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Biomedical subjects

C Y Lin

Publications and source records attributed to C Y Lin.

At least 127 records · Page 7Linked to original sources
PubMed1999

Alpha-1-antichymotrypsin polymorphism in schizophrenia: frequency, age at onset and cognitive function.

A common polymorphism in the alpha1-antichymotrypsin (ACT) gene is associated with Alzheimer's disease. ACT is also a trophic factor in the hippocampal neurons. In order to examine if the ACT gene plays a role in the pathogenesis of schizophrenic disorders, patients (n = 175) and control subjects (n = 114) were genotyped for ACT. We also investigated the relationship between genotypes and patients' cognitive function as evaluated by the Clinical Dementia Rating Scale and the Mini-Mental State Examination. The results demonstrated no association between schizophrenia and/or cognitive deficit in schizophrenia and ACT polymorphism. The data suggest that the ACT gene is not of major importance for the genesis of schizophrenia. Further studies measuring ACT expression as messenger RNA or serum ACT level may help to exclude the role of ACT in the pathogenesis of schizophrenia.

Adult↗
PubMed1999

Transient electroencephalographic suppression with initiation of cardiopulmonary bypass in pigs: blood versus nonblood priming.

Electroencephalographic (EEG) changes have been reported with cardiopulmonary bypass (CPB). We tested whether the type of priming solution (blood versus nonblood) affected the EEG. Twenty-six anesthetized pigs (29.5+/-1.6 kg) were cannulated for CPB primed with 1 liter plasmalyte and 500 ml 6% hetastarch (nonblood prime). EEG signals were recorded during the initiation of normothermic CPB. Three minutes later, animals were weaned from CPB and allowed to stabilize. CPB was reinstituted using the animals' hemodiluted blood as prime. We found that with nonblood prime, abrupt and marked EEG suppression lasting 12.6+/-0.7 s was found in all animals, followed by gradual resumption of baseline EEG activity. In contrast, CPB with blood prime caused no detectable EEG changes. We conclude that severe reductions in EEG activity occur after initiating CPB with nonblood prime; these reductions are not seen when using blood prime. The cause of EEG suppression is unknown, but may represent transient impairment of oxygen delivery to the brain caused by nonblood perfusion.

Animals↗
PubMed1999

Human leukocyte antigen polymorphisms in the Taiwanese population.

Polymorphisms of human leukocyte antigens (HLA) are important in transplantation medicine, anthropologic studies, and paternity testing. We investigated the polymorphisms of HLA classes I and II in the Taiwanese population by means of serologic typing and polymerase chain reaction (PCR) analysis with sequence-specific primers. We calculated the HLA-A, -B, and -C gene frequencies in 673 Taiwanese subjects and the HLA-DRB1, and HLA-DQB1 gene frequencies in 204 subjects with available DNA samples. Haplotype frequencies and linkage-disequilibrium were analyzed on the basis of these data. The common HLA class I antigens were A11 (gene frequency, 34.9%), A2 (29.3%), A24 (15.8%), and A33 (9.8%); B60 (21.9%), B46 (13.1%), B58 (9.7%), and B13 (8.5%); and Cw1 (18.8%), Cw7 (15.3%), and Cw10 (10.7%). The common HLA-DRB1 and HLA-DQB1 alleles were DRB1*12 (15.2%), DRB1*09 (15.2%), DRB1*08 (12.0%), and DRB1*04 (12.0%); and DQB1*0301 (23.5%), DQB1*0303 (15.2%), DQB1*0601 (14.5%), and DQB1*02 (10.8%). The common two-locus haplotypes were A2-B46 (frequency, 9. 7%), A11-B60 (9.6%), and A33-B58 (6.8%); DRB1*09-DQB1*0303 (14.9%), DRB1*12-DQB1*0301 (14.2%), and DRB1*08-DQB1*0601 (10.7%). This study is the first to report the gene frequencies of HLA-DQB1 alleles and the common HLA-DR-DQ haplotypes among Taiwanese. Comparison of our results with those from two other Chinese populations in mainland China reveals that Taiwanese are more closely related to southern Han than to northern Han Chinese.

China↗
PubMed1999

Apolipoprotein E-dependent cholesterol efflux from macrophages: kinetic study and divergent mechanisms for endogenous versus exogenous apolipoprotein E.

