Biomedical subjects

M Hou

Publications and source records attributed to M Hou.

At least 55 records · Page 3Linked to original sources

PubMed1998

Induction of immune tolerance in adult rabbits undergoing heterotopic cardiac transplantation.

OBJECTIVE: To induce experimental immune tolerance in rabbits and observe its effects on heterotopic cardiac transplantation. METHODS: Donor's splenic lymphocytes pretreated with platinum metal chelator were injected into the recipient's mesenteric-portal vein. Cyclosporin A was perfused through the donor's heart. RESULTS: The injection of donor's splenic lymphocytes before transplantation could significantly prolong the survival time of the heterotopically transplanted heart. The effect of two injections was better than that of one. Radioactive tracer studies showed that the 99mTc-HMPAO tagged lymphocytes injected into the recipient rabbit were later concentrated in the liver, though initially they were distributed in multiple organs. The induced immune tolerance was antigen-specific, and it neither affect the other immune functions of the lymphatic system prominently nor exert any harmful effect on the recipient's liver and renal functions. The perfusion of cyclosporin A through the donor heart could block the glycosyl groups, such as D-glucose, D-mannose or N-acetyl-galactosamine on the surface of the myocardial cells, thus might change the antigenic expression, effectively preventing rejection of the graft by the host, and might be considered as a new method to block graft rejection in cardiac transplantation. The combined use of the above-mentioned two methods acted on both the host and the donor, thus reducing the exposed antigens on the donor organ as well as the immune reaction against the donor antigens, and resulting in synergistic effect in inducing immune tolerance in adult rabbits, and resulting in relatively long-term survival of transplanted hearts. CONCLUSION: This report may provide the experimental basis for inducing immune tolerance in clinical transplantation.

Animals↗

PubMed1997

Multiple quinine-dependent antibodies in a patient with episodic thrombocytopenia, neutropenia, lymphocytopenia, and granulomatous hepatitis.

A 58-year-old man experienced episodes of fever, vomiting, and diarrhea over a 2-year period. The laboratory evaluation during these attacks consistently disclosed thrombocytopenia, leukopenia, and elevated liver enzymes. A liver biopsy performed at one of these attacks showed a typical picture of granulomatous hepatitis. In retrospect, all episodes seemed to be associated with the ingestion of quinine. Indeed, such a correlation was established by a challenge with quinine. By using flow cytometry, quinine-dependent IgG antibodies to platelets were detected in the patient serum. By a two-color flow cytometric assay, the patient serum was also found to hold quinine-dependent antibodies specific for neutrophils, T lymphocytes, and B lymphocytes. Moreover, serum absorbed with neutrophils in the presence of quinine continued to react with platelets, T lymphocytes, and B lymphocytes; serum that was absorbed with mononuclear cells continued to react with neutrophils and platelets. These experiments indicated that the antigen targets were different on platelets, neutrophils, and lymphocytes. Further, the patient serum in the presence of quinine immunoprecipitated surface-labeled platelet proteins with electrophoretic mobilities closely resembling those of glycoprotein (GP) Ib/IX and GPIIb/IIIa. By a modified monoclonal antibody-specific immobilization of platelet antigens assay, the patient serum in the presence of quinine reacted with platelet GPIb/IX and GPIIb/IIIa. Also, the patient serum in the presence of quinine immunoprecipitated an uncharacterized 15-kD double-band from surface-labeled granulocyte proteins. We conclude that our patient's thrombocytopenia, neutropenia, and lymphocytopenia were caused by quinine-dependent antibodies and that these antibodies recognized cell lineage-specific epitopes.

Antibodies↗

PubMed1997

Immunoglobulins targeting both GPIIb/IIIa and GPIb/IX in chronic idiopathic thrombocytopenic purpura (ITP): evidence for at least two different IgG antibodies.

