Biomedical subjects
Publications and source records attributed to M Sugimoto.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
CONTEXT: Japan's maternal mortality rate is higher than that of other developed countries. OBJECTIVES: To identify causes of maternal mortality in Japan, examine attributes of treating facilities associated with maternal mortality, and assess the preventability of such deaths. DESIGN AND SETTING: Cross-sectional study of maternal deaths occurring in Japan between January 1, 1991, and December 31, 1992. SUBJECTS: Of 230 women who died while pregnant or within 42 days of being pregnant, 197 died in a hospital and had medical records available, 22 died outside of a medical facility, and 11 did not have records available. MAIN OUTCOME MEASURES: Maternal mortality rates per 100,000 live births by cause (identified by death certificate review and information from treating physicians or coroners); resources and staffing patterns of facilities where deaths occurred; and preventability of death, as determined by a 42-member panel of medical specialists. RESULTS: Overall maternal mortality was 9.5 per 100,000 births. Hemorrhage was the most common cause of death, occurring in 86 (39%) of 219 women. Seventy-two (37%) of 197 deaths occurring in facilities were deemed preventable and another 32 (16%) possibly preventable. Among deaths that occurred in a medical facility with an obstetrician on duty, the highest rate of preventable deaths (4.09/100,000 live births) occurred in facilities with 1 obstetrician. Among the 72 preventable deaths, 49 were attributed to 1 physician functioning as the obstetrician and anesthetist. While the unpreventable maternal death rate was highest in referral facilities, the preventable maternal death rate was 14 times lower in referral facilities than in transferring facilities. CONCLUSIONS: Inadequate obstetric services are associated with maternal mortality in Japan. Reducing single-obstetrician only delivery patterns and establishing regional 24-hour inpatient obstetrics facilities for high-risk cases may reduce maternal mortality in Japan. JAMA. 2000;283:2661-2667.
Forty patients with fatty liver were studied by peritoneoscopic examination after intravenous administration of indocyanine green (ICG). Although diffuse or centrilobular steatosis was observed in both nonalcoholic and alcoholic fatty liver, periportal steatosis was seen only in alcoholic fatty liver. Vascular markings were more prominent in alcoholic fatty liver, especially in those with fibrosis, compared with nonalcoholic fatty liver. Fat was not stained with ICG. Unstained red patches, observed after ICG administration in both nonalcoholic and alcoholic fatty liver, were thought to be due to congestion in the former and to lobular inflammation as well as congestion in the latter. Acinar markings were indistinct in the fatty liver with fibrosis but became clearer after ICG administration.
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BACKGROUND AND OBJECTIVES: Clinical evidence suggests that stellate ganglion block (SGB) might modulate the immune system. Little is known, however, about the immunologic effects of SGB. We examined how SGB affected immune functions by analyzing the activation response of lymphocytes during SGB. METHODS: Twenty-four volunteers were randomly subdivided into three groups. The SGB group (SGB; n = 9) received 6 mL 1% lidocaine at the sixth cervical vertebra (C6) transverse process and showed Horner's sign and elevation of ipsilateral facial and upper limb temperature. The lidocaine group (n = 7) had 6 mL 1% lidocaine injected into subcutaneous tissue at the neck and showed no remarkable clinical effects. The saline group (placebo; n = 8) received 6 mL saline solution injected at approximately the C6 transverse process and showed no remarkable clinical effects. Peripheral blood samples were drawn before and 30 minutes after drug administration. Samples were incubated for 4 hours under the stimulation of mitogen. Using flow cytometry, we measured the de novo expression of CD69, which is one of the initial markers of lymphocyte activation and which reflects the cell activation process. The changes in pre- and post-values were calculated and compared among the three groups. RESULTS: In only the SGB group, the helper T-cell activation was significantly reduced, and the cytotoxic T-cell activation also tended to decrease after SGB. CONCLUSIONS: SGB may depress immune system activity for a short time, as reflected in the T-cell activation response.
Bone morphogenetic protein-4 is a potent inducer of ectopic bone and cartilage formation in vivo. Expression of the bone morphogenetic protein-4 gene has been detected in bone cells during fracture repair but not in normal adult bone cells. To examine whether the gene is expressed by bone cells during embryonic development, in situ hybridization and reverse transcription polymerase chain reaction methods were used to detect murine bone morphogenetic protein-4 specific complementary DNA in murine developmental bone tissues. Bone morphogenetic protein-4 messenger RNA was detected in the cells of various developing bone tissues, but it was not detected in these tissues after birth. Combined with previous reports, our findings indicate that the bone morphogenetic protein-4 gene is expressed during embryogenesis and bone repair and suggest that its product may be a potent bone-forming factor in bone development and fracture repair.
A case of giant symptomatic myelolipoma is described in which clinical differentiation was difficult. It was considered to be an extremely rare case of giant myelolipoma arising in the adrenal gland. Histologically the present case contained more lipomatous elements than others reported to data. This is a case of giant adrenal myelolipoma with a few foci of myeloid elements and it is suggested that this case has a true neoplastic nature rather than a hyperplastic or metaplastic one.
