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J X Li

Publications and source records attributed to J X Li.

At least 55 records · Page 3Linked to original sources

[Molecular recognition between GlcNAc and Plasmodium falciparum merozoites].

In this study p-aminophenyl-2-acetamido-2-deoxy-beta-D-glucopyranoside was bound covalently to bovine serum albumin (BSA) to form neoglycoprotein (GlcNAc-BSA). The antigenicity of BSA and the pyranose structure of the sugar was preserved. By using the neoglycoprotein antibody against BSA and staphylococcal protein A-gold (SPA-gold), Plasmodium falciparum FCC-1/HN merozoites were immunolabeled. The labelled sample was observed under transmission electron microscope (TEM). The TEM pictures showed that colloidal gold pellets were distributed all over the merozoite surface. This is the first report on the direct experimental evidence of molecular recognition between GlcNAc-BSA (or GlcNAc) and Plasmodium falciparum merozoites. But free GlcNAc or even GlcN can inhibit the immunolabeleation. The results support the hypothesis that, besides N-acetylneuraminic acid, GlcNAc is involved as another recognized site on GPA for Plasmodium falciparum. Thus we further confirmed that N-acetyl of GlcNAc is not necessary for the recognition.

Acetylglucosamine↗

Capsular type-specific polysaccharide partially inhibits group B Streptococcus-induced pulmonary hypertension.

Capsular type-specific polysaccharide is thought to be an important pathogenetic factor in Group B streptococcus (GBS) sepsis. To determine the effects of capsular type-specific polysaccharide on GBS-induced hemodynamic responses, anesthetized infant piglets were infused for 3 h with three related GBS Type lb strains that express different amounts of capsular type-specific polysaccharide. A larger capsule strain and a smaller capsule strain were isolated from an infected infant and its mother, respectively. A capsule-deficient mutant was then made from the larger capsule strain by transposon insertion mutagenesis. The smaller capsule strain and capsule-deficient mutant caused similar elevations in mean pulmonary artery pressure and pulmonary vascular resistance index and reductions in cardiac index. The larger capsule strain caused moderate pulmonary hypertension, but this response was smaller than for the other two GBS strains. Further comparisons in responses between the large capsule strain and its capsule-deficient mutant were then performed using unanesthetized piglets. The mutant caused significantly greater pulmonary hypertension and arterial plasma thromboxane B2 levels than the large capsule strain. The pulmonary hypertension induced by both strains was reversed by dazmegrel, a thromboxane A2 synthase inhibitor. These results suggest that (1) capsular type-specific polysaccharide is not an essential component in the generation of acute hemodynamic responses; (2) expression of large amounts of capsular type-specific polysaccharide on the organism surface partially inhibits GBS-induced pulmonary hypertension; and (3) the inhibition of the pulmonary responses is due to reduced thromboxane A2 release.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

Age-related differences in responses to endotoxin infusion in unanesthetized piglets.

Newborn endotoxic shock syndrome is associated with high morbidity and mortality, yet presents with different clinical manifestations than in older patients. To determine the influence of age on hemodynamic and metabolic responses to endotoxin, we developed a chronically instrumented endotoxic shock model using eight 1-3-day-old and seven 2-3-week-old piglets. Three days after surgery, 10 mg/kg of endotoxin was infused intravenously over 10 min in the younger group, and 5-10 mg/kg was given to the older animals. Two older piglets died immediately after infusion of 5 mg/kg of endotoxin, and five of the seven died within 4 hr, while all eight younger animals lived longer than 4 hr. Pulmonary artery pressure increased significantly after endotoxin in both groups, and there were no differences between groups. Systemic artery pressure and cardiac index fell by 44 +/- 10% and 70 +/- 15%, respectively, 5 min after endotoxin infusion in the older group, while these values did not change significantly in the younger group. Endotoxin infusion also caused greater elevation in pulmonary vascular resistance index in the older animals. In the later phase, which began 30 min after endotoxin, both groups displayed systemic hypotension and pulmonary hypertension, and the groups did not differ from one another in this regard. With progression of endotoxic shock, more severe metabolic acidosis developed in the older animals than in the younger animals. Plasma thromboxane B2 levels in the older group were about double those in younger piglets. Plasma 6-keto-PGF1 alpha and TNF alpha levels in both groups were similar and were significantly increased in the later phase.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

Delayed thromboxane synthesis inhibition, but not cholinergic blockade, reverses group B streptococcus-induced pulmonary hypertension.

