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M T Lin

Publications and source records attributed to M T Lin.

At least 145 records · Page 8Linked to original sources

The greater omentum is the primary site of neutrophil exudation in peritonitis.

BACKGROUND: Peritonitis remains a major infectious problem. Neutrophil influx into the peritoneal cavity is one of the most important host defense mechanisms. However, no studies have focused on the site of neutrophil exudation. This study examined the primary anatomic site of neutrophil exudation in bacterial peritonitis. STUDY DESIGN: Fifty-five rats were injected intraperitoneally with saline solution (control group) or 10(7) Escherichia coli (peritonitis group). In experiment 1, 1 x 10(6) fluorescein-labeled neutrophils were infused 3 hours after the challenge. Then, peritoneal-lavaged fluids and peritoneal tissues (the greater omentum, mesentery, parietal peritoneum, colon, and ileum) were obtained. Subpopulations of peritoneal exudative cells and numbers of labeled neutrophils in tissues were counted. In experiment 2, labeled neutrophils were infused at 10 minutes and at 1 and 5 hours after the challenge. Peritoneal tissues were also harvested. The number of labeled neutrophils in each tissue was determined. RESULTS: In experiment 1, numbers of labeled peritoneal neutrophils and exudative neutrophils were higher in the peritonitis group than in the control group. Numbers of exudative neutrophils showed a positive correlation with numbers of labeled peritoneal neutrophil. In experiment 2, at 1 and 5 hours after the challenge, the number of labeled neutrophils was higher in the peritonitis group than in the control group. The number of neutrophils in the omentum was higher than the number in other peritoneal tissues. CONCLUSIONS: Our fluorescence microscopic method is useful for detecting neutrophil adhesion. Neutrophil exudation into the peritoneal cavity was most marked in the omentum. The greater omentum may play an important role in host defense as a source of exudative neutrophils.

Animals↗

Interleukin-1 receptor antagonist increases survival in rat heatstroke by reducing hypothalamic serotonin release.

During onset of heatstroke, rats displayed higher values of hypothalamic serotonin release and score f hypothalamic neuronal damage, and lower values of mean arterial pressure and hypothalamic blood flow compared with normothermic control rats. In another group in which interleukin-1 receptor antagonist (IL-1 ra; 200 micrograms/kg, i.v.) was injected 30 or 60 min after the start of heat exposure, the augmented hypothalamic serotonin release, diminished hypothalamic blood flow, arterial hypotension and hypothalamic neuronal damage during heatstroke were reduced as compared to the saline control group. The survival time (interval between onset of heatstroke and death) of the heatstroke rats was prolonged by treatment with IL-1 ra. The data indicate that IL-1 ra increases survival during rat heatstroke by reducing hypothalamic serotonin release.

Animals↗

Correlation of cytogenetic results with immunophenotype, genotype, clinical features, and ras mutation in acute myeloid leukemia. A study of 235 Chinese patients in Taiwan.

Of 235 consecutive patients with de novo acute myeloid leukemia (AML), clonal chromosomal abnormalities were detected in 151 (64%) of them. Twenty-four of the 71 patients with M2 AML had t(8;21), 35 of the 36 M3 patients had t(15;17), and 11 of the 45 M4 leukemia disclosed inv(16). Six of the eight patients with 11q23 abnormality had M4 or M5 subtype of leukemia. The incidence of t(15;17) and t(8;21) was higher in our patients than in patients from most Western countries. Immunophenotyping was performed on 197 patients. Patients with t(15;17) were associated with negativity to HLA-DR, CD11b, and CD34. Patients with t(8;21) expressed CD13 and CD33 less frequently than other patients, but all showed CD15 positivity. Coexpression of lymphoid-associated antigens on the leukemic blasts was detected in 52 patients (26%), including all 7 patients with t(9;22), 3 of the 8 patients with t/del(11)(q23), 2 of the 25 patients with t(15;17), and 2 of the 22 patients with t(8;21). Seven (35%) of the 20 patients coexpressing lymphoid markers showed immunoglobulin heavy chain or T-cell receptor beta-chain gene rearrangements, while only 2 (4%) of the 53 patients without lymphoid antigen expression did so. Patients with inv(16), t(8;21), and t(15;17) had a better prognosis than other patients. Of all surface antigens tested, only CD15, CD11b, and HLA-DR were of prognostic value: CD15 with a higher complete remission (CR) rate and CD11b or HLA-DR with a shorter CR duration. N-ras mutations were detected in 7 (18%) of the 40 patients in the study, including two of the three patients with inv(16). This study demonstrated differences in clinical features, immunophenotypes, and genotypes among different cytogenetic subgroups.

