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Biomedical subjects

J Masuyama

Publications and source records attributed to J Masuyama.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1996

Activation of human monocyte functions by tumor necrosis factor: rapid priming for enhanced release of superoxide and erythrophagocytosis, but no direct triggering of superoxide release.

Tumor necrosis factor (TNF), like granulocyte-macrophage colony-stimul ating factor (GM-CSF), rapidly primed human monocytes for enhanced release of superoxide (O-2) stimulated by receptor-mediated agonists, N-formyl-methionyl-leucyl-phenylalanine (FMLP) and concanavalin A (Con A), but not by phorbol myristate acetate (PMA), which bypasses the receptors to stimulate the cells. The optimal priming was obtained by pretreatment of suspended monocytes with 10 U/mL TNF for 10 minutes at 37 degrees C. The potency of the maximal priming effect was TNF> GM-CSF, and the combined effect of TNF and GM-CSF was greater than that of each cytokine alone. GM-CSF induced an increase in cytoplasmic pH but TNF did not. These findings suggest that TNF and GM-CSF activate monocytes through different mechanisms. TNF and GM-CSF by themselves never triggered O-2 release in suspended monocytes or monocytes adherent to endothelial cells, although both cytokines triggered massive release of O-2 in human neutrophils. In additions, TNF and GM-CSF induced tyrosine phosphorylation of a 42-kD protein in neutrophils but not in monocytes. These findings suggest that the TNF-receptor- or GM-CSF-receptor-mediated signaling pathways for triggering O-(2) release is active in neutrophils but inactive or defective in monocytes. TNF also enhanced phagocytosis of sialidase-treated autologous erythrocytes by monocytes, and this effect was further potentiated in the presence of autologous fresh serum. The significant enhancement of erythrophagocytosis was obtained at 1 U/mL TNF. At this concentration of TNF, the expression of C3bi-receptor (CD11b/CD18) was upregulated. These findings show that TNF rapidly primes human monocytes for enhanced release of O-(2) and erythrophagocytosis and suggest that TNF activates monocytes through autocrine or paracrine mechanisms at the inflammatory sites inasmuch as TNF is primarily produced by activated monocytes/macrophages.

Adult↗
PubMed1995

Migration of distinct subsets of CD8+ blood T cells through endothelial cell monolayers in vitro.

The immune response in many infections and to allografts is dependent on CD8+ cytotoxic T lymphocytes (CTL). Influx of CD8+ CTL from the blood has been documented during antigen challenge. We have previously found that a subset of CD8+ T cells from normal blood can migrate through endothelial cell monolayers in vitro. To further characterize migration-prone CD8+ T cells from normal blood, we examined the expression of CD28 and a restricted epitope of CD18/CD11a (S6F1), a CTL marker. Although normal blood CD8bright+ T cells were heterogeneous in their expression of CD28, three populations could be identified (CD28low, CD28moderate, and CD28high). CD8+ cells migrating across endothelial cell monolayers were enriched for CD8bright+ CD28high cells and a subset of CD8dim+ cells, which were CD28high. Both adherent and migrating CD8+ cells were exclusively (> 95%) S6F1high. There was also preferential adhesion and migration of CD8+ cells expressing the low-molecular-weight form of the leukocyte common antigen, CD45RO. Cytokine activation of the endothelium did not significantly alter preferential migration of these subsets. These data suggest that certain subsets of CD8+ memory T cells in normal human blood are prone to, adhere to, and migrate through allogeneic endothelial cells and would thus be likely to be recruited to sites of antigen challenge.

Adult↗
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

Suppressive role of endogenous endothelial monocyte chemoattractant protein-1 on monocyte transendothelial migration in vitro.

