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Biomedical subjects

S Akizuki

Publications and source records attributed to S Akizuki.

At least 55 records · Page 3Linked to original sources
PubMed1994

[Case report: infective endocarditis caused by Streptococcus agalactiae].

A 42-year-old male was admitted to our hospital because of high grade fever on October 6, 1992. He had no history of cardiac and underlying disease. For the past 10 days, he had complained of high grade fever and noticed arthralgia on his left shoulder. Physical examination on admission revealed that there was a body temperature of 39.0 degrees C and tenderness in the left shoulder. There were no abnormal findings for the chest or abdomen. On the second hospital day, he developed a diastolic murmur which had not been present on admission. And blood culture was positive for Streptococcus agalactiae. Ultrasonic-cardiogram indicated the presence of vegetation. He was diagnosed as infective endocarditis and treated with PCG 20 million units/day, IPM/CS 2 g/day and ISP 400 mg/day. But he was not responding to the chemotherapy. Aortic valve replacement was done on 22nd, October. Valve surgery succeeded and he became well after that time. Endocarditis caused by S. agalactiae is extremely rare, and is an important condition which carries a high mortality. Only seven cases of S. agalactiae endocarditis have been reported in Japan. It is difficult to treat these cases with antibiotic therapy alone. Therefore, we suggest that early surgery should be considered in infective endocarditis caused by S. agalactiae.

Adult↗
PubMed1994

Premature termination mutations in two patients with deficiency of lactate dehydrogenase H(B) subunit.

Two patients with low lactate dehydrogenase (LD) activity were discovered during healthcare examinations and were found to be homozygous for LD-H (heart) subunit deficiency by electrophoretic isoenzyme analysis of serum and erythrocyte hemolysate. The molecular nature of the genetic mutations was characterized by amplification by the polymerase chain reaction and DNA sequencing. In one case, a single-base substitution (T-->G transversion) at codon 147 of the LD-H(B) gene resulted in a nonsense mutation; in the other case, a deletion of 2 base pairs had occurred at codon 139, resulting in a frameshift translation and premature termination.

Adult↗
PubMed1994

Disseminated Trichosporon infection. A case report and immunohistochemical study.

An autopsy case of disseminated Trichosporon beigelii infection in a patient with acute promyelocytic leukemia is presented. We diagnosed the T beigelii infection with immunoperoxidase method using our rabbit antiserum to T beigelii. The diagnosis of T beigelii infection is difficult, because of its close resemblance to Candida species in both clinical features and histopathologic findings. We could consistently identify T beigelii in tissue sections with the present immunohistologic method. We conclude that the immunoperoxidase method using antiserum to T beigelii is very useful to diagnose T beigelii infection.

Cadaver↗
PubMed1993

[Disseminated Trichosporon beigelii infection: report of nine cases and review].

Trichosporon beigelii (formerly called Trichosporon cutaneum) is an emerging pathogen of disseminated trichosporonosis in immunocompromised patients. We conducted postmortem microbiological examinations of lung aspirates and blood in the heart. T. beigelii was isolated from the samples of 7 (2.24%) of 313 patients. Five of 7 patients isolated were diagnosed as having trichosporonosis based on histochemical and clinical findings. The other two were considered as colonization. Immunohistochemical study using Cryptococcus neoformans-absorbed antiserum to T. beigelii was carried out on the sections of autopsied tissues with deep mycoses. The sections from seven patients were positively stained, which were formerly diagnosed as candidiasis and/or aspergillosis. Consequently, 9 patients had disseminated trichosporonosis caused by T. beigelii. In Japan, 43 patients including the present 9, 31 males and 12 females, aged 51 (range, 2-84), were reported in the literature. Thirty-seven (86%) patients had hematologic malignancy, and the majority of them revealed profound neutropenia due to cytotoxic chemotherapy. Thirty-eight (88%) patients died despite the anti-fungal chemotherapy including amphotericin B. New strategies for refractory disseminated trichosporonosis in immunocompromised patients is needed.

Adolescent↗
PubMed1992

Identification of a tissue-specific regulatory element within the murine CD14 gene.

