduced infarct size by 65% and 57%, respectively, which improved blood pressure, left ventricular systolic pressure, and relaxation and contractility (+/-dP/dt) compared with vehicle controls 24 h later. Neutrophil infiltration, myeloperoxidase activity, and the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule 1 were reduced. Thus PR-39 and PR-11 effectively inhibit myocardial ischemia-reperfusion injury in the rat in vivo. This effect is mediated by inhibition of I kappa B alpha degradation and subsequent inhibition of nuclear factor-kappa B-dependent adhesion molecules. The active sequence is located in the first 11 amino acids, suggesting a potential for oligopeptide therapy as an adjunct to revascularization.

Animals↗

Morphology and current-voltage characteristics of nanostructured pentacene thin films probed by atomic force microscopy.

Atomic force microscopy was used to study the growth modes (on SiO2, MoS2, and Au substrates) and the current-voltage (I-V) characteristics of organic semiconductor pentacene. Pentacene films grow on SiO2 substrate in a layer-by-layer manner with full coverage at an average thickness of 20 A and have the highest degree of molecular ordering with large dendritic grains among the pentacene films deposited on the three different substrates. Films grown on MoS2 substrate reveal two different growth modes, snowflake-like growth and granular growth, both of which seem to compete with each other. On the other hand, films deposited on Au substrate show granular structure for thinner coverages (no crystal structure) and dendritic growth for higher coverages (crystal structure). I-V measurements were performed with a platinum tip on a pentacene film deposited on a Au substrate. The I-V curves on pentacene film reveal symmetric tunneling type character. The field dependence of the current indicates that the main transport mechanism at high field intensities is hopping (Poole-Frenkel effect). From these measurements, we have estimated a field lowering coefficient of 9.77 x 10(-6) V-1/2 m1/2 and an ideality factor of 18 for pentacene.

Crystallization↗

Association of plasma antibodies against the inducible Hsp70 with hypertension and harsh working conditions.

Autoantibodies against certain stress or heat shock proteins (Hsps) may play a role in the pathogenesis and/ or prognosis of some diseases. Using immunoblotting with human recombinant Hsps and univariate and multivariate logistic regression models, we have investigated the presence of antibodies against Hsp70, the inducible member of the 70-kDa family of heat shock proteins, and analyzed its possible association with hypertension and working conditions. Plasma and serum were collected from 764 steel mill workers from 6 work sites exposed to (1) severe noise; (2) severe noise and dust; (3) noise, dust, and heat; (4) noise and heat; (5) severe noise and heat; and (6) office conditions (control). Workers with prolonged exposure to stresses such as noise, dust, and high temperature and a combination of these in the workplace had a high incidence (26.6% to 40.2%) of antibodies to Hsp70 compared to the lowest incidence (18.6%) of antibodies to Hsp70 in the control group of office workers. Moreover, there was a statistical association of antibodies against Hsp70 with hypertension. The statistical correlation between the presence of antibodies to Hsp70 and hypertension is higher in the group of workers with blood pressure of 160/95 mmHg than in the 140/90-mmHg group after excluding possible effects of the workplace stresses. These results suggest that harsh workplace conditions can increase the production of antibodies against Hsp70 and that the presence of antibodies to this stress protein may be associated with hypertension. The precise mechanism for the elevation of antibodies against Hsps by environmental and workplace stresses and their relation to hypertension remains to be established.

Autoantibodies↗

Polymorphonuclear neutrophils and their mediators in gingival tissues from generalized aggressive periodontitis.