Adolescent↗

Changes of protein kinase C subspecies in staphylococcal enterotoxin-B-induced thymocyte apoptosis.

Our previous studies demonstrated that intravenous administration of staphylococcal enterotoxin B (SEB) to BALB/c mice resulted in thymocyte apoptosis. In the present study, we evaluated the role of protein kinase C (PKC) in thymocyte apoptosis induced by SEB. Our results showed that the level of protein phosphorylation in the thymocytes was reduced after the in vivo SEB treatment for 24 h. The activity of classical PKC subspecies was decreased in both cytosolic and membrane fractions of thymocytes following SEB administration. The lowest level of PKC activity was reached by 24 and 48 h, then was recovered gradually after 72 h. Furthermore, the mRNA expression of PKC-beta and, to a much less extent, PKC-alpha, but not PKC-sigma, in thymocytes was reduced by SEB. The decrease of mRNA level of PKC-beta showed good correlation with the pattern of PKC activity. These results provide direct evidence showing the changes in PKC subspecies mRNA expression during the process of apoptosis.

Animals↗

Nigrostriatal dopamine system mediates baroreflex sensitivity in rats.

Both sham-operated rats and rats with lesions of the nigrostriatal dopamine (DA) pathway were subjected to increasing or decreasing carotid sinus pressure (respectively produced by phenylephrine injection or bilateral carotid occlusion) and their striatal DA release and baroreflex responses were compared. In sham-operated rats, phenylephrine produced both increased striatal DA release and decreased heart rate, while bilateral carotid occlusion produced the opposite effects. Both the striatal DA release and baroreflex responses produced by phenylephrine or carotid occlusion were attenuated by lesions of the nigrostriatal DA pathway induced by intramedial forebrain bundle injection of 6-hydroxydopamine. The data indicate that the nigrostriatal DA pathway mediates baroreflex sensitivity in rats.

Animals↗

Suppression of natural killer cell activity in mouse spleen lymphocytes by several dopamine receptor antagonists.

The effects of dopaminergic receptor inhibitors such as thiothixine (D1/D2), fluphenazine (D1/D2), trifluoperazine (D1/D2), pimozide (D2), flupenthixol (D1/D2), (+/-)-SKF 83566 (D1), and spiperone (D2) on splenic natural killer (NK) cell cytotoxic activities were assessed in vitro using mouse spleen lymphocytes or enriched NK cells. Both the activities of the splenic NK cell cytotoxicity and the effector-target cell conjugation were suppressed by thiothixine, fluphenazine, and trifluoperazine at concentrations from 2.64 to 14.78 microM. In addition, the augmentation of the cytolytic activity of NK cells induced by interferon-alpha or interleukin-2 was antagonized by pretreatment with these neuroleptic compounds. However, neither the splenic NK cell cytotoxicity nor the effector-target cell conjugation were affected by treatment with other neuroleptic compounds such as pimozide, flupenthixol, (+/-)-SKF 83566, and spiperone. Thus, it appears that neuroleptic compounds such as thiothixine, fluphenazine, and trifluoperazine may act through the mechanisms other than a dopaminergic pathway to affect the NK cell-target cell interaction.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Detrimental effects of a nitric oxide synthase inhibitor (N-omega-nitro-L-arginine-methyl-ester) in a murine sepsis model.

