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Biomedical subjects

T Yoshio

Publications and source records attributed to T Yoshio.

At least 37 records · Page 2Linked to original sources
PubMed1998

Acute acalculous cholecystitis in systemic lupus erythematosus: a case report and review of the literature.

A 27-year-old woman with systemic lupus erythematosus (SLE) was found to have acute acalculous cholecystitis. At the time of admission, the patient was not under corticosteroid or immunosuppressive therapy. Computed tomography (CT) and ultrasonography revealed findings in the gall bladder consistent with acute acalculous cholecystitis. Her abdominal pain completely disappeared following corticosteroid therapy, with dramatic improvement in the images of CT and ultrasonography. Six similar cases of SLE complicated with acute acalculous cholecystitis have been reported in the literature and they were all treated surgically by cholecystectomy or cholecystostomy. This is the first case report in which acute acalculous cholecystitis accompanying SLE was treated successfully by corticosteroid without surgical intervention.

Acute Disease↗
PubMed1998

A close temporal relationship of liver disease to antiribosomal P0 protein antibodies and central nervous system disease in patients with systemic lupus erythematosus.

OBJECTIVE: To determine whether there is a close temporal relationship of liver disease to serum IgG and/or IgM antiribosomal P0 protein antibodies (anti-P0) and central nervous system (CNS) lupus in patients with systemic lupus erythematosus (SLE). METHODS: The study included 70 patients with active SLE. Of these, 30 had IgG and/or IgM anti-P0 and 14 had CNS lupus other than psychiatric disease (nonpsychiatric CNS lupus). Of these 14 patients, 11 had anti-P0. Laboratory manifestations of liver disease were retrospectively analyzed. RESULTS: Liver disease not attributed to any cause other than SLE (SLE liver disease) was present in 8 of the 11 patients with anti-P0 with nonpsychiatric CNS lupus (72.7%), in none of the 19 patients with anti-P0 without nonpsychiatric CNS lupus (0%), and in one of the 40 patients without anti-P0 (2.5%). The prevalence of SLE liver disease was significantly greater in patients with anti-P0 with nonpsychiatric CNS lupus than in the other 2 groups (p < 0.0001). Mean levels of liver enzymes (lactate dehydrogenase, glutamic oxaloacetic transaminase, glutamate pyruvate transaminase, gammaglutamyl transpeptidase) were significantly higher in patients with anti-P0 with nonpsychiatric CNS lupus than in the other 2 groups. Serial studies in 3 patients showed that the appearance of anti-P0 and liver dysfunction slightly preceded the onset of nonpsychiatric CNS lupus. CONCLUSION: Anti-P0 may be related to the pathogenesis of CNS lupus and SLE liver disease found simultaneously in SLE. The appearance of anti-P0 and liver dysfunction may predict onset of CNS lupus.

Adolescent↗
PubMed1997

Preferential binding with Escherichia coli hsp60 of antibodies prevalent in sera from patients with rheumatoid arthritis.

One hundred thirty-two patients with various connective tissue disorders, including 60 with rheumatoid arthritis (RA), had antibodies against human as well as Escherichia coli hsp60 in titers significantly higher than those of normal controls. There was a correlation between titers of antibody to human hsp60 and those to E. coli hsp60. Levels of antibodies against human and E. coli hsp60 were lower in joint fluids than in sera, indicating little production of antibodies in the joint. Antibodies affinity-purified with E. coli hsp60 bound strongly with the homologous hsp60, but weakly with human hsp60. However, antibodies affinity-purified with human hsp60 bound comparably with both E. coli hsp60 and human hsp60. Antibodies affinity-purified with Mycobacterium tuberculosis hsp65 bound to human hsp60 with a reactivity similar to the reactivity of those affinity-purified with human hsp60. The reactivity to the three hsp60 species was lost when sera were absorbed with E. coli hsp60, while the reactivity to E. coli hsp60 remained after extensive absorption with M. tuberculosis hsp65 or human hsp60. These results indicate that anti-hsp60 antibodies in patients with RA and other connective tissue disorders are raised by infection with intestinal microorganisms such as E. coli. They may represent another example of autoimmune responses triggered by antigenic mimicry of host proteins to microbes and suggest that the reactivity of antibodies from RA patients with M. tuberculosis hsp65 might have been a cross-reaction with the E. coli homologue.