BACKGROUND: Impaired polymorphonuclear neutrophil (PMN) functions were generally considered to be related to the onset of generalized aggressive periodontitis (GAgP). However, some research has indicated that the hyperreactivity of PMN seems to be involved in the inflammatory response of GAgP. The present study's main purpose was to provide more evidence about the role of PMN in the pathogenesis of GAgP by surveying PMN infiltration in gingiva and its relationship with the expression of their mediators including intercellular adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8), interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha). The inflammatory response in GAgP was also compared with that in adult periodontitis (AP) and periodontally healthy subjects. Since these PMN mediators were reported to be produced mainly by macrophages, the association between the expression of these PMN mediators and the distribution of macrophages was also investigated. METHODS: A total of 25 gingival specimens were obtained from 10 GAgP patients, 10 AP patients, and 5 periodontally healthy subjects. Serial sections were obtained from each specimen, and the following techniques were adopted to investigate the distribution and interrelation of different cells and cytokines. Infiltration of PMN was observed by using hematoxylin and eosin staining. Distribution of the macrophages, identified as CD68+, was shown by using immunohistochemistry. Immunohistochemistry and in situ hybridization were used to detect the expression of ICAM-1, IL-8, IL-1beta, and TNF-alpha in gingival tissues. These techniques were performed in serial sections from each individual specimen. RESULTS: Large numbers of infiltrating PMNs were observed in gingiva from GAgP. In gingiva from both GAgP and AP, the strongest protein and mRNA expression of IL-8, ICAM-1, IL-1beta, and TNF-alpha were located in pocket epithelium and adjacent connective tissue with large numbers of infiltrating PMNs. In tissues without abundant PMN infiltration, the appearance of positive cells expressing IL-8, ICAM-1, IL-1beta, and TNF-alpha was scattered. CD68+ was distributed sparsely in connective tissue and was hardly seen in pocket epithelium with large numbers of PMN infiltration. The degree of leukocyte infiltration and connective tissue destruction in gingiva from GAgP patients was not distinctly different from that in gingiva from AP. The gingival specimens with heavy PMN infiltration from both GAgP and AP patients presented strong expressions of IL-1beta and TNF-alpha; showed more extensive inflammatory cell infiltration; had severe connective tissue destruction; and presented severe elongation and ulceration of pocket epithelium. In gingiva from healthy subjects, inflammation was minor with visually no PMN, CD68+, or the positive cells of IL-8, ICAM-1, IL-1beta and TNF-alpha expression. CONCLUSIONS: Enhanced accumulation of PMN, which is associated with the upregulation of IL-8, ICAM-1, IL-1beta, and TNF-alpha expression, relates to the severity and activity of GAgP. In addition to macrophages, PMN and/or epithelial cells might also be important sources of IL-8, IL-1beta, and TNF-alpha production in gingiva.

Adult↗

Clear cell odontogenic carcinoma: a clinicopathologic and immunocytochemical study of 5 cases.

CONTEXT: Odontogenic tumor composed predominantly of clear cells is a rare neoplasm of the jaws that was initially designated as clear cell odontogenic tumor. Subsequent reports in the literature, however, all have indicated that this tumor exhibits an aggressive behavior characterized by infiltrative local growth, recurrence, or metastases. OBJECTIVE: To ascertain the clinicomorphologic features and biologic behavior of this tumor group, we present 5 additional cases using the term clear cell odontogenic carcinoma. DESIGN: Histologic and immunohistochemical examinations were performed on clear cell odontogenic carcinomas from 5 patients. Clinical and follow-up data were recorded, and the literature was reviewed. RESULTS: The patients were 1 man and 4 women with an average age of 42.4 years at diagnosis. Three tumors occurred in the mandible and the other 2 in the maxilla. Four of the 5 cases occurred in the anterior or premolar areas of the jaws, appearing as poorly marginated radiolucencies. All cases consisted of islands and sheets of large clear cells and small basaloid cells with scanty eosinophilic cytoplasm, which were separated by thin, mature, fibrous septae. The tumors were unencapsulated and showed aggressive infiltration of the surrounding muscle and perineural tissues. Most of the clear cells contained cytoplasmic glycogen. Immunocytochemically, the tumor cells were positive for pan-keratin, cytokeratin 19, and epithelial membrane antigen, but were negative for vimentin, S100 protein, desmin, smooth muscle actin, human melanoma antigen (HMB-45), and alpha(1)-antichymotrypsin. Follow-up data showed 4 of 5 patients to have multiple local recurrences, and 1 of these 4 had submandibular lymph node metastasis and a fatal outcome due to uncontrollable tumor growth. CONCLUSION: These results suggest that odontogenic clear cell neoplasms are at least low-grade malignancies and should be classified as carcinomas.

Adenocarcinoma, Clear Cell↗

The thromboxane A2 receptor activates mitogen-activated protein kinase via protein kinase C-dependent Gi coupling and Src-dependent phosphorylation of the epidermal growth factor receptor.