In these studies, we have utilized a J774 macrophage model in order to compare phospholipid and cholesterol efflux kinetics in macrophage cells that do not express endogenous apoE to cells transfected to express physiologic levels of human apoE. This model was also used to compare the effect of exogenously added versus endogenously expressed apoE on cholesterol efflux kinetics from macrophages. ApoE expression increased free cholesterol and phospholipid efflux into the medium, but did not change the free cholesterol/phospholipid molar ratio of secreted lipids. Kinetic examination showed that free cholesterol and phospholipid appeared simultaneously in the medium, and that cholesterol loading widened the difference in the rate of cholesterol efflux between apoE-expressing and non-expressing macrophages. Addition of exogenous lipid-free apoE added to non-expressing cells, at a >2-fold higher medium concentration than that produced by endogenous expression, produced less cholesterol efflux than that observed from apoE-expressing cells. The addition of phosphatidylcholine liposomes substantially increased cholesterol efflux from apoE-expressing and non-expressing J774 cells. Addition of these liposomes eliminated the enhanced cholesterol efflux produced by addition of exogenous apoE. On the other hand, even in the presence of phosphatidylcholine liposomes, cholesterol efflux rates remained significantly higher from apoE-expressing macrophages than non-expressing cells. Similar results were obtained when efflux was studied in the presence of cyclodextrin. These results suggest that endogenous expression of apoE by macrophages alters cell cholesterol balance via mechanisms distinct from those utilized by the extracellular addition of apoE, and may involve intracellular or pericellular mechanisms.

Animals↗
PubMed1999

Intussusception in a child infected with enterovirus: case report.

Most intussusceptions in childhood are idiopathic. The association of viral infection has been suspected for decades. We report a case of ileocolonic intussusception in a child during a course of enterovirus infection. A 20-month-old girl with vomiting and irritable crying of 4 days' duration was found to have intussusception by sonography. She had suffered from herpangina one week earlier. Due to her peritoneal signs, she underwent surgical manual reduction. A cluster of enlarged lymph nodes in the intussuscipiens was noted preoperatively by high resolution ultrasound. Two swollen lymph nodes were removed for pathologic evaluation and examined for a viral genome by polymerase chain reaction (PCR) amplification. Panenterovirus base pairs were confirmed on the electrophoresis print. During postoperative sonographic follow-up, significant shrinkage of previous mesenteric lymphoid hyperplasia was observed. In this article, we present the first case of childhood intussusception in associated with enterovirus infection, in which the panenterovirus genome was identified in the patient's mesenteric lymph nodes. This was also the first evaluation of the role of mesenteric lymph nodes in intussusception by high resolution sonography.

Enterovirus Infections↗
PubMed1999

Intrarenal infusion of supernatant from cytokine-activated human mesangial cells may cause glomerular damage.

BACKGROUND: The pathogenesis of glomerular damage in glomerulonephritis (GN) is not fully understood. Several studies have suggested that reactive oxygen molecules play a role in renal disease. It is known that, during GN, mesangial cells are activated. In a previous study, we demonstrated that in vitro interleukin (IL)-1 plus IL-6 stimulated cultured human mesangial cell (HMC) activation to release free oxygen radicals. METHODS: In this study, we measured hydrogen peroxide (H2O2) and superoxide anion (O2-) levels after stimulation by IL-1 plus IL-6 in cultured HMCs. We then infused H2O2 directly into the left renal arteries of Sprague-Dawley rats. We also infused the culture supernatants of HMCs after stimulation by IL-1 plus IL-6 into the left renal arteries of rats. Two hours after stopping the infusion, the kidneys were removed and fixed using Carson's modified Millonig's buffer for electron microscopy. RESULTS: Both 100 microM H2O2 and supernatants of HMCs stimulated by IL-1 10 U/ml plus IL-6 1,000 U/ml caused similar glomerular damage, including blebbing and sloughing of endothelial cells, and denuded basement membrane in glomeruli. When 100 microM H2O2 or supernatants of cytokine-activated HMCs were infused into renal arteries, they caused hematuria and proteinuria. CONCLUSIONS: These results suggest that activated HMCs may secrete free radicals and cause glomerular damage.

Adolescent↗
PubMed1998

Identification and subcellular localization of a novel Cu,Zn superoxide dismutase of Mycobacterium tuberculosis.