Anisodamine, an anticholinergic drug, is widely used in China for treatment of infants with septic shock and has been reported to inhibit thromboxane synthesis in cultured cells. Thromboxane A2 plays an important role in the early pulmonary hypertension in sepsis; however, the role of thromboxane A2 later in sepsis is unclear. We tested the hypothesis that thromboxane A2 synthesis inhibition with dazmegrel, and cholinergic blockade with anisodamine, would attenuate the later phase of pulmonary hypertension induced by 4 h of group B streptococcus (GBS) infusion. 1 mg/kg of dazmegrel reversed the pulmonary hypertension and slightly increased cardiac output; these hemodynamic improvements persisted for 30-60 min. Plasma thromboxane B2 levels returned toward pre-GBS baseline values after dazmegrel treatment. Thus, thromboxane A2 is still a major mediator of pulmonary hypertension in piglets after 4 h of continuous GBS infusion. 0.5 mg/kg of anisodamine had no significant hemodynamic effect. 2 and 4 mg/kg of anisodamine each caused transient, dose-related decreases in systemic artery pressure; cardiac output also fell after the highest anisodamine dose. Pulmonary hypertension was not alleviated by anisodamine. All hemodynamic changes induced by anisodamine were short-lived and returned to preanisodamine values within 10 min. Anisodamine did not ameliorate thromboxane-mediated pulmonary hypertension in this animal model, and therefore may not inhibit thromboxane synthesis in vivo. The results of this study do not support the use of anticholinergic therapy to improve hemodynamics in GBS sepsis, but do suggest that thromboxane synthesis inhibition may be a clinically useful therapy in advanced GBS sepsis.

Animals↗

Role of capsule in pulmonary hypertension induced by group B streptococcus.

The type-specific polysaccharide capsule of group B streptococcus (GBS) is thought to be an important factor in the pathogenesis of disease. We used an acutely instrumented piglet model to assess the hemodynamic effects of rapid infusions of two heat-killed GBS type Ib strains isolated from the spinal fluid of an infant with late-onset meningitis and from the vaginal culture of his mother. These strains expressed different amounts of capsule, as determined by buoyant density centrifugation and electron micrographs, and they produced different hemodynamic effects in the piglets. The mother's strain, which had a smaller capsule, caused significantly higher increases in pulmonary artery pressure and vascular resistance than did the infant's strain, which had a larger capsule. Transposon mutants were then made from the infant's isolate to further study the role of capsule in pulmonary hypertension. Two mutants lacking detectable capsular type-specific polysaccharide were compared with the original isolate and with an isogenic mutant containing transposons but having a large capsule. The nonencapsulated mutants caused significantly higher changes in pulmonary artery pressure and resistance than did the encapsulated strains. Pulmonary hypertension may play a role in the pathophysiology of GBS sepsis, but the presence of a large capsule may partially cloak the hemodynamically active component(s) of the bacteria. The lower initial host response to heavily encapsulated GBS may play a role in pathogenesis by helping the organisms avoid host defense mechanisms.

Animals↗

[Clinico-pathologic studies on 143 cases of tonsillar malignancies with special reference to lymphomas].