We report the arthroscopic treatment of pigmented villonodular synovitis (PVNS) in a 13-year-old Japanese boy with congenital partial deficiency of plasminogen activator inhibitor-1 (PAI-1). He was admitted to our hospital with recurrent haemarthrosis of his right knee. Characteristic abnormalities of fibrinolysis included shortened euglobulin lysis time, low PAI-1 activity and low PAI-1 antigen levels. In addition, levels of "active PAI" in the plasma, which is a measure of total PAI bound to exogenous plasminogen activator, were very low. These parameters remained low after venous occlusion. The diagnosis of PVNS was established by synovial membrane biopsy, and arthroscopic synovectomy was performed with adjuvant administration of intravenous tranexamic acid. Subsequent bleeding episodes have been well controlled by oral administration of tranexamic acid on demand.
In the present study, we investigated thirty uveitis patients who had a possible diagnosis of ocular sarcoidosis, no respiratory symptoms, and normal chest X-rays, in order to determine whether bronchoalveolar lavage was useful for establishing a diagnosis of subclinical pulmonary involvement of sarcoidosis. Sixteen of 30 uveitis patients showed bronchoalveolar lymphocytosis (39 +/- 11%) as compared to normal controls (14 +/- 3%). Ten of these 16 patients were associated with significantly increased proportions of CD3+ cells with elevated CD4+/CD8+ ratios (P less than 0.01). These data were consistent with those of patients with active pulmonary sarcoidosis (stage 1 and 2) except for total cell count in lavage fluid, but different from those of patients with hypersensitivity pneumonitis. Transbronchial lung biopsy showed noncaseating epithelioid cell granuloma in 4 of 10 uveitis patients with bronchoalveolar T-lymphocytosis and increased CD4+/CD8+ ratios. Immunohistochemical studies of biopsied lung tissues showed many CD3+ cells and CD4+ cells with very few CD8+ cells in the granuloma. These results suggest that T-lymphocytosis with elevated CD4+/CD8+ ratios in bronchoalveolar lavage fluid could be a good marker in predicting the pulmonary involvement of sarcoidosis in patients with suspected ocular sarcoidosis and normal chest X-rays.
Ten patients with human T lymphotropic virus type I-associated myelopathy (HAM), 5 asymptomatic HTLV-I carriers and 11 healthy normal volunteers were studied to determine if peripheral blood lymphocytes spontaneously release IL-2 and soluble IL-2 receptors. Peripheral blood lymphocytes obtained from HAM patients proliferated spontaneously when cultured for 5 days in vitro. Proliferating cells were CD3+ lymphocytes and both CD4+ cells and CD8+ cells as shown by morphologic and immunohistochemical observations. These T cell responses were also found in asymptomatic carriers, but the responses were not as marked as those of HAM patients. IL-2 activity in the culture supernatants was much higher in HAM patients than in asymptomatic carriers; IL-2 activity correlated well with the intensity of spontaneous proliferation of lymphocytes. Furthermore, soluble IL-2 receptors in the cell-free supernatants from HAM patients were markedly increased compared to those from asymptomatic carriers. These results indicate that spontaneous proliferation of T cells is intimately related to HTLV-I infection and is probably due to autocrine or paracrine pathways which involve IL-2 and IL-2 receptor system.
A 24-year-old man showed thyrotoxic symptoms with hypokalemic periodic paralysis. Serum thyroid hormone levels were high and thyrotropin (TSH) was undetectable. 123I-thyroidal uptake was suppressed. TSH-binding inhibitor immunoglobulin (TBII) was positive. After a month without any treatment, he became hypothyroid. Thyroid hormone level was decreased and TSH was increased to above the normal range. 123I-thyroidal uptake was increased. TBII activity was still positive. From the clinical findings, a diagnosis of silent thyroiditis was made. Sera obtained in the hypothyroid state revealed the presence of thyroid-stimulation-blocking antibodies (TSBAb), but there were no thyroid-stimulating antibodies (TSAb). These results suggest that the hypothyroidism in this patient was due to the presence of TSBAb with TBII activity.
BACKGROUND: Modern plasma-derived clotting factor concentrates are produced using various virus-inactivation protocols and are assumed to be safer than they were previously with regard to the risk for transmitting viral infections such as human immunodeficiency virus, hepatitis B, and hepatitis C. The risks from viruses that are relatively resistant to the current inactivation procedures remain uncertain. PATIENT: A 7-year-old with mild hemophilia A who had not been previously infused with any blood products was treated with a plasma-derived, monoclonal antibody-purified factor VIII concentrate to cover orthopedic surgery after traumatic fracture of his left arm. RESULTS: A typical primary human parvovirus (HPV)-B19 infection was observed associated with transient hypoplastic anemia. Retrospective studies including serologic examination and polymerase chain reaction analysis confirmed that the HPV-B19 infection was transmitted by the factor VIII concentrate. CONCLUSIONS: Clotting factor concentrates for the treatment of hemophilia retain a risk for HPV-B19 contamination. HPV-B19 viral infection might induce hypoplastic anemia in these patients, particularly during enhanced hemopoiesis after acute blood loss.