Periplasmic copper, zinc superoxide dismutases (Cu,ZnSOD) of several Gram-negative pathogens have been shown to play an important role in protection against exogenous superoxide radicals and in determining virulence of the pathogens. Here we report the cloning and characterization of the sodC gene, encoding Cu,ZnSOD, from the Gram-positive Mycobacterium tuberculosis. The predicted protein sequence contains 240 amino acids with a putative signal peptide at the N-terminus and shows approximately 25% identity to other bacterial sodC. Recombinant proteins of a full-length sodC and a truncated form lacking the putative signal peptide were overexpressed in Escherichia coli and affinity purified. Renatured recombinant M. tuberculosis sodC protein possessed characteristics of a Cu,ZnSOD. Immunoblotting with an antiserum against the recombinant M. tuberculosis Cu,ZnSOD allowed detection of a single polypeptide in the lysate of M. tuberculosis. This polypeptide has a similar size as the recombinant protein without the putative signal peptide indicating that the endogenous Cu,ZnSOD in M. tuberculosis might be processed and secreted. Furthermore, immunogold electron microscopic image showed that Cu,ZnSOD is located in the periphery of M. tuberculosis. The enzymatic activity and subcellular localization of this novel Cu,ZnSOD suggest that it may play a role in determining virulence of M. tuberculosis.

Amino Acid Sequence↗
PubMed1998

Phospholipid- and GTP-dependent activation of cholera toxin and phospholipase D by human ADP-ribosylation factor-like protein 1 (HARL1).

ADP-ribosylation factors (ARFs), 20-kDa guanine nucleotide-binding proteins named for their ability to activate cholera toxin (CT) ADP-ribosyltransferase activity, have a critical role in vesicular transport and activate a phospholipase D (PLD) isoform. Although ARF-like (ARL) proteins are very similar in sequence to ARFs, they were initially believed not to activate CT or PLD. mRNA for human ARL1 (hARL1), which is 57% identical in amino acid sequence to hARF1, is present in all tissues, with the highest amounts in kidney and pancreas and barely detectable amounts in brain. Relative amounts of hARL1 protein were similar to mRNA levels. Purified hARL1 (rARL1) synthesized in Escherichia coli had less activity toward PLD than did rARF1, although PLD activation by both proteins was guanosine guanosine 5'-(gamma-thio)triphosphate (GTPgammaS)-dependent. ARL1 stimulation of CT-catalyzed ADP-ribosylation was considerably less than that by rARF1 and was phospholipid dependent. GTPgammaS-binding by rARL1 was also phospholipid- and detergent-dependent, and in assays containing phosphatidylserine, was greater than that by rARF1. In vitro, the activities of rARL1 and rARF1 are similar. Rather than being a member of a separate subfamily, hARL1, which activates PLD and CT in a phospholipiddependent manner, appears to be part of a continuum of ARF family proteins.

ADP-Ribosylation Factors↗
PubMed1998

Frequent mutation in Chinese patients with infantile type of GSD II in Taiwan: evidence for a founder effect.

Glycogen storage disease type II (GSD II, Pompe's disease), an autosomal recessive inherited disease, is caused by the deficiency of acid alpha-D-glucosidase, which results in the impaired glycogen degradation in lysosome and causes excess glycogen accumulation in lysosome. In Taiwan, the infantile form of GSD II is the most common type of glycogen storage diseases. The frequency of C1935A mutant allele is 0.8 in these Chinese patients. In this study, we analyzed four single point polymorphic markers (324, 1203, 2065, 2338) by ACRS-based RFLP We observed that the alleles possessing the C1935A mutation in 19 of 25 Chinese patients who were heterozygous or homozygous have conserved polymorphic markers, and all of C1935A mutant alleles in these patients are linked to a specific haplotype. The allele frequency of this specific haplotype in 19 Chinese patients and in 42 normal individuals is 0.95 and 0.17, respectively (P<0.005, chi2 = 66.018). This result suggests that the C1935A mutation in Chinese patients with infantile form of GSD II is due to the founder effect.

Alleles↗
PubMed1998

IgG subclass/IgM ratio and response to therapy in focal segmental glomerulonecrosis.