Antibodies↗
PubMed1997

Undectable expression of hMLH1 protein in sporadic colorectal cancer with replication error phenotype.

PURPOSE: Four DNA mismatch repair genes have been identified as being susceptible genes for hereditary nonpolyposis colorectal cancer. Deficiency of one of the mismatch repair genes causes the replication error phenotype in more than 80 percent of patients with hereditary nonpolyposis colorectal cancer and in 10 to 30 percent of patients with sporadic colorectal cancer. To determine which mismatch repair gene is lacking the function in patients with replication error-positive colorectal cancer, several approaches have been used at the nucleic acid and protein levels. We studied replication error in 40 samples of randomly selected colorectal cancers and expression of hMSH2 and hMLH1 proteins analyzed by immunoblot in the tumor and normal tissues of the replication error-positive and replication error-negative samples. MATERIALS AND METHODS: Frozen tumor and normal tissues were obtained from 40 Japanese patients who had colorectal cancer. According to the Amsterdam criteria, those patients were classified as having 39 sporadic and 1 unknown colorectal cancers. Genomic DNA was extracted from tumor and normal tissues for determining replication error with eight microsatellite markers. Expression of hMSH2 and hMLH1 proteins in cell lysates of tumor and normal tissues of 16 patients was analyzed by immunoblot. RESULTS: The replication error phenotype was found in 6 (15 percent) of the 39 sporadic cases. hMLH1 protein was not detected in two of the six replication error-positive tumor tissues and not in the normal tissues, indicating that the tumor cells of the two patients had severe mutations in both alleles of the hMLH1 gene. Another four replication error-positive and ten replication error-negative tumors and normal tissues expressed hMLH1 protein. hMSH2 protein was detected in all samples. CONCLUSION: hMLH1 protein was undetectable in the two tumor tissues of the six replication error-positive samples of sporadic colorectal cancer. The detection procedure used here may have potential use for determining a dysfunctional mismatch repair gene product.

Adaptor Proteins, Signal Transducing↗
PubMed1997

Association of interleukin 6 release from endothelial cells and pulmonary hypertension in SLE.

OBJECTIVE: To investigate how sera from 37 patients with systemic lupus erythematosus (SLE) stimulate interleukin (IL) 6 release from IL-1beta pretreated endothelial cells and compare these effects to those of sera from 16 normal controls. METHODS: Endothelial cells pretreated 18 h with IL-1beta (5 U/ml) were incubated 2 h with sera diluted 10-fold with phosphate buffered saline (PBS). IL-6 concentrations in endothelial culture supernatants collected after incubation were measured by ELISA. RESULTS: Compared with PBS, sera from controls and 24 patients with SLE suppressed IL-6 release from IL-1beta pretreated cells. However, sera from 13 patients with SLE augmented IL-6 release. Of note, sera from 5 patients with pulmonary hypertension induced the highest level of IL-6 release. IgG from control sera suppressed IL-6 release, whereas F(ab')2 did not. Both IgG and F(ab')2 from the sera of patients with SLE with pulmonary hypertension augmented IL-6 release from IL-1beta pretreated cells. CONCLUSION: IgG antiendothelial cell antibodies from patients with SLE may be associated with the pathogenesis of SLE and pulmonary hypertension.

Adolescent↗
PubMed1997

Detection of large macrophage colony forming cells in the peripheral blood of patients with rheumatoid arthritis.