143 cases of tonsillar malignancies consulted or treated in our hospital during the past 33 years (1958-1991) were studied morphologically and histochemically. There were 126 non-Hodgkin's lymphomas (NHL), 14 squamous cell carcinomas and one each of mucoepidermoid carcinoma, malignant melanoma and histiocytic lymphoma. The results showed that: 1. The ratio of peripheral T-cell and B-cell lymphoma was high (2.08:1), of which the reason is unexplained, 2. Many tonsillar NHLs had been misdiagnosed as undifferentiated carcinomas, poorly differentiated carcinomas or reticular cell sarcomas in the past, and 3. Most of the B-cell lymphomas belong to the high grade malignant large cell lymphomas, like the large non-cleaved and immunoblastic type. These findings are different from what is generally believed and known.

Aged↗

Abnormalities of ion-exchange proteins of the red cell membrane in iron deficiency anemia.

The influences of iron deficiency on erythrocyte spanning membrane proteins, band 3 protein and Na(+)-K(+)-ATPase, were studied in the growing rats with iron deficient anemia. The main findings were (1) reduction of band 3 and increment of band 4.1 protein. (2) diminished rate constant of pyruvate-chloride exchange (Kp:Cl.h-1) of the erythrocytes and (3) significant decrease of Na(+)-K(+)-ATPase activity only at the early stage of iron exhaustion. In addition, there was a significant negative correlation between Kp:Cl.h-1 and Na(+)-K(+)-ATPase activity both in iron deficient rats and in the controls. It is suggested that the composition and function of the erythrocyte spanning-membrane proteins for ion exchange could be affected by iron deficiency.

Anemia, Hypochromic↗

[Extracranial meningioma--a report of 6 cases].

Six cases of extracranial meningioma (EM) are reported. In addition to the routine paraffin section and HE stain as examined by light microscope, immuno-histochemical studies with antibodies against vimentin, EMA, CK1, and S-100 were done. One specimen was examined by electron microscopy as well. For subdivision, 4 belonged to meningotheliomatous type and each of the rest belonged to transitional and psammomatous types respectively. According to Lopez's classification, 5 were Type II and 1 was Type III. The significance of Lopez's classification of this tumor in clinical diagnosis and differential diagnosis, in histogenesis and pathogenesis are discussed.

Adult↗

[Effects of 4-(4"-(2",2",6",6"-tetramethyl-1"-pipe-ridinyloxy) amino)-4'-demethylepipodophyllotoxin on nucleic acids, proteins, and DNA strand of L7712 cells in vitro].

The antitumor activity of GP-7, a new spin-labeled epipodophyllotoxin, was studied by liquid scintillation spectrometry. There were many similarities between GP-7 and etoposide. Both GP-7 and etoposide inhibited the incorporation of [3H]TdR, [3H]UR, and [3H]Leu into DNA, RNA, and protein synthesis in leukemia 7712 cells. The inhibition correlated with drug concentration and duration. IC50 of GP-7 and etoposide on DNA synthesis at 24 h were 0.21 and 0.37 micrograms.ml-1, respectively. The inhibition of GP-7 or etoposide on DNA synthesis retained even after the drug were washed out for 3 h. GP-7 and etoposide caused DNA single-strand breaks, with a well concentration-response relationship. These data suggest that the inhibition of DNA synthesis by GP-7 or etoposide is likely due to the damage of DNA template and breaking of single-strand DNA.

Animals↗

O6-methylguanine-DNA methyltransferase and human cancer chemotherapy.

Two kinds of human tumor cell strains having different activity of O6-methylguanine-DNA methyltransferase (O6-MT) were transplanted into nude mice. Then the mice were injected intraperitoneally with bifunctional alkylating agent 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU). The tumors with low O6-MT activity were quickly suppressed or cured. The result suggests that some tumors, if provisionally determined with low O6-MT activity, might be efficiently cured by treatment with ACNU. This probably opens a new way for human cancer chemotherapy.

Animals↗

[Molecular recognition between glycophorin A and Plasmodium falciparum merozoites].