Focal segmental glomerulosclerosis (FSGS) is relatively steroid resistant and no clinical or histological marker can predict the response to therapy. To investigate the role of serum immunoglobulin subclass/IgM in predicting the response to therapy in FSGS, serum concentrations of total IgG, IgG subclasses, and the ratio of serum IgG subclasses to total IgG (% IgG subclass) were measured in 27 children during the acute nephrotic state. Prednisolone, cyclophosphamide, and Persantine (dipyridamole) were given for 12 weeks. We divided the patients into good responders or poor responders according to clinical response. The clinical and nephrotic status were similar in both groups. Fourteen patients were good responders with higher serum IgGI/IgM than that of non-responders (4.00+/-0.67 vs. 1.61+/-0.20, P<0.05). There was no significant difference in IgG2/IgM between these two groups. These results suggest that higher serum IgGI/IgM ratios may be associated with a better clinical response. These changes may reflect dysregulation of immunoglobulin class switching in patients with FSGS.

Acute Disease↗
PubMed1998

Formalin treatment of refractory hemorrhagic cystitis in systemic lupus erythematosus.

Hemorrhagic cystitis is a potentially life-threatening complication in systemic lupus erythematosus (SLE). No safe, effective and conservative treatment exists for patients who fail to respond to standard therapy. We report a 17-year-old girl with SLE who suffered from severe hemorrhagic cystitis. Initially, she received frequent red blood cell and platelet transfusions, continuous bladder irrigation, and blood clots were evacuated. Numerous kinds of treatment were tried, including electrocoagulation of bleeding foci, prostaglandin E1 bladder instillation, and hyperbaric oxygen. However, she remained severely anemic and thrombocytopenic necessitating daily transfusions of blood products. After intravesical formalin instillation was performed twice, the hematuria ceased completely.

Adolescent↗
PubMed1998

Chinese herbs as modulators of human mesangial cell proliferation: preliminary studies.

In the hope of identifying agents of therapeutic value in immunoglobulin A nephropathy (IgA-N), we tested crude methanol extracts of 15 Chinese herbs for their effect on human mesangial cel proliferation in vitro. The results indicated that 7 out of the 15 crude extracts inhibited human mesangial cell proliferation activated by interleukin-1beta and interleukin-6. The extracts and their median inhibitory concentrations were as follows (in microg/ml): Selaginella tamariscina (MLS-032), 56.0 +/- 2.0; Ixeris chinensis (MLS-033), 62.7 +/- 1.7; Polygonum hypoleucum Ohwi (MLS-034), 25.0 +/- 1.5; Scutellaris rivularis (MLS-036), 39.6 +/- 1.1; Condonacanthus paucifiorus (MLS-042),63.6 +/- 2.6; Xanthium strumarium (MLS-043), 42.8 +/- 1.3; Daemonoropus margaritae (MLS-044), 56.1 +/- 1.9. These findings indicate that human mesangial cells were most sensitive to MLS-034 treatment. These herbs also decreased interleukin-1beta and tumor necrosis factor-alpha production. Moreover, TNF-alpha mRNA expression was inhibited by MLS-034. It is unlikely that cytotoxicity was involved, because no cell deaths were observable. We hypothesize that the inhibitory mechanisms of these Chinese herbs may be related to the impairments of gene expression and production of cytokines in human mesangial cells. Plans are underway for the isolation of pure compounds from these Chinese herbs and the elucidation of their mechanisms of action.

Adolescent↗
PubMed1998

Identification and characterization of a hyperglycemic hormone from freshwater giant prawn, Macrobrachium rosenbergii.

Crustacean hyperglycemic hormone (CHH), a physiologically important neurohormone stored in the sinus gland of eyestalks, primarily regulates carbohydrate metabolism and also plays significant roles in reproduction, molting and other physiological processes. In the freshwater giant prawn, Macrobrachium rosenbergii, an injection of X-organ sinus gland (XOSG) extract evoked a hyperglycemic response, peaked in 1 h. The hyperglycemic effect of the eyestalk extract was maximal at the dose of 0.5 eyestalk equivalent. CHH fractionated by RP-HPLC, in M. rosenbergii was identified by its hyperglycemic activity and partial amino acid sequence, and the molecular weight of 8534 was determined by matrix-assisted laser desorption ionization mass spectrometry--time of flight analysis (MALDI-TOF). The amino acid sequence of the first 25 residues of CHH showed 72% homology with the first 25 residues of CHH A and CHH B of the American lobster Homarus americanus.

Animals↗
PubMed1998

Seasonal changes in symptomatic duodenal ulcer activity in Taiwan: a comparison between subjects with and without haemorrhage.