Monocyte chemoattractant protein-1 (MCP-1, or monocyte chemotactic and activating factor) is thought to play an important role in monocyte infiltration into tissue, but little is known about its effect on monocyte-endothelium interaction. We examined the effect of MCP-1 produced by cytokine-activated endothelial cells (ECs) on monocyte-endothelium adhesion and subsequent transendothelial migration by using a double-chamber vessel model. Unstimulated ECs showed no MCP-1 expression, but exposure to interleukin-1 beta (IL-1 beta, 25 U/mL) induced marked MCP-1 mRNA expression and protein synthesis. When placed in the lower compartment, recombinant human (rh) MCP-1 (100 ng/mL) produced a 1.9-fold and a 2.7-fold increase in adhesion and migration, respectively, compared with a corresponding 51% and 59% decrease when placed in the upper compartment. Migration of monocytes was dependent on a gradient of rh-MCP-1 from the apical to basilar side of the EC layer. Furthermore, a forward gradient of MCP-1 induced adherent cells to increase their subsequent migration, whereas a reverse gradient induced the cells to detach and completely inhibited their subsequent migration. Pretreatment with IL-1 beta for 4 and 24 hours produced a 20% and 63% increase in monocyte migration, respectively. In the presence of anti-MCP-1 antibody, the increase was further enhanced by 52% and 152%, respectively. These results suggest that endogenous endothelial MCP-1, when secreted by IL-1-stimulated ECs, suppresses monocyte migration in the presence of MCP-1 on the basilar side of the EC layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies↗
PubMed1995

Induction of monocyte chemoattractant protein-1 synthesis in human monocytes during transendothelial migration in vitro.

Monocyte chemoattractant protein-1 (MCP-1, or monocyte chemotactic and activating factor) plays important roles in the recruitment of monocytes and thus in the development of atherosclerosis. In this study, we determined whether MCP-1 synthesis was induced by the cellular interaction between monocytes and endothelial cells during the process of transendothelial migration. We found that when human peripheral blood monocytes (2.5 x 10(6) cells) and umbilical vein endothelial cells (HUVECs; 5.0 x 10(5) cells) were cocultured for 5 hours, 7.9 ng/mL MCP-1 was secreted into the medium, whereas when the two were cultured separately, MCP-1 levels were 1.0 and 0.9 ng/mL, respectively. Furthermore, the use of interleukin-1 beta (IL-1 beta)-pretreated HUVECs in cocultures induced twice the levels of MCP-1 as in unstimulated HUVEC culture. Conditioned medium had transendothelial chemotactic activity for monocytes, and this activity was completely abolished by addition of anti-MCP-1 antibody. Although MCP-1 mRNA levels were very low or undetectable in HUVECs or monocytes alone, message could be detected after 2 hours of coculture in total mRNA preparations from both monocytes and HUVECs. mRNA levels increased by 4 hours and had declined slightly by 24 hours. The rapid induction of message suggests that cell contact between monocytes and HUVECs induces the de novo synthesis of MCP-1 protein. Anti-interleukin (IL)-1 alpha/beta and anti-tumor necrosis factor-alpha antibodies, or anti-lymphocyte function-associated antigen-1 and very late antigen-4 antibodies, had little or no inhibitory effects on MCP-1 secretion by cocultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion Molecules↗
PubMed1995

Effects of endogenous endothelial interleukin-8 on neutrophil migration across an endothelial monolayer.