OBJECTIVE: To examine the effects of a nitric oxide synthase inhibitor on host elimination of bacteria, tumor necrosis factor (TNF) production, and survival in a murine sepsis model. DESIGN: Prospective randomized experimental trials. SETTING: Laboratory. MATERIALS: Female Balb/c mice. INTERVENTIONS: Balb/c mice were injected with Escherichia coli (10(8) colony-forming units per body) into the peritoneal cavity. N-omega-Nitro-L-arginine-methyl-ester (L-NAME), an inhibitor of nitric oxide synthase, was given intraperitoneally at 10 mg/kg (N10 group) or 100 mg/kg (N100 group) 1 hour before bacterial challenge. MAIN OUTCOME MEASURES: Thirty animals were observed for survival. Samples of peritoneal lavaged fluid (PLF), blood, liver, and lungs were obtained at 4 and 6 hours after bacterial challenge (n = 60). The peritoneal exudative cells were counted. Viable bacterial counts were determined in PLF, blood, and organs. The TNF levels also were determined in plasma, PLF, and supernatant samples of cultured peritoneal exudative cells. RESULTS: Survival times after E coli challenge were significantly reduced by pretreatment with L-NAME (100 mg/kg intraperitoneally). Numbers of viable bacteria in the peritoneal cavity and plasma TNF level 4 hours after E coli challenge were higher in both L-NAME-treated groups than in the control group. The number of bacteria in the blood and the plasma TNF level 6 hours after E coli challenge were higher in the L-NAME-treated group (N100 group) than in the control group. Conversely, the number of hepatic bacteria in the control group was significantly higher than in the L-NAME-treated groups. Plasma TNF level showed significant positive correlations with numbers of bacteria in the PLF and in the blood 4 hours after challenge. No significant differences were noted in TNF levels in PLF and peritoneal exudative cell cultured supernatants. CONCLUSION: Inhibition of nitric oxide production is detrimental in this gram-negative sepsis model.

Animals↗

Growth hormone and insulinlike growth factor I enhance host defense in a murine sepsis model.

OBJECTIVE: To investigate the effects of exogenous growth hormone (GH) and insulinlike growth factor I (IGF-I) on host defense and survival in a murine model of Escherichia coli sepsis. DESIGN: Prospective randomized experimental trials. SETTING: Laboratory. MATERIALS: Nine-week-old female BALB/c mice. INTERVENTIONS: Mice were injected subcutaneously with 4.8 or 0.48 mg/kg of body weight per day of GH, 24 or 2.4 mg/kg of body weight per day of IGF-I or, as a control, normal saline solution, for 6 days. Mice were then challenged intraperitoneally with 1 x 10(8) colony-forming units per body of E coli. MAIN OUTCOME MEASURES: Fifty mice were observed for survival. In the next experiments, samples from the high-dose GH, high-dose IGF-I, and saline control groups were harvested before or at 4 or 6 hours after challenge. Numbers of peritoneal exudative cells and tissue-viable bacterial counts were determined. Peritoneal exudative cells were cultured with lipopolysaccharide (10 micrograms/mL) for 24 hours. Levels of tumor necrosis factor, interleukin-1, and interleukin-6 in the peritoneal lavage fluid, plasma and supernatants of peritoneal exudative cell culture were measured. RESULTS: Both high and low doses of GH and high-dose IGF-I significantly prolonged survival. Growth hormone and IGF-I significantly increased peritoneal exudative cell numbers and reduced viable bacterial counts in the peritoneal lavage fluid and the liver. These hormones significantly suppressed excessive systemic cytokine production, while enhancing in vitro cytokine production and preserving local cytokine responses. CONCLUSION: The immunomodulation produced by administration of GH or IGF-I leads to improved host defense in this murine model of E coli sepsis.

Analysis of Variance↗

Consistent presence of isochromosome 7q in hepatosplenic T gamma/delta lymphoma: a new cytogenetic-clinicopathologic entity.

Peripheral T-cell lymphoma (PTL), which is characterized by hepatosplenic presentation and the gamma/delta T-cell receptor (TCR) phenotype on the malignant cells, is a rare but distinct subtype of non-Hodgkin's lymphomas. Little is known about the chromosomal changes in these lymphomas. We report the cytogenetic analysis of three patients who had neoplastic proliferation of T gamma/delta cells in the spleen, bone marrow, and liver, but not in lymph nodes or skin. Isochromosome 7q and trisomy 8 were observed in all three patients. Isochromosome 7q as the sole abnormality has been previously reported in one patient with similar clinicopathologic features. It is suggested that i(7q) is a primary, nonrandom chromosomal abnormality in hepatosplenic T gamma/delta PTL.