OBJECTIVES: To examine if climatic changes may influence the presentation of pain and haemorrhage in patients with duodenal ulcers. DESIGN: Cross-sectional study. SETTING: Tertiary referral centre. SUBJECTS: A total of 10,331 symptomatic duodenal ulcer diseases were diagnosed from 1989 to 1996. The patients who had any extrinsic factors that might influence the exacerbation of duodenal ulcer were not included. Patients were divided into those whose ulcer bled once or repeatedly as distinct from those whose ulcers caused pain without haemorrhagic complications. Patients with acute cholangitis diagnosed in the same period were studied as controls. RESULTS: During the 7-year period, 10,331 symptomatic duodenal ulcer diseases were diagnosed. Amongst these, 5328 showed active duodenal ulcer without haemorrhage, 2088 showed acute duodenal ulcer with stigmata of recent haemorrhage, and 2915 showed a deformed bulb. The incidence of total duodenal ulcers showed significant monthly variation and was found to be more common from November to March (P < 0.001). The monthly incidence of total episodes of upper gastrointestinal tract bleeding peaked from November to March (P < 0.001) with significant variation. The monthly incidence of bleeding episodes from duodenal ulcer only was the same (P < 0.001). In patients whose duodenal ulcers repeatedly caused pain without haemorrhage, there were significant monthly fluctuations, with peak months from December to March (P < 0.001). In the control diagnosis, there were no significant calendar variations (P = 0.85). CONCLUSIONS: Our study has shown that both groups of patients demonstrated similar monthly fluctuations. The incidence is significantly higher during the cold seasons. These data suggest that climatic changes may influence the presentation of pain and haemorrhage in duodenal ulcer patients.

Adult↗
PubMed1998

Leached components from dental composites in oral simulating fluids and the resultant composite strengths.

The aim of this study was to analyse the leached moieties of dental composites after storage in ethanol and organic acids of plaque and further evaluate the resultant effect on the diametral tensile strength (DTS) of the composites. Three commercial composites were used: Bis-GMA-based Z100, Bis-GMA/UDMA-based Heliomolar, and Bis-MPEPP-based Marathon One. The solutions used were: 99.9% acetic acid, 99% propionic acid and 75% ethanol. Specimens (4 mm diam. x 2 mm thick) were stored at 37 degrees C in 3 mL of solution for up to 30 days. Gas chromatography/mass spectrometry was used to characterize the leached moieties and DTS of the specimens after immersion was evaluated. Data were analysed using ANOVA and Tukey LSD test. The eluted substances were not all the same in different solutions and composites but mostly increased with immersion time, and included diluents (TEGDMA and decamethacrylate) and some additives, such as an ultra-violet stabilizer (TINUVINP), plasticizers (dicyclohexyl phthalate and bis(2-ethylhexyl) phthalate), initiator (triphenyl stibine), coupling agent (gamma-methacryloxypropyl trimethoxysilane), and phenyl benzoate. The chief polymerizing monomers were not found. More kinds of components were found in the acetic acid and ethanol groups studied. The fewest kinds and quantities of leached moieties were found for Bis-GMA specimens and then Bis-GMA/UDMA ones, most of which are diluent agents. Bis-MPEPP specimens leached the most substances, which were composed mostly of a short phenyl group chain structure. The BisGMA composite showed the highest DTS (54.8 +/- 5.7 MPa), which was not greatly affected by the length of storage. Bis-GMA/UDMA (36.2 +/- 6.8 MPa) and Bis-MPEPP (26.1 +/- 4.5 MPa) composites were significantly reduced (P < 0.05) after 30 days storage in the ethanol (35-50%), in the propionic acid (25-30%), and in the acetic acid (40-60%). Irreversible processes such as the leaching of components occur in fluids simulating an oral environment, which may contribute to irreversible material degradation, especially for non-Bis-GMA-based composites.

Acetates↗
PubMed1998

Clinical efficacy of cyclosporin a neoral in the treatment of paediatric lupus nephritis with heavy proteinuria.