OBJECTIVE: Recent studies suggest that interleukin-8 (IL-8) is involved in the neutrophil infiltration of subendothelial myocardial tissue in the ischaemia/reperfusion injury associated with acute myocardial infarction. The aim of this study was to investigate the effects of IL-8 on transendothelial neutrophil migration using an in vitro three dimensional double chamber migration assay system. METHODS: Human neutrophils were incubated with human endothelial cell monolayers for 1 h, and adherent and migrated neutrophils were then counted. Expression of IL-8 mRNA and secretion of its protein by endothelial cells were analysed respectively by northern blotting and ELISA. RESULTS: Recombinant human (rh) IL-8 (50 ng.ml-1) placed in the lower compartment significantly increased neutrophil adhesion 1.7-fold and transmigration 2.3-fold, compared with control conditions using medium alone in both compartments. In contrast, rh IL-8 (50 ng.ml-1) in the upper compartment significantly inhibited neutrophil adhesion and transmigration by 53% and 61% respectively compared with controls. Neutrophil adhesion and transmigration was dependent on the IL-8 concentration gradient between upper and lower compartments. Unstimulated endothelial cells showed no IL-8 expression, but endothelial cells pretreated with IL-1 beta (25 U.ml-1) markedly induced endogenous IL-8 mRNA and protein accumulation. When endothelial cells were cocultured with neutrophils, enhanced endogenous IL-8 production was observed. Pretreatment of endothelial cells with IL-1 beta for 4 and 24 h increased neutrophil transmigration 2.8-fold and 3.0-fold respectively, compared with unstimulated endothelial cells. The addition of anti-IL-8 monoclonal antibody (12.5 micrograms.ml-1) to the upper compartment with IL-1 beta-pretreated endothelial cells further enhanced transmigration from 2.8- to 3.3-fold and from 3.0- to 4.3-fold respectively. CONCLUSIONS: Endogenous endothelial IL-8, secreted from activated endothelial cells into the apical side of endothelial cell monolayers, has an inhibitory effect on transendothelial migration of neutrophils, suggesting that IL-8 may prevent excessive neutrophil infiltration of myocardial tissue from circulating blood in the reperfusion injury associated with acute myocardial infarction.

Blotting, Northern↗
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

Involvement of adhesion molecules in human monocyte adhesion to and transmigration through endothelial cells in vitro.

Although the accumulation of monocyte-derived foam cells in the subendothelium is a key step in early atherogenesis, the mechanism responsible for monocyte adhesion to and subsequent transmigration through endothelial cells (ECs) has not been defined fully. We investigated the kinetics and the role played by adhesion molecules in the adhesion and transmigration of human monocytes using an in vitro three-dimensional model system comprising ECs cultured on collagen gels. Monocyte adhesion to untreated EC layers increased with time, reached a maximum after 3 h, and then declined. Monocyte transmigration through untreated EC layers also increased with time and reached a plateau after 3-4 h. Prestimulation of ECs with interleukin-1 beta (IL-1 beta; 25 U/ml) for 4 h enhanced monocyte adhesion (40.7 +/- 1.4%) and transmigration (37.9 +/- 1.6%) significantly compared with the value for untreated EC layers. In unstimulated EC layers, anti-leukocyte function-associated antigen-1 (LFA-1) plus anti-intercellular adhesion molecule-1 (ICAM-1) monoclonal antibodies (mAbs) inhibited monocyte adhesion and transmigration significantly by 19% and 20%, respectively, whereas anti-very late antigen-4 (VLA-4) plus anti-vascular cell adhesion molecule-1 (VCAM-1) mAbs did not. In IL-1 beta-stimulated EC layers, anti-LFA 1 plus anti-ICAM-1 mAbs inhibited the adhesion and transmigration by 32% and 30%, respectively and anti-VLA-4 plus anti-VCAM-1 mAbs did so by 18% and 27%, respectively. These results suggest that the monocyte-EC interaction in unstimulated ECs is mediated, in part, by the LFA-1-ICAM-1 pathway and in IL-1 beta-stimulated ECs, in part, by both LFA-1-ICAM-1 and VLA-4-VCAM-1 pathways.

Antibodies, Monoclonal↗
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↗
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

[Long-term retrospective study of patients with connective tissue diseases accompanied by pulmonary hypertension].