OBJECTIVE: To test for the presence of colony forming cells, that form large macrophage colonies (> 2.5 mm in diameter, > 10,000 cells), in the peripheral blood of patients with rheumatoid arthritis (RA) and to determine its association with the clinical and laboratory features of RA. METHODS: Peripheral blood mononuclear cells (PBMC) from 96 patients with RA and 20 healthy controls were assayed for in vitro colony formation. In addition, PBMC from 38 patients with other rheumatic diseases including systemic lupus erythematosus (SLE), progressive systemic sclerosis (SSc), and polymyositis/dermatomyositis (PM/DM); 23 patients with infectious inflammatory diseases were also assayed. RESULTS: Large macrophage colony forming cells were detected in the peripheral blood of 19% of patients with RA (18/96), but not in that of healthy controls. In addition, these cells were detected in the peripheral blood of 11 of the 38 patients with other rheumatic disease (7/13 SSc and 4/11 PM/DM), but not in the 23 patients with infectious diseases. In the patients with RA, interstitial lung disease was significantly more frequently observed among patients in whom colony forming cells were found than among those in whom they were not found (p < 0.001). CONCLUSION: Based on the size of the colonies they formed, the macrophage colony forming cells detected in patients with RA probably corresponded to primitive hematopoietic progenitor cells, defined as high proliferative potential colony forming cells (HPP-CFC). Our observations provide preliminary evidence of the appearance of HPP-CFC in the circulation during inflammation of RA, and during that in other rheumatic diseases such as SSc and PM/DM, and of the association of HPP-CFC with interstitial lung disease in patients with RA.

Adult↗
PubMed1996

Selective accumulation of anti-histone antibodies in glomeruli of lupus-prone lpr mice.

Immunoglobulins were eluted from glomeruli of 50 lupus-prone, lpr mice and their physicochemical properties and specificity were compared with those in sera pooled from the same mice. Although immunoglobulins in glomeruli had higher isoelectric points than those in sera, there were no appreciable differences in the relative contents of neutral and acidic immunoglobulins between them. The proportion of IgG3 subclass was slightly higher in glomerular than serum immunoglobulins. Both anti-single-stranded and anti double-stranded DNA antibodies were twofold higher in glomerular than serum immunoglobulins, while anti-Sm antibodies were not recovered in glomerular eluate despite their high activity in serum. Antibodies in glomerular eluate reacted most strongly with histones, especially with core histones, while those in sera bound preferentially with histone H1, Sm-B, -B', and -D antigens. Since histones are very basic, they would have a higher affinity for negatively charged glomerular constituents, leading to an in situ formation of immune complexes involving fixed histones and their binding with antibodies for the induction of nephritides. Otherwise, such immune complexes themselves might retain positive charges sufficient for an affinity with the glomerular basement membrane. These results indicate that histone-anti-histone antibody system may play a role in the perpetuation of murine lupus nephritis.

Animals↗
PubMed1996

Histiocytic cytophagic panniculitis which developed during interferon-alpha therapy.

A 59-year-old woman developed edema of the face and eyelids during interferon (IFN)-alpha-2b therapy for chronic hepatitis C with a cumulative dose of 6 million x 47 units. Despite cessation of the therapy, the edema progressed and was followed by exophthalmos, pyrexia, liver dysfunction, pancytopenia, and disseminated intravascular coagulation. Two months after initial presentation, she died of hemorrhagic shock and was diagnosed with histiocytic cytophagic panniculitis at autopsy. This may be a hitherto unrecognized adverse effect of therapeutic IFN alpha.

Antiviral Agents↗
PubMed1995

Endothelin-1 release from cultured endothelial cells induced by sera from patients with systemic lupus erythematosus.

OBJECTIVES: To clarify the pathophysiological role of endothelin-1 (ET-1) in the vascular injury associated with systemic lupus erythematosus (SLE) by investigating the effect of sera from patients with SLE on ET-1 release from cultured human umbilical vein endothelial cells. METHODS: Confluent monolayers of cultured human umbilical vein endothelial cells were incubated with serum samples (diluted 1:10) from 25 patients with SLE and 16 normal controls for two hours at 37 degrees C and ET-1 concentration in the culture supernatant was measured by enzyme immunoassay. RESULTS: The mean release of ET-1 from endothelial cells in the presence of serum from SLE patients was greater than in the presence of serum from normal controls (p < 0.005). ET-1 release from endothelial cells significantly correlated with the titre of IgM anti-endothelial cell antibodies (IgM-AECA) and immune complex concentration in sera from SLE patients (p < 0.05 and p < 0.01, respectively). After gel chromatography of the serum from an SLE patient, those fractions containing IgM-AECA or immune complex were shown to stimulate ET-1 release from endothelial cells. Heat aggregated IgG also stimulated ET-1 release from endothelial cells in a concentration dependent manner. CONCLUSIONS: IgM-AECA and immune complexes may stimulate ET-1 release from endothelial cells and ET-1 may play an important role in the initiation and development of vascular injury, such as pulmonary hypertension and lupus nephritis, in SLE.