By using purified human erythrocyte membrane glycophorin A (GPA) and glycopeptide of GPA, antibodies against GPA and against GPA-glycopeptide, and SPA-colloidal gold, Plasmodium falciparum FCC-1/HN merozoites were immunolabeled. The labeled samples were observed under transmission electron microscope (TEM). The TEM pictures showed that colloidal gold pellets were distributed over all of the merozoite surface. This is the first report on the direct experimental evidence of molecular recognition and combination between GPA (or glycopeptide of GPA) and Plasmodium falciparum merozoites. The results strongly support the hypothesis that GPA is involved as a recognized receptor on erythrocytes for Plasmodium falciparum and the glycopeptide domain of GPA is the receptor site for Plasmodium falciparum.

Animals↗

D-3-hydroxyacyl coenzyme A dehydratase from rat liver peroxisomes. Purification and characterization of a novel enzyme necessary for the epimerization of 3-hydroxyacyl-CoA thioesters.

Rat liver peroxisomal D-3-hydroxyacyl-CoA dehydratase, which in combination with enoyl-CoA hydratase catalyzes the epimerization of 3-hydroxyacyl-CoA, was purified by a five-step procedure to yield a highly purified preparation as judged by gel electrophoresis of the native and denatured enzyme. Since the molecular mass of the native dehydratase was estimated to be twice that of its 44-kDa subunit, the enzyme seems to be composed of two, possibly identical subunits. This dehydratase catalyzes the reversible dehydration of D-3-hydroxyacyl-CoA to 2-trans-enoyl-CoA, but, in contrast to enoyl-CoA hydratase, does not act on 2-cis-enoyl-CoA. The dehydratase is virtually inactive toward crotonyl-CoA, but exhibits high activity with 2-trans-hexenoyl-CoA as a substrate and acts with decreasing efficiency on all 2-enoyl-CoAs tested from 2-hexenoyl-CoA to 2-hexadecenoyl-CoA. The pH optimum of the enzyme is close to 8. Equilibrium ratios of 3-hydroxyoctanoyl-CoA/2-trans-octenoyl-CoA and 3-hydroxyoctanoyl-CoA/2-cis-octenoyl-CoA were found to be close to 3 and 137, respectively. It is suggested that 2-cis-enoyl-CoA intermediates formed during the beta-oxidation of polyunsaturated fatty acids in peroxisomes are hydrated by enoyl-CoA hydratase to D-3-hydroxyacyl-CoAs which are epimerized to their L-isomers by the sequential actions of D-3-hydroxyacyl-CoA dehydratase and enoyl-CoA hydratase.

Animals↗

Influence of radiation on the blood-brain barrier and optimum time of chemotherapy.

A pilot study of the destructive effects of radiation on the blood-brain barrier (BBB) was made on 14 patients with localized and limited brain tumors by 99MTc-GH imaging from August 1988 to November 1989. Count/pixel data were obtained from the unirradiated, irradiated, and tumor areas before and after radiotherapy of 30-40 Gy. It was observed that, a) the BBB in the unirradiated area outside the radiation portal was not changed, b) the degree of destructive effect on the BBB in the irradiated normal area was directly proportional to the radiation dose. For 30-40 Gy, the count/pixel change enhances to average 24.7% [(147.6-118.4)/118.4], and c) the BBB in the tumor area is partially destroyed on an average of 22.1% [(206.8-169.4)/169.4] by the tumor. The radiotherapy further enhances this effect to an average of 74.7% [(206.8-118.4)/118.4]. Case 3 showed that before radiation, the degree of destructive effect on the BBB in the tumor area was 22% [(167-137)/137] higher than normal brain tissue. After a dose of 30 Gy of irradiation, it increased to 76.7% [(242-137)/137]; 8 months later it decreased to 17% [(160.3-137)/137]. It has been proven that the BBB can recover at least partially. Based on these observations, the authors believe that in the combined treatment of operated brain tumors, radiotherapy should precede chemotherapy so as to enhance the destruction of the BBB, facilitating the incorporation of drugs into the tumor. The dose at which to start chemotherapy is 20-30 Gy.