Antiplatelet antibodies in chronic idiopathic thrombocytopenic purpura (ITP) mainly target glycoprotein (GP) IIb/IIIa and GPIb/IX. Previous studies, employing modern antigen-specific assays, indicate that serum reactive with both GPIIb/IIIa and GPIb/IX is not an uncommon finding in chronic ITP. However, the mechanism behind this dual reactivity remains unclear. We studied sera from 72 patients with chronic ITP using modified GPIIb/IIIa- and GPIb/IX-specific MAIPA assays. Among the 34 positive sera, seven showed strong reactivity against both GPIIb/IIIa and GPIb/IX. These seven dual reactive ITP sera were further analysed by absorption studies. It was found that sera absorbed with immobilized GPIb/IX lost nearly all serum IgG specific for GPIb/IX but fully retained the IgG specific for GPIIb/IIIa. Conversely, sera absorbed with immobilized GPIIb/IIIa retained their reactivity only with GPIb/IX. These findings demonstrate that ITP sera, reactive with both GPIIb/IIIa and GPIb/IX, contain at least two different IgG antibody populations, each reactive with only one of the GP complexes.

Adolescent↗

PubMed1996

Light chain-restricted autoantibodies in chronic idiopathic thrombocytopenic purpura, but no evidence for circulating clone B-lymphocytes.

In chronic idiopathic thrombocytopenic purpura (ITP) platelet destruction is caused by antibodies directed against platelet membrane glycoproteins (GP), and the predominant autoantigens are known to be GPIb/IX and GPIIb/IIIa. In a recent study we reported that these antibodies frequently had a restricted light chain phenotype, thereby supporting a clonal origin. Similar findings and the presence of clonal B-cell populations in immune thrombocytopenias have been reported by others. In the present study we further explored the hypothesis of clonal B-cell expansions in chronic ITP. Twenty patients with chronic ITP were investigated. Antibodies were detected with an ELISA (MAIPA) specific for GPIb/IX and GPIIb/IIIa; circulating clonal B lymphocytes were assessed by flow-cytometric (FACS) clonal-excess analysis and by analyzing Ig-gene rearrangements (CDR3) with the PCR technique. Nine patients displayed a GP-specific antibody restricted to either kappa or lambda phenotype. However, FACS analysis and Ig-gene rearrangement studies did not disclose any circulating clonal B-cell population. Considering the sensitivity of the FACs analysis and Ig-gene rearrangement for detection of clonal B-cell populations, the hypothesis of clonally derived autoantibodies in ITP is still valid. Most probably, the clonal B-cell expansion responsible for the production of autoantibodies in ITP, if present, is below the detection limit for the techniques employed.

Adolescent↗

PubMed1996

Blood group A antigen expression in platelets is prominently associated with glycoprotein Ib and IIb. Evidence for an A1/A2 difference.

Blood group ABH antigens are associated with platelets as intrinsic determinants and extrinsically adsorbed antigens, and exist both on glycosphingolipids and on glycoproteins (GPs). We now provide direct evidence that the blood group ABH antigens are prominently associated with platelet GPIb and GPIIb. By immunoprecipitation, a murine monoclonal anti-A antibody precipitated surface-biotin-labelled blood group A1 platelet membrane proteins with electrophoretic characteristics identical to those of GPIb/IX and GPIIb/IIIa. By immunoblotting of SDS-PAGE separated blood group A1 platelet proteins the monoclonal anti-A antibody bound to proteins with electrophoretic characteristics identical to those of GPIb and GPIIb. When immunoaffinity purified GPIb/IX and GPIIb/IIIa, derived from blood group O, A1 and A2 platelets, were employed for immunoblotting, GPIb and GPIIb only from A1 platelets bound the monoclonal anti-A antibody. By ELISA, wherein monoclonal antibodies specific for GPIb (APl) and the GPIIb/IIIa complex (AP2) were used to capture and hold antigens from platelet lysate, human anti-A antibodies reacted with these proteins derived from blood group A1 platelets; proteins from blood group A2, O and B platelets showed no reactivity. These results indicate that blood group A antigen is associated with GPIb and GPIIb derived from blood group A1 but not A2 platelets.

ABO Blood-Group System↗

PubMed1996

Evidence for an expression of blood group A antigen on platelet glycoproteins IV and V.