Adolescent↗
PubMed1995

[Progressive systemic sclerosis (PSS) and cancer--increasing coincidence rate of cancer in 67 PSS patients].

The coincidence rate of cancer and PSS has been increasing according to reports from Nippon Byori Boken Shuho (Annual of Pathological Autopsy Cases in Japan), reaching 12.3% in the most recent report. Therefore we reviewed the histories of 67 PSS patients seen at our division over an 18-year period between 1974 and 1992, and found a high coincidence rate (14.6%) of cancer, reflecting the increasing tendency reported in the Nippon Byori Boken Shuho. The most frequent type of cancer was gastrointestinal cancer, including gastric and colon cancer and duodenal carcinoid. There were no significant differences in the clinical and laboratory findings between PSS patients with cancer and those without. Twenty-six of the 67 PSS patients died. Cancer was the cause of death in four, ranking second behind respiratory failure. The reason for the increasing coincidence rate of cancer and PSS is unclear at present. However, it is very important to discover cancer in PSS patients as early as possible, since it has a marked effect on prognosis.

Adult↗
PubMed1995

Quantification of antiribosomal P0 protein antibodies by ELISA with recombinant P0 fusion protein and their association with central nervous system disease in systemic lupus erythematosus.

OBJECTIVE: Using solid phase ELISA with recombinant P0 fusion protein as the antigen for detecting antiribosomal P0 protein antibody, we analyzed the association of this antibody and anticardiolipin antibody (aCL) with central nervous system (CNS) disease in patients with active systemic lupus erythematosus (SLE). METHODS: Sera from 70 randomly selected Japanese patients with active SLE were assayed for IgG and IgM antiribosomal P0 protein antibody titers and IgG aCL. RESULTS: IgG and IgM antiribosomal P0 protein antibodies were present in 29 and 12 (41.4 and 17.1%) of the 70 patients, respectively. The incidence of CNS disease, excluding lupus psychosis, was significantly higher in patients with IgG and IgM antiribosomal P0 protein antibodies than in those who lacked them (IgG antiribosomal P0 protein antibody 11/29 vs 3/41; IgM antiribosomal P0 protein antibody 7/12 vs 7/58). In addition, both IgG and IgM antiribosomal P0 protein antibody titers were significantly higher in patients with CNS disease, excluding lupus psychosis, than those without. No significant association was observed between antiribosomal P0 protein antibodies and lupus psychosis. No significant association was observed between IgG aCL and CNS disease. Serial studies of antiribosomal P0 protein antibodies and aCL in patients with transverse myelopathy also showed that IgG and IgM antiribosomal P0 protein antibodies, but not IgG aCL, were associated with CNS disease, excluding lupus psychosis. CONCLUSION: These data suggest a strong association of IgG and IgM antiribosomal P0 protein antibodies with CNS disease, excluding lupus psychosis, in SLE.

Adolescent↗
PubMed1994

Antiendothelial cell antibodies and their relation to pulmonary hypertension in systemic lupus erythematosus.

OBJECTIVE: Antiendothelial cell antibodies (aECA) have been demonstrated in patients with systemic lupus erythematosus (SLE), but their role in the pathogenesis of this disease remains unclear. We investigated the association of aECA and anticardiolipin antibodies (aCL) with clinical and laboratory findings in patients with active SLE. METHODS: Sera from 28 patients with active SLE and 22 healthy controls were assayed for IgG and IgM-aECA by cellular ELISA method using cultured human umbilical vein endothelial cells and IgG-aCL by ELISA method. RESULTS: Serum titers of both IgG and IgM-aECA were significantly higher in active SLE than in healthy controls. Titers of IgG-aECA were unrelated to titers of IgG-aCL. Patients with pulmonary hypertension demonstrated a marked elevation of serum titer of both IgG and IgM-aECA compared with patients without pulmonary hypertension. In addition, patients with digital vasculitis showed a significant elevation of serum titer of both IgG and IgM-aECA compared with patients without digital vasculitis. Serum titers of IgG-aECA in patients with Raynaud's phenomenon and of IgM-aECA in patients with serositis were each significantly increased compared with patients without such findings. CONCLUSION: aECA were unrelated to aCL. Serum titers of aECA are elevated in patients with active SLE, especially with pulmonary hypertension, digital vasculitis, Raynaud's phenomenon or serositis. Since pulmonary hypertension in SLE has been associated with digital vasculitis, Raynaud's phenomenon and serositis, aECA may be involved in the pathogenesis of vascular injury, leading to these manifestations.