Adult↗

Subunit interaction enhances enzyme activity and stability of sweet potato cytosolic Cu/Zn-superoxide dismutase purified by a His-tagged recombinant protein method.

The coding region of copper/zinc-superoxide dismutase (Cu/Zn-SOD) cDNA from sweet potato, Ipomoea batatas (L.) Lam. cv. Tainong 57, was introduced into an expression vector, pET-20b(+). The Cu/Zn-SOD purified by His-tagged technique showed two active forms (dimer and monomer). The amount of proteins of dimer and monomer appeared to be equal, but the activity of dimeric form was seven times higher than that of monomeric form. The enzyme was dissociated into monomer by imidazole buffer above 1.0 M, acidic pH (below 3.0), or SDS (above 1%). The enzyme is quite stable. The enzyme activity is not affected at 85 degrees C for 20 min, in alkali pH 11.2, or in 0.1 M EDTA and also quite resistant to proteolytic attack. Dimer is more stable than monomer. The thermal inactivation rate constant kd calculated for the monomer at 85 degrees C was 0.029 min-1 and the half-life for inactivation was about 28 min. In contrast, there is no significant change of dimer activity after 40 min at 85 degrees C. The enzyme dimer and monomer retained 83% and 58% of original activity, respectively, after 3 h incubation with trypsin at 37 degrees C, while those retained 100% and 31% of original activity with chymotrypsin under the same condition. These results suggest subunit interaction might change the enzyme conformation and greatly improve the catalytic activity and stability of the enzyme. It is also possible that the intersubunit contacts stabilize a particular optimal conformation of the protein or the dimeric structure enhances catalytic activity by increasing the electrostatic steering of substrate into the active site.

Base Sequence↗

Leukotriene E4 selectively increase the delivery of methotrexate to the C6 gliomas in rats.

Leukotriene E4 (LTE4) infused into the carotid artery ipsilateral to an experimental glial tumor will selectively increase the blood-tumor permeability within the tumor. In this study the effects of intracarotid infusion of LTE4 on blood-tumor barrier (BTB) permeability for intravenously administered 14C-aminoisobutyric acid, 14C-5-fluorouracil (5-FU) 14C-sucrose and 3H-methotrexate (MTX) were examined in C6 gliomas of rats. The intracarotic administration of LTE4 selectively opened the BTB, without affecting permeability of normal brain tissue, to all of the above tracers. Intracarotid infusion of LTE4 had the tendency to increase the uptake of intravenously administered 5-FU within the tumor, but this effect was not statistically significant. The intracarotid infusion of LTE4, however, increased the uptake of intravenously injected MTX about twofolds within the tumor (Ki = 19.48 +/- 1.06 vs 10.12 +/- 1.19, p < 0.01) without increasing the uptake in the normal brain tissue.

Animals↗

Detection of dural involvement by magnetic resonance imaging in adult patients with acute leukemias--preliminary experience.

Retrospectively, the dura in 18 adult patients with acute leukemia were evaluated by gadolinium-enhanced T1-weighted magnetic resonance imaging (MRI). Abnormal dural enhancements were detected in three of four patients with positive cerebrospinal fluid (CSF) cytology, in one of five with suspicious central nervous system (CNS) disease, and in two of nine asymptomatic patients. Computed tomography failed to demonstrate any dural abnormality in these six patients. The abnormal dural enhancement was found in either (a) the brain and the spine, (b) the thoracolumbar spine, or (c) the area adjacent to the parenchymal lesions. Three of the patients were in hematological remission stage; disappearance of the abnormal dural enhancement was observed 1-2 months after radiotherapy and high-dose systemic chemotherapy. The results suggest that MRI is a sensitive and noninvasive imaging modality and superior to CT in detecting dural disease in leukemic patients.

Adolescent↗

Differential inhibition of reverse transcriptase and cellular DNA polymerase-alpha activities by lignans isolated from Chinese herbs, Phyllanthus myrtifolius Moon, and tannins from Lonicera japonica Thunb and Castanopsis hystrix.