Blood group ABO antigens are known to be carried by several platelet glycoproteins (GP), e.g. GPIb, GPIIa, GPIIb, GPIIa and PECAM. Beside these proteins, we recently observed that blood group A antigen was also expressed on some other uncharacterized platelet proteins (70-90 kDa) having electrophoretic mobilities closely resembling those of GPIV and GPV. These findings prompted us further to characterize these latter ABO-expressing platelet proteins. By antigen capture ELISA, wherein the monoclonal antibodies (mAbs) CLB-IVC7 and CLB-SWI6 were used to hold the corresponding antigens GPIV and GPV, human anti-A specifically bound to these proteins derived from A1-platelets; neither GPIV nor GPV derived from A2-, B- or O-platelets bound anti-A. In a Western blot assay using immunoprecipitated GPIV and GPV as antigens, mAb anti-A immunostained GPIV and GPV precipitated from A1, but not from A2 and O platelets. These results conclusively demonstrate that blood group A antigen is expressed on platelet GPIV and GPV.

ABO Blood-Group System↗

PubMed1996

Genotyping of the platelet-specific alloantigen HPA-5 (Br(a)/Br(b)) using polymerase chain reaction with sequencespecific primers (PCR-SSP).

A DNA-based one-stage technique, polymerase chain reaction with sequence-specific primers (PCR-SSP) was developed for genotyping of the platelet specific alloantigen HPA-5 (Bra/Brb). Sequence-specific primers, matching the wild type and the point mutation responsible for the HPA-5 (Bra/Brb) phenotype, were constructed. Conjointly a fragment of the gene coding for glycoprotein (GP) IIIa was amplified as an internal control of the enzyme reaction. Using these HPA-5 (Bra/Brb) sequence-specific primers the correct fragment of the GPIa gene was amplified, as evidenced by the PCR product size, the restriction map and by the nucleotide sequence. This assay was applied on 187 Swedish blood donors; 157 individuals were found to have a homozygous HPA-5a (Bra/Brb) genotype and 30 individuals a heterozygous HPA-5a,b (Bra/Brb) genotype. None of the donors was found to display a homozygous HPA-5b (Bra/Brb) genotype. Thus, the (HPA-5b) Bra antigen frequency in this population will be approximately 16.0% with a gene frequency of 8.0%. It is concluded that this assay is an attractive technique for genotyping of the HPA-5 (Bra/Brb) alloantigens on genomic DNA. The technique can replace serological alloantigen typing, especially in cases where platelets and rare human alloantisera are not available.

Adult↗

PubMed1996

[Usefulness of percutaneous transluminal coronary angioplasty in silent myocardial ischemia].

The usefulness of percutaneous transluminal coronary angioplasty (PTCA) was assessed in patients with exercise-induced asymptomatic myocardial ischemia (silent ischemia) and compared with exercise-induced symptomatic myocardial ischemia (symptomatic ischemia). Patients with single vessel coronary artery disease (51 with angina pectoris, 40 with old myocardial infarction) and evidence of stress-induced ischemia on thallium-201 single photon emission computed tomography (SPECT) underwent successful PTCA. Thirty-seven percent of angina patients and 60% of infarction patients showed asymptomatic exercise-induced ischemia. There was no significant difference in population characteristics between silent and symptomatic patients. Patients with silent angina had significantly higher percentage thallium uptake and washout rate than symptomatic patients. After PTCA, both percentage diameter stenosis and percentage thallium uptake were improved in all patients with angina irrespective of the presence or absence of symptoms. There were no significant differences in percentage thallium uptake and washout rate between patients with silent and symptomatic infarction. After PTCA, percentage diameter stenosis, percentage thallium uptake, and washout rate improved in all infarction patients irrespective of the symptoms. Zero percent of silent angina patients, 12% of symptomatic angina patients, 12% of silent infarction patients, 19% of symptomatic infarction patients had cardiac events during about 4.5 years after PTCA. The incidence of cardiac events did not significantly differ in any patient group. PTCA improved myocardial perfusion in all patients, and the incidence of cardiac events did not differ between the silent and symptomatic groups. Revascularization with PTCA is suitable for patients with silent as well as symptomatic ischemia.