We previously isolated and sequenced the 5'-flanking region of the mouse CD14 (mCD14) gene (Matsuura, K., Setoguchi, M., Nasu, N., Higuchi, Y., Yoshida, S., Akizuki, S., and Yamamoto, S. (1989) Nucleic Acids Res. 17, 2132). To define the regulatory elements that control expression of the mCD14 gene, we analyzed the structure of the 5' end of the gene, including a region further upstream of that determined previously. Sequentially 5'-deleted, chimeric, and point mutated clones were tested for the ability to stimulate chloramphenicol acetyltransferase. An 8-base pair sequence, TGATTCAC, at position -255, which resembled the consensus sequence of the 12-O-tetradecanoylphorbol-13-acetate-responsive element (TRE), enhanced the expression of the chloramphenicol acetyltransferase gene in macrophage (aHINS-B3) and non-macrophage (glioblastoma G203 and myeloma NS1) cells. The enhancing ability of the TRE-like sequence (TLS), however, was markedly reduced in G203 cells but not in aHINS-B3 cells when the TLS was followed by the sequence immediately downstream. The TLS and sequence immediately downstream were capable of binding nuclear proteins which were unique to aHINS-B3 cells and macrophages, suggesting that these unique protein regulate the specific expression of the mCD14 gene. Binding of AP-1 to the TLS was also found in aHINS-B3 and G203 cells. Although it is uncertain whether AP-1 is involved in expression of the mCD14 gene, the effect of AP-1 in non-macrophage cells was inhibited by a nuclear protein which binds to the sequence immediately downstream of the TLS.

Animals↗
PubMed1992

Presence of HTLV-I proviral DNA in central nervous system of patients with HTLV-I-associated myelopathy.

The polymerase chain reaction (PCR) method was used to determine the presence and amount of human T lymphotropic virus type I (HTLV-I) proviral DNA in central nervous system (CNS) tissue obtained at autopsy from 6 patients with HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP), 1 patient with adult T-cell leukemia (ATL) and CNS infiltration of leukemic cells, and 9 control subjects with other neurological disorders. HTLV-I pX and env but not pol DNA were detected in CNS tissue from 5 of 6 patients with HAM/TSP. The ATL samples were positive for pX, env, and pol DNA by PCR. None of the control samples was consistently positive for HTLV-I by PCR, but all showed positive bands on beta-globin PCR. Quantitative PCR combined with histological studies showed no correlation between HTLV-I proviral DNA amounts and extent of perivascular mononuclear cell infiltration in the HAM/TSP CNS. Also, the amounts of pX and probably env DNA were greater in the HAM/TSP samples than in the ATL sample, although the extent of mononuclear cell infiltration was far less in the HAM/TSP samples than in the ATL sample. Therefore, in addition to infiltrating mononuclear cells, constituent cells of the CNS may harbor the HTLV-I genome, at least in the pX and env regions, in patients with HAM/TSP.

Base Sequence↗
PubMed1992

Predictive value of liver tissue flow in assessment of the viability of liver grafts after extended preservation in pigs.

The crucial damage in cold storage of liver allografts is to the hepatic sinusoidal lining (microcirculation). Using different solutions, we studied whether determinations of graft tissue flow were valuable in estimating the viability of liver grafts. Twenty-three pairs of female pigs underwent orthotopic liver transplantation and were assigned to five groups according to the cold preservation time or solutions used: in group I the liver grafts were stored in Euro-Collins solution (EC) for 4 h (n = 3), in group II the grafts were stored in EC for 12 h (n = 5), in group III the donor was pretreated with azathioprine (AZA), 1 mg/kg per day, orally (p.o.) for 3 days before harvesting and the graft was implanted after 12 h cold storage with EC (n = 6), in group IV the graft was stored in modified University of Wisconsin solution (mUW) for 4 h (n = 3), and in group V the graft was stored in mUW for 24 h (n = 6). Liver tissue blood flow (LTBF) was measured, using a laser doppler device, at 60 min after recirculation of the graft. In the case of EC preservation, LTBF (ml/100 g of liver tissue per min) correlated well with 4-day survival: 21.2 +/- 3.0 ml/100 g of tissue per min mean +/- SD, in group I (3/3, 100%); 10.0 +/- 2.8 ml/100 g of tissue per min in group II (0/5, 0%); and 19.1 +/- 3.4 ml/100 g of tissue per min in group III (5/6, 83.3%) (P < 0.05, group II vs I and III). All grafts with LTBF of more than 15 ml/100 g tissue per min functioned well. However, changes in microcirculation of the mUW-stored livers did not correlate with early function of the graft: 23.0 +/- 2.3 ml/100 g of tissue per min in group IV (4-day survival; 3 of 3, 100%) and 23.5 +/- 9.1 ml/100 g of tissue per min in group V (0 of 6, 0%). This was accompanied by graft dehydration during storage and an increased number of erythrocytes in the hepatic sinusoids post-recirculation. We concluded that assessment of liver tissue flow by LDF was very helpful and easy to apply in predicting liver graft failure in the case of preservation with Euro-Collins solution. However, LTBF should be carefully evaluated as a marker of liver graft viability when the liver graft is preserved with mUW.

Animals↗
PubMed1992

Turner's syndrome associated with Hashimoto's thyroiditis and sarcoidosis: a case report.