The mitogen-activated protein kinase signaling cascade is used by many G protein-coupled receptors to initiate functional events. In this study, activation of the Gq/G11-coupled thromboxane A2 (TxA2) receptor (TP) by the TxA2 mimetic IBOP in ECV304 cells was found to induce extracellular regulated kinase (ERK) phosphorylation and tyrosine phosphorylation of the epidermal growth factor receptor (EGFR), which were inhibited by the TP antagonist SQ29548, the EGFR kinase inhibitor AG1478, the Src family kinase inhibitor PP1, the Gi/o protein inhibitor pertussis toxin (PTX), or the protein kinase C (PKC) inhibitor calphostin C. TP activation also increased Src kinase activity, which was blocked by PTX, PP1, and calphostin C, but not by AG1478, indicating that Src activation occurs before phosphorylation of EGFR. Blockade of Src activity by expression of dominant negative mutant of Src inhibits mitogen-activated protein kinase (MAPK) activation induced by TxA2. ERK activation induced by the PKC activator phorbol myristate acetate was inhibited by PTX, PP1, AG1478, and calphostin C. In contrast, activation of ERK by lysophosphatidic acid, a Gi-coupled receptor activator, was inhibited by PTX, PP1, and AG1478, but not by calphostin C. Thus, TP-stimulated ERK activation requires Gi, which in turn requires PKC activation. Immunoprecipitation of Galphai showed increased association of Galphai with TPalpha following PKC activation. In conclusion, TPalpha is directly coupled to the Gi protein by a PKC-regulated mechanism; Gi coupling causes Src-dependent transactivation of the EGFR, which is the dominant pathway in TP-mediated ERK activation.

Cell Line↗

[An ECG waves separation technique based on mathematical morphology].

An ECG waves separation technique based on mathematical morphology is suggested and discussed in this paper. Without detection of QRS complexes, the QRS complexes can be eliminated by series morphological operations. Then the start points and end points of P-wave and T-wave can be decided and the waves of ECG are separated qualitatively and quantitatively. The results of qualitative separations are rather satisfied and the SDs of quantitative separation results are not very large. Also, ECG signals are filtered and baseline is normalized by morphological method.

Algorithms↗

Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin: a study by magnetic resonance imaging, 1H- and 31P-magnetic resonance spectroscopy.

Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin were investigated 1, 3, 5 and 7 days after infarction by means of magnetic resonance imaging (MRI), 1H- and 31P-magnetic resonance spectroscopy (MRS). A region of T2 hyperintensity was observed in left temporal neocortex in infarction group and batroxobin group 1, 3, 5 and 7 days after infarction. The volume of the region gradually decreased from 1 day to 7 days after infarction. The ratio of NAA/Cho + Cr in the region of T2 hyperintensity in the infarction group was significantly lower than that in the corresponding region in the sham-operated group 3, 5 and 7 days after infarction respectively (P < 0.05). Lac appeared in the region of T2 hyperintensity in the infarction group 1, 3, 5 and 7 days after infarction, but it was not observed in the corresponding region in sham-operated group at all time points. Compared with the sham-operated group, the ratios of beta ATP/PME + PDE and PCr/PME + PDE of the whole brain in the infarction group were significantly lower 1, 3 and 5 days after infarction respectively (P < 0.05), and the ratio of beta ATP/PCr also was significantly lower 1 day after infarction (P < 0.05). Batroxobin significantly decreased the volume of the region of T2 hyperintensity 1 and 3 days after infarction (P < 0.05), significantly increased the ratio of NAA/Cho + Cr in the region 5 and 7 days after infarction (P < 0.05), significantly decreased the ratios of Lac/Cho + Cr and Lac/NAA in the region 5 and 7 days after infarction (P < 0.05), and significantly increased the ratios of beta ATP/PME + PDE and beta ATP/PCr in the whole brain 1 day after infarction (P < 0.05). The results indicated that the infracted region had severe edema, increased Lac and apparent neuronal dysfunction and death, and energy metabolism of the whole brain decreased after focal infarction, and that batroxobin effectively ameliorated the above-mentioned abnormal changes.

Animals↗