Aged↗

PubMed1996

Naturally occurring IgG autoantibodies to platelet cytoskeleton tropomyosin.

We have observed that naturally occurring serum antibodies generated a 30 Kd band in a platelet immunoblot assay. The target protein had the same molecular weight (30 Kd) under nonreduced and reduced electrophoretic conditions, and could be immunoblotted from either autologous or homologous platelet lysates. Also, the 30 Kd reactive autoantibodies could be totally adsorbed by platelet cytoskeletons. From these data one likely candidate for the autoantibody target was the intracellular platelet protein tropomyosin. Indeed, a commercially available monoclonal anti-tropomyosin antibody reacted with proteins comigrating with this 30 Kd band; affinity purified human platelet tropomyosin was bound by the antibodies that recognized the 30 Kd protein. This body of evidence conclusively demonstrated that naturally occurring serum autoantibodies reacted with the platelet cyto-skeleton protein-tropomyosin. These tropomyosin specific antibodies were found in roughly the same percentage of sera from patients with chronic idiopathic thrombocytopenic purpura (ITP) as from normal individuals.

Adult↗

PubMed1995

Evidence for a light chain restriction of glycoprotein Ib/IX and IIb/IIIa reactive antibodies in chronic idiopathic thrombocytopenic purpura (ITP).

To address the assumption of clonally restricted antibodies in immune thrombocytopenias we studied sera from 19 patients with chronic ITP known to possess antibodies reactive with glycoprotein (GP) Ib/IX and/or GPIIb/IIIa. These sera were re-analysed using the standard monoclonal antibody immobilization of platelet antigens (MAIPA) assay and 16 patients exhibited IgG antibodies reactive with GPIIb/IIIa; seven patients showed also a reactivity with GPIb/IX. Employing a light-chain-specific MAIPA assay, 75% (12/16) of these sera displayed GPIIb/IIIa-specific antibodies that were light chain restricted; only 13% (2/16) of the GPIIb/IIIa reactive sera showed a mixed kappa and lambda phenotype. A light-chain-restricted phenotype was also seen for the GPIb/IX reactive antibodies. To further substantiate these findings, the MAIPA assay was modified in order to avoid interference from human anti-mouse antibodies. A high frequency of light-chain restricted platelet antibodies was also found using the modified MAIPA technique. These results support the hypothesis of a clonal B-cell expansion in immune thrombocytopenias, producing antibodies with a restricted idiotype repertoire and reacting with a limited number of epitopes.

Adult↗

PubMed1995

Fab-mediated binding of glycoprotein Ib/IX and IIb/IIIa specific antibodies in chronic idiopathic thrombocytopenic purpura.

The antibody domain responsible for the interactions between platelet glycoproteins (GP) and serum IgG autoantibodies in patients with chronic idiopathic thrombocytopenic purpura (ITP) was studied. Sera from nine non-transfused ITP patients and 20 normal controls and a serum containing an anti-PlA1 antibody were employed. Serum, purified IgG and F(ab')2 fragments were prepared and their binding to platelet GPIb/IX and GPIIb/IIIa were analysed using a modified MAIPA assay and an antigen capture ELISA. In all experiments most of the autoantibodies studied behaved identically to the anti-PlA1 antibody in that the IgG-F(ab')2 fragments retained their ability to bind to the respective glycoprotein. Substituting the enzyme-conjugated secondary antibody (Fab specific), in the MAIPA assay, with an Fc specific antibody removed all reactivities observed against platelet GPs, produced by IgG-F(ab')2 fragments. Furthermore, in an antigen-capture ELISA, IgG autoantibodies against platelet GPIb/IX and/or GPIIb/IIIa were blocked preferentially by pre-incubating the ITP sera with a goat anti-human IgG (F(ab')2 specific) antibody, but not with an anti-Fc antibody. We conclude that these ITP patients produced antibodies specific for platelet GPIb/IX and/or GPIIb/IIIa, and that the autoantibody-platelet interaction was mediated by the classic Fab binding.

Adult↗

PubMed1995

Glycoprotein IIb/IIIa autoantigenic repertoire in chronic idiopathic thrombocytopenic purpura.