Two lignans, phyllamycin B and retrojusticidin B isolated from Phyllanthus myrtifolius Moon have been demonstrated to have a strong inhibitory effect on human immunodeficiency virus-1 reverse transcriptase activity (HIV-1 RT), but much less inhibitory effect on human DNA polymerase-alpha (HDNAP-alpha) activity. Fifty percent inhibitory concentrations of phyllamycin B and retrojusticidin B were determined to be 3.5 and 5.5 microM for HIV-1 RT, and 289 and 989 microM for HDNAP-alpha, respectively. The mode of inhibition was found to be non-competitive inhibition with respect to template-primer and triphosphate substrate. Several tannins such as caffeoylquinates (CQs) isolated from Lonicera japonica Thunb, galloylquinates (GQs) and galloylshikimates (GSs) purified from Castanopsis hystrix were shown to have a much less selective inhibitory effect on HIV-1 RT.

DNA Polymerase II↗

Interleukin-1 receptor antagonist attenuates the heat stroke-induced neuronal damage by reducing the cerebral ischemia in rats.

The effects of interleukin-1 receptor antagonist (IL-Ira) on both local cerebral blood flow and neuronal damage of the hypothalamus, corpus striatum, cortex or thalamus were assessed in rats with heat stroke. Heat stroke was induced by exposing the urethane-anesthetized rats to a high ambient temperature (42 degrees C). Damage to the hypothalamus, corpus striatum, cortex or thalamus was scored on a scale of zero to three modified from the grading system of Pulsinelli and colleagues in which: 0 = normal, 1 = few neurons damaged, 2 = many neurons damaged, and 3 = all neurons damaged. During the onset of heat stroke, as compared to those of normothermia controls, the heat stroke rats displayed a higher value of colonic temperature or neuronal damage score, as well as a lower value of local cerebral blood flow or mean arterial blood pressure. In addition, compared to those of normothermic, control rats, the heat stroke rats had increased interleukin-1 and tumor necroting factor production in the diencephalon, brain stem and cortex. The heat stroke-induced neuronal damage and diminished local cerebral blood flow in different brain structures, as well as the systemic hypotension, were attenuated in animals pretreated with IL-1ra (200 micrograms/kg, iv) 30 min before the onset of heat stroke. The results indicate that IL-1ra attenuates the heat stroke-induced cerebral neuronal damage by reducing cerebral ischemia in rats.

Animals↗

Long-term disease-free survival after autologous bone marrow transplantation in a primary plasma cell leukaemia: detection of minimal residual disease in the transplant marrow by third-complementarity-determining region-specific probes.

Primary plasma cell leukaemia (PPCL) is a rare form of plasma cell neoplasm. Treatments of PPCL have been most disappointing. A patient with PPCL received high-dose melphalan plus total body irradiation and autologous bone marrow transplantation (ABMT). By using third-complementarity-determining region (CDRIII)-specific probes, minimal residual disease (MRD) was detected in remission marrow, collected 1 month before ABMT. MRD was no longer detected by CDRIII-specific probes 6, 19 and 26 months after transplantation. The patient remained in complete remission up to 59 months after ABMT.

Adult↗

Brain serotonin depletion attenuates diabetogenic effects of streptozotocin.

The diabetogenic effects of streptozotocin (STZ) were studied on blood glucose, plasma insulin, feeding and drinking, body weight, islet morphology, and hypothalamic serotonin (5-HT) release in vehicle-pretreated rats and in rats pretreated with either intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT; a 5-HT nerve fiber depletor), intraperitoneal injection of p-chlorophenylalanine (PCPA; a tryptophan hydroxylase inhibitor), or intraperitoneal injection of p-chloroamphetamine (PCA; a neurotoxin for 5-HT nerve fiber). At four days after STZ administration, vehicle-treated rats displayed hyperglycemia, polydipsia, polyphagia, decreased plasma insulin level, derangement of islet morphology (few insulin cells, accumulation of glucagon cells), and elevated 5-HT release in the hypothalamus. The above diabetogenic effects of STZ were attenuated by brain serotonin depletion induced by 5,7-DHT, PCPA, or PCA. Furthermore, the STZ-induced hyperglycemia or derangement of islet morphology was attenuated by peripheral sympathectomy or adrenalectomy. It is concluded that brain serotonin depletion attenuates diabetogenic effects of STZ by reducing sympathetic efferent activity in rats.

5,7-Dihydroxytryptamine↗