Antibodies, Anticardiolipin↗
PubMed1994

[Study on relationship between intratumoral DNA heterogeneity and clinicopathological findings in colorectal cancer].

We studied the relationship between intratumoral DNA heterogeneity and clinicopathological findings in 85 colorectal cancers. DNA ploidy was analyzed in 5 specimens from different sites of each tumor. When the difference in the DNA index (D.I) between several peaks in the same tumor was more than 0.1, the tumor was considered to consist of heterogeneous subpopulations with different DNA clones. DNA heterogeneity was found in 34 cases (40.0%). There was no relationship between DNA heterogeneity and depth of tumor invasion, lymph node metastasis or stage. The incidence of heterogeneity was significantly higher in the tumor with lower differentiation, liver metastasis or vessel invasion.

Colorectal Neoplasms↗
PubMed1993

[Two cases of pneumococcal septic arthritis complicating rheumatoid arthritis].

It is reported that most of the causative organisms of suppurative arthritis complicating rheumatoid arthritis (RA) is Staphylococcus aureus and that Streptococcus pneumoniae is rare, representing less than 5% of cases of suppurative arthritis complicating RA. We here report two cases of pneumococcal septic arthritis complicating RA. Both were female, and 68 and 64 years old, respectively. They had active, long-standing RA with destructed changes. Infected joints included both knees (case 1) and right knee (case 2). Pain and loss of motion in the septic joints were prominent. On admission, the physical examination showed severe redness, swelling and tenderness of the septic joints and the range of motion of those was markedly decreased. The radiograph of affected joints showed stage III. Laboratory data showed markedly elevated ESR of 127 mm/hr (case 1) and 142 mm/hr (case 2) and C-reactive protein of 49.91 mg/dl (case 1) and 30.36 mg/dl (case 2). Aspirate of the left knee of case 1 showed numerous neutrophils. Cultures of the joint fluid grew S. pneumoniae. Grossly purulent material was aspirated from the right knee of case 2 and cultures also grew S. pneumoniae. They were started on intravenous antibiotics with a good response and the function of involved joints returned to preseptic condition. The source of infection on case 1 was presumed to be otitis media because she had discharge from left ear concurrently with the exacerbation of joint symptoms. Case 2 had productive cough and cultures of sputum also disclosed S. pneumoniae when pain of right knee joint developed. The suggested source of infection was upper respiratory tract.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[Anti-endothelial cell antibodies].

Anti-endothelial cell antibodies (AECA) are demonstrated in connective tissue diseases (CTD) such as systemic lupus erythematosus (SLE) and progressive systemic sclerosis (PSS), but their role in the pathogenesis of CTD is unknown. Sera from 33 patients with SLE, 10 patients with PSS, 10 patients with polymyositis/dermatomyositis, 10 patients with mixed connective tissue diseases, 6 patients with rheumatoid arthritis (RA), 6 patients with malignant RA and 22 normal controls were examined for IgG-AECA and IgM-AECA by cellular ELISA method using cultured human umbilical vein endothelial cells. Each patient group except RA had significantly elevated levels of both IgG-AECA and IgM-AECA compared with that of normal controls. Furthermore, the possible relationship of AECA to clinical and laboratory findings in 28 patients with active SLE was analysed. The levels of both IgG-AECA and IgM-AECA in patients with either pulmonary hypertension (PH) or digital ulcer were significantly increased compared with those in patients without such abnormalities. IgG-AECA levels in patients with Raynaud's phenomenon and IgM-AECA levels in patients with serositis were significantly increased compared with those in patients without such abnormalities. PH and digital ulcer result from vasculitis and PH in SLE is reported to be associated with Raynaud's phenomenon, digital ulcer and serositis. These results suggest that AECA might play an important role in the pathogenesis of vasculitis and vascular injury in these organs. Further studies are required to characterize the nature of endothelial cell antigens with which AECA react and the role of AECA in vascular injury.

Arteritis↗