The objective of the present study was to further disclose the autoantigenic repertoire carried by the platelet glycoprotein (GP) IIb/IIIa complex. IgG-F(ab')2 fragments were prepared from two prototype ITP patients, and their ability to block the binding of GPIIb/IIIa reactive antibodies derived from other patients with ITP was evaluated using a modified MAIPA asay; a PlA1 alloantiserum and 20 normal sera were included as controls. It was found that the two prototype IgG-F(ab')2 fragments were each able to significantly block the binding of serum IgG to GPIIb/IIa in six (55%) and seven (64%) out of 11 patients with chronic ITP, respectively. No significant blocking effect was observed for IgG-F(ab')2 fragments prepared from normal subjects. Also, the binding of the PlA1 alloantiserum to its epitope on GPIIIa was not affected by any of the blocking IgG-F(ab')2 fragments exploited in the study. These data substantiate that in chronic ITP at least half of the GPIIb/IIIa reactive sera bind to homogenous autoepitopes.

Adolescent↗

PubMed1995

Antibodies against platelet GPIb/IX, GPIIb/IIIa, and other platelet antigens in chronic idiopathic thrombocytopenic purpura.

Antibodies involved in the pathogenesis of chronic idiopathic thrombocytopenic purpura (ITP) react most frequently with platelet glycoprotein (GP) Ib/IX and GPIIb/IIIa. However, uncertainty as to the specificity, frequency, and clinical significance of such antibodies still remains. By using a modified antigen-capture ELISA (MACE), an immunoprecipitation assay, and an immunoblot assay, sera from 60 patients with chronic ITP were analyzed. GP-specific antibodies were found in 50% (30/60) of the patients, with 14 patients having antibodies directed solely to GPIIb/IIIa, 8 holding antibodies specific only for GPIb/IX, and 8 possessing antibodies against both antigens. Serum antibodies were more frequently (p < 0.01) detected in either active and/or non-splenectomized ITP patients. Moreover, in patients displaying antibodies against GPIb/IX, significantly (p < 0.05) lower platelet counts were observed. Using the immunoblot assay, antibodies specific for a 30 kD platelet antigen were detected in 12 of 60 patients. This antigen could not be immunoprecipitated from surface labelled platelet membranes, indicating an intracellular location. We conclude that in chronic ITP, (1) the frequency of anti-GPIIb/IIIa antibodies is close to that of anti-GPIb/IX antibodies, (2) anti-GP antibodies are more likely to be detected in patients with an active disease status and, (3) a 30 kD internal platelet protein is another frequent antigen.

Adult↗

PubMed1994

Secretion of progesterone and 20 alpha-dihydroprogesterone during the estrous cycle in goats.

The secretion of progesterone and 20 alpha-dihydroprogesterone (20 alpha-DHP) during the estrous cycle and the effects of prostaglandin F2 alpha (PGF2 alpha) and 20 alpha-DHP on the secretion of these two steroids during the midluteal phase in goats were studied. The mean progesterone concentration in the peripheral plasma was extremely low (< 0.01 ng/mL) on the day of estrus. The concentration increased to a maximum (7.80 ng/mL) on about day 10 after estrus, and decreased rapidly during the last 3 days of the cycle. The plasma concentration of 20 alpha-DHP also was low (0.86 ng/mL) on the day of estrus, but increased gradually after estrus and decreased gradually in the last 5 days of the cycle (to 3.22 ng/mL). The ratio of progesterone to 20 alpha-DHP was > 1 after day 2 of estrus, but decreased and fell to < 1 during the last 3 days of the cycle. An injection of 3 mg of PGF2 alpha decreased the secretion of progesterone within 30 min, but affected the secretion of 20 alpha-DHP little until 2 h. The ratio of progesterone to 20 alpha-DHP fell to < 1 after 24 h. Three of the five goats given such an injection came into estrus within 2 days, and the other two came into estrus within 3 days. An injection of 15 mg of 20 alpha-DHP did not affect progesterone secretion or the estrous cycle length. These results indicate that in the goat after estrus, there is much 20 alpha-DHP in the peripheral plasma. Progesterone may be catabolized to the biologically inactive steroid, 20 alpha-DHP, during luteolysis.