To determine clinical and serological features that are related with the prognosis of connective tissue diseases with pulmonary hypertension (PH), we studied a long-term prognosis of 14 patients (4 SLE, 1 PSS, 3 MCTD, 2 primary Sjögren's syndrome, and 5 OL) accompanied by PH. The patients were divided into three groups; group A (4 cases) that is alive for 5-12 years until present, group B (6 cases) in which PH was the main cause of death, and group C (4 cases) was dead of pulmonary fibrosis and pericardial tamponade. No significant difference was observed in background connective tissue diseases among the three groups. However, the mean ages at the onset of PH was obviously younger in group B (25.7 yrs.) than both in group A (38.3 yrs.) and in group C (42.0 yrs.) (group A vs group B, p < 0.02, and group B vs group C, p < 0.05). Sudden death occurred in 5 of the 6 in group B, whereas it was not observed either in group A or in group C. Also, the interval between onset of PH and death was shorter in group B (1.3 yrs.) than in group C (3.5 yrs.). The incidence of digital necrosis and pericardial effusion was higher in group B (83% and 83%, respectively) than both in group A (0% and 25%, respectively) and in group C (25% and 40%, respectively). A large amount of pericardial effusion was detected in 4 of 5 cases in group B. The incidence of digital necrosis between group A and group B was significantly different (p < 0.05, Fisher's test).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Evidence for recent as well as long term activation of T cells migrating through endothelial cell monolayers in vitro.

As T cells actively extravasate from blood, they adhere to endothelium and then migrate out of the vessel with a locomotive activity. Although both adhesion and locomotion are properties associated with activated T cells, the two processes are not necessarily associated with identical activation states. Using human endothelial cells (EC) cultured to confluence on collagen gel, we examined the activation state of human peripheral blood T cells that adhere to and migrate through EC monolayers with three different methods: flow cytometric analysis of cell surface activation-related molecules, incorporation of tritiated nucleotide, and cell cycle analysis. The results were as follows. 1) Although expression of very late activation Ag integrins VLA-2 and VLA-3 by the initial blood T cell population (unseparated cells) and of adherent T cells was minimal, 40 to 45% of migrating cells were positive for VLA-2 and VLA-3. 2) The percentage of IL-2R+ cells in both unseparated and adherent cells was below 5% whereas the percentage of IL-2R+ cells among the migrating cells was 22 +/- 9% (range, 12 to 31%, n = 6). 3) Migrating cells expressed the highest CD26, whereas CD26 of adherent (nonmigrating) cells was divided into negative and high expression; in contrast, leukocyte adhesion molecule-1 (L-selectin) of both adherent and migrating cells was mostly low or negative. 4) [3H]Uridine incorporation of migrating and adherent cells was 2.1- to 2.5-fold and 1.4- to 1.7-fold higher, respectively, than that of unseparated cells, indicating that RNA synthesis of migrating cells as well as adherent cells was enhanced. 5) Cell cycle analysis showed that 23.5% of migrating cells appeared to enter the G1 phase but not S or G2 + M phases whereas 2.2% of unseparated cells and 8.0% of adherent cells that did not migrate had an RNA content consistent with entry into G1. These results suggest that cells migrating from normal human blood through unactivated EC have been activated recently as well as showing evidence of long term activation. The activation state of migrating cells is consistent with the hypothesis that previous in vivo activation is required for cells to migrate through EC in this system.

Animals↗
PubMed1992

[A systemic lupus erythematosus patient with multiple aseptic bone necroses, thrombosis of superior mesenteric artery and anti-phospholipid antibody].

A 38 year old woman with systemic lupus erythematosus (SLE) was admitted because of epigastralgia and fever. The diagnosis of SLE was made 22 years ago based on Raynaud's phenomenon, butterfly rash, hair loss, photosensitivity and positive antinuclear antibody. She had episodes of consciousness disturbance, transient visual disturbance of the left eye, and a necrosis of the left big toe. She underwent artificial arthroplasty of bilateral femoral heads 11 years ago, when multiple aseptic necroses of thirteen bones were found, and when anti-cardiolipin (CL) antibody was found to be positive. An echogram of abdomen suggested an obstruction of superior mesenteric artery (SMA) when she was admitted. Selective angiography revealed a complete obstruction of SMA and splenic artery, and incomplete obstruction of celiac artery. Conservative treatment with urokinase infusion and prednisolone 50 mg/day was not effective, and small intestine and right colon were resected on the 23rd hospital day. The pathological examination showed thrombosis of SMA. There was no evidence of arteritis or atherosclerosis. Anti-CL antibody and lupus anticoagulant were positive on admission, but the level of both anti-DNA antibody and complement was normal. Therefore, it was suggested that the thrombosis was related with anti-phospholipid antibody. The characteristic clinical feature were multiple aseptic bone necroses and thromboses of several arteries. We discussed the relationship of thrombosis and the etiology of multiple bone necrosis in this case with anti-phospholipid antibody.