Antineoplastic Agents↗

Plant regeneration from protoplasts of a super Chinese rice (Oryza sativa L.) cultivar--Zhonghua NO.8.

Green rice plants were regenerated from protoplasts, which were derived from cell suspension of Oryza sativa L. cut. Zhonghua No. 8, a super Chinese rice cultivar with high productivity, good quality and high resistance to both bacterial blight and blast. The embryogenic calli were initiated from mature embroys. It took about 4 months to establish the cell suspenion. The regeneration plants from protoplasts were obtained in 2 months after the isolation of protoplasts.

Cells, Cultured↗

[Antitumor activity of 4-(4''-(2'',2'',6'',6''-tetramethyl-1''-piperidinyoxy)amino)-4'- demethyl epipodophyllotoxin in vitro].

The antitumor activity of a new podophyllotoxin spin-labeled derivative, 4-(4''-(2'',2'',6'',6''-tetramethyl-1''-+piperidinyoxy)amino)-4'- demethylepipodophyllotoxin (GP-7) First synthesized by us, was studied in vitro. It was found that the proliferation of SGC-7901 cells was markedly inhibited by GP-7 depending the concentration and exposure time. At concentration of 0.04-100 mg/L, the inhibition rates were 15.5-92.6% ID50 was 0.42 mg/L. After exposure to GP-7 greater than 0.5 mg/L for 24, 48, 72 and 96 h, the inhibition rates of cells were 25.1, 49.0, 71.4 and 84.9% respectively. The dose-response curve of GP-7 on SGC-7901 cell was similar to that of etoposide (VP-16). The colony formation of SGC-7901 cell was also inhibited by GP-7 in a concentration dependent fashion with ID50 1.63 mg/L. At concentrations of 0.1-0.5 mg/L, the inhibitory effects were stronger than that of VP-16. GP-7 decreased the mitotic index (MI) of SGC-7901 cell and had no effect on microtubule assembly and disassembly in vitro, which suggested that GP-7 did not act on M phase.

Antineoplastic Agents↗

[Midline peripheral T-cell lymphoma--a disease entity recognized anew].

Thirty-one cases of midline peripheral T-cell lymphoma (MPTL), treated during the past two years in our hospital, are reported. All were proven by immunohistochemical stain on frozen section, using a panel of antibodies: IIIC4 (CD5), Leu-2, Leu-3, Leu-4, T,p55, T11, Ia, Ki-1, IL2-R, B1/DAKO-CD22, Kappa, Lambda and IgM. Three cases were also stained with LCA, UCHL-1, MT1, MT2, MB1 and MB2 monoclonal antibodies in paraffin sections, and the results conformed with the frozen-sectionmethod. According to our present and previous reports, it is worthy of note that most of the so-called midline malignant reticuloses (MMR) in the past, including necrotic granulomatosis and malignant granulomatosis, are actually MPTL. In view of MPTL being highly malignant and not very rare in this country, it is emphasized that this disease should be paid more attention and recognized anew. More active treatment should be given to improve the results.

Adolescent↗

The 3-hydroxyacyl-CoA epimerase activity of rat liver peroxisomes is due to the combined actions of two enoyl-CoA hydratases: a revision of the epimerase-dependent pathway of unsaturated fatty acid oxidation.

Chromatography of a rat liver extract on DEAE-cellulose resulted in the near total loss of 3-hydroxyacyl-CoA epimerase activity. The activity was regained either when fractions were recombined or when purified crotonase was added to the early column fractions. A new enoyl-CoA hydratase present in these early fractions catalyzes the conversion of D-3-hydroxyacyl-CoA to 2-trans-enoyl-CoA which can be hydrated by crotonase or the peroxisomal bifunctional enzyme to L-3-hydroxyacyl-CoA. Thus, the 3-hydroxyacyl-CoA epimerase activity is due to the combined actions of two enoyl-CoA hydratases with opposite stereospecificities.

Animals↗