20-alpha-Dihydroprogesterone↗

PubMed1994

[Pathological and immunohistochemical study on anorectal melanoma].

Forty two cases of anorectal melanoma were studied which constituted 1.19% of all the anorectal malignancies collected in this series. 90% of the tumors located near by the dentate line. Grossly, the masses were nodular, fungiform or ulcerated. Histologically, pleomorphic tumor cells mixed together giving a feature somewhat like either carcinomatoid or sarcomatoid, with a predominance of one kind of the malignant cells. Histopathologic observation supported the idea that this tumor developed from the melanocytes and nevus cells located at the basal layer of the epithelium. Immunohistochemistry proved that melanocytes originated from the neural crest. S-100 protein was marker with high sensitivity but the specificity not ideal, so that, varied markers are recommended in order to improve the accuracy of diagnosis.

Adult↗

PubMed1994

Evaluation of the efficacy of nicorandil in patients with ischemic heart disease by exercise Tl-201 myocardial SPECT.

The effect of nicorandil on myocardial perfusion in ischemic heart disease was studied using exercise-load Tl-201 myocardial SPECT (Ex-SPECT). ExSPECT was carried out in 12 patients with previous myocardial infarction (OMI) and 9 with angina pectoris (AP) before and after administration of nicorandil 15 mg/day, for three or more weeks; %Tl uptake and the washout rate in infarcted or ischemic areas were calculated from short axial images using the Bull's eye method. In the OMI group, %Tl uptake and washout rates in the infarction areas improved significantly from 52.4% and 0.25 before nicorandil to 60.4% and 0.38 after nicorandil. In the AP group, too, %Tl uptake and washout rates showed a significant improvement from 56.9% and 0.10 before to 69.1% and 0.33 after administration of nicorandil. Six subjects who had not received the drug, and who showed negative washout rates, had high improvement rates when nicorandil was administered, suggesting that the drug could increase myocardial perfusion during exercise loading as well as suppressing coronary spasm. Ex-SPECT was carried out in 4 subjects before and after the administration of nicarandil and after subsequent surgical treatment (PTCA or CABG) and the effects of the two therapies were compared. The washout rate was improved from 0.01 to 0.34 by the administration of nicorandil, and a notable increase in coronary artery blood flow was achieved compared to the level after surgical treatment, i.e. 0.50. It is concluded that normal dosages of nicorandil have a powerful direct effect of dilating the coronary arteries without any influence on preload or afterload.

Adult↗

PubMed1993

[A study on RBC immunofunction in experimental traumatic uveitis].

Examination of the RBC immunofunction in rabbit experimental traumatic uveitis with Guo's method of complement-labelled yeast revealed that the percentage of RBC C3b receptor rosette and the activity of red cell immune adherence (RCIA) enhancing factor in sera were markedly lower, while the percentage of RBC surface immune complex rosette, the activity of the RCIA-inhibiting factor and the CIC in sera were higher than those in the normal controls, indicating that the lowered RBC immunofunction was involved in pathogenesis of the experimental traumatic uveitis.

Animals↗

PubMed1992

[Effect of Cordyceps sinesis on T-lymphocyte subsets in chronic renal failure].

Synchronous measurements of renal function and T-cell subsets were taken in 51 cases of chronic renal failure (CRF) patients. Cordyceps sinesis 3-5 g/d was given to 28 out of these 51 patients, which was considered as follow-up group. The results were stated as follows: (1) Obvious decrease of OKT3, OKT4, OKT4/OKT8 was found in CRF (P < 0.01). (2) OKT4 and OKT4/OKT8 were proportional to plasma albumin and Hb levels (P < 0.05). (3) After administration of Cordyceps sinesis, improvement of renal function and OKT4, OKT4/OKT8 were confirmed. This study indicated that cellular immune function was decreased in CRF. Administration of Cordyceps sinesis might improve their renal function and as the same time enhance the cellular immune function in CRF.

Adult↗