Adult↗
PubMed1991

Polymorphonuclear leukocyte-induced detachment of cultured epidermal carcinoma cells from the substratum.

In an in vitro study, intended to develop tumoricidal therapy with the use of human leukocyte, an interesting phenomenon was found. Normal human polymorphonuclear leukocytes (PMN) plated on a cell line established from malignant trichilemmal cyst (DJM-1), a kind of squamous cell carcinoma, in a serum-free media and incubated for 48 h induced the detachment of DJM-1. The detachment was more extensive as the number of PMN increased. The detachment rate was 97.0% when the number of PMN and DJM-1 in a well was in a ratio 2.4:1 and the viability of detached DJM-1 was 96.5%. Two kinds of proteinase inhibitors, especially the inhibitor of neutrophil elastase, fetal bovine serum, and monoclonal anti-laminin antibody inhibited the detachment significantly. Furthermore, when PMN were seeded in a chamber with a filter membrane bottom to prevent direct contact with DJM-1, DJM-1 detachment decreased to 14.2%. In view of these results, the following mechanism was postulated. Activated by their adhesion to DJM-1, especially between laminin receptor on PMN and laminin on DJM-1, PMN secreted proteinases, resulting in DJM-1 detachment. This phenomenon might be an expression of cytotoxicity of PMN to cancer cells, because cultured cancer cells of epithelium origin such as DJM-1 can grow only after they are firmly attached to the substratum. This phenomenon, in turn, may explain the final step in the induction of epidermal-dermal separation in subepidermal bullous diseases with PMN infiltration such as bullous pemphigoid and dermatitis herpetiformis if we could regard DJM-1 as normal keratinocyte.

Carcinoma, Squamous Cell↗
PubMed1991

[A case of primary Sjögren's syndrome presenting as osteomalacia secondary to renal tubular acidosis].

We report a 43-year-old female with primary Sjögren's syndrome (SjS) who presented as osteomalacia due to distal renal tubular acidosis (RTA). Osteomalacia was thought to be a rare complication of RTA in SjS, although it had been often described in association with RTA in general. In 1979, she presented with dry mouth, parotid gland swelling and leg purpura. A diagnosis of primary SjS and hyperglobulinemic purpura was made on the basis of positive staining with Rose Bengal stain, sialography of the parotid gland and histological examination of the salivary gland of the lip. She was admitted to Jichi Medical School Hospital in March 1988 with chest pain. X-ray films revealed pseudofractures of bilateral ribs. Bone scanning showed abnormal multiple accumulation of RI on the same parts. Laboratory studies on admission revealed: GOT 50 IU/ml, GPT 9 IU/ml, ALP 190 IU/ml, LDH 301 IU/ml, BUN 11.0 mg/dl, creatinine 1.0 mg/dl, uric acid 2.7 mg/dl, total protein 7.4 g/dl (gamma globulin 22.3%), sodium 141 mEq/l, potassium 3.7 mEq/l, chloride 106 mEq/l, calcium 8.9 mg/dl, and phosphorus 2.4 mg/dl. Arterial blood gas studies on room air showed: PO2 96.7mmHg, PCO2 35.5mmHg, HCO3-19.1 mEq/l, PH 7.347 and base excess -5.4 mEq/l. The urinalysis showed: specific gravity 1.008, PH 7.0, and no protein and glucose. Immunologically, antinuclear antibody was positive at 1:640 with a speckled pattern. Anti-DNA antibody was negative. Antibodies to SS.A and SS.B were 1:64 and 1:32 respectively. Distal RTA was confirmed by the sodium bicarbonate and NH4Cl loading test.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