Cyclosporin A (CsA) was introduced in recent years for the treatment of lupus nephritis in patients with steroid resistance or in those with severe corticosteroid toxicity. Our previous study on paediatric patients showed that Neoral (a new microemulsion formulation) had better bioavailability than CsA capsules. To evaluate the clinical efficacy of Neoral in children with lupus nephritis compared with conventional therapy, we performed an open randomized study on 40 children, ranging from 9 to 14 yr old, with class III-V lupus nephritis and heavy proteinuria. They were randomly assigned to either Neoral (5 mg/kg/day), administered q.12.h, or prednisolone (2 mg/kg/day) plus cyclophosphamide (2 mg/kg/day) for 1 yr. Both groups showed a significant decrease in proteinuria (Neoral: 4.62 +/- 1.93 to 0.35 +/- 0.29 g/day, P < 0.05; prednisolone plus cyclophosphamide: 4.52 +/- 1.86 to 0.62 +/- 0.21 g/day, P < 0.01). The CH50 haemolytic assay titre decreased after 1 yr of Neoral treatment (26.5 +/- 0.9 to 21.4 +/- 2.2 U/ml, P < 0.05). Serum C3 and anti-double-stranded (ds) DNA antibody levels also fell with Neoral (C3: 86.2 +/- 6.8 to 76.3 +/- 4.5 mg/dl; anti-ds DNA antibodies: 14.1 +/- 3.2 to 8.2 +/- 1.4 IU/ml, P < 0.05). The Neoral group had a significant increase in growth rate over the prednisolone plus cyclophosphamide group (8.2 +/- 1.1 cm/yr vs 2.7 +/- 0.6 cm/yr, P < 0.01) with improvement of growth status. During the study period, patients tolerated Neoral well with no significant changes in renal function, liver function or lipid profile. Our study implies that Neoral appears to be effective in suppressing proteinuria. Neoral should be regarded as being adjunctive therapy, perhaps with a steroid-sparing effect, in paediatric lupus nephritis. However, its long-term use awaits further studies.

Adolescent↗
PubMed1998

Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs.

BACKGROUND: The aim of this study was to determine whether progressive levels of hypothermia (37, 34, 31, or 28 degrees C) during cardiopulmonary bypass (CPB) in pigs reduce the physiologic and metabolic consequences of global cerebral ischemia. METHODS: Sagittal sinus and cortical microdialysis catheters were inserted into anesthetized pigs. Animals were placed on CPB and randomly assigned to 37 degrees C (n = 10), 34 degrees C (n = 10), 31 degrees C (n = 11), or 28 degrees C (n = 10) management. Next 20 min of global cerebral ischemia was produced by temporarily ligating the innominate and left subclavian arteries, followed by reperfusion, rewarming, and termination of CPB. Cerebral oxygen metabolism (CMRO2) was calculated by cerebral blood flow (radioactive microspheres) and arteriovenous oxygen content gradient. Cortical excitatory amino acids (EAA) by microdialysis were measured using high-performance liquid chromatography. Electroencephalographic (EEG) signals were graded by observers blinded to the protocol. After CPB, cerebrospinal fluid was sampled to test for S-100 protein and the cerebral cortex was biopsied. RESULTS: Cerebral oxygen metabolism increased after rewarming from 28 degrees C, 31 degrees C, and 34 degrees C CPB but not in the 37 degrees animals; CMRO2 remained lower with 37 degrees C (1.8 +/- 0.2 ml x min[-1] x 100 g[-1]) than with 28 degrees C (3.1 +/- 0.1 ml x min[-1] x 100 g[-1]; P < 0.05). The EEG scores after CPB were depressed in all groups and remained significantly lower in the 37 degrees C animals. With 28 degrees C and 31 degrees C CPB, EAA concentrations did not change. In contrast, glutamate increased by sixfold during ischemia at 37 degrees C and remained significantly greater during reperfusion in the 34 degrees C and 37 degrees C groups. Cortical biopsy specimens showed no intergroup differences in energy metabolites except two to three times greater brain lactate in the 37 degrees C animals. S-100 protein in cerebrospinal fluid was greater in the 37 degrees C (6 +/- 0.9 microg/l) and 34 degrees C (3.5 +/- 0.5 microg/l) groups than the 31 degrees C (1.9 +/- 0.1 microg/l) and 28 degrees C (1.7 +/- 0.2 microg/l) animals. CONCLUSIONS: Hypothermia to 28 degrees C and 31 degrees C provides significant cerebral recovery from 20 min of global ischemia during CPB in terms of EAA release, EEG and cerebral metabolic recovery, and S-100 protein release without greater advantage from cooling to 28 degrees C compared with 31 degrees C. In contrast, ischemia during 34 degrees C and particularly 37 degrees C CPB showed greater EAA release and evidence of neurologic morbidity. Cooling to 31 degrees C was necessary to improve acute recovery during global cerebral ischemia on CPB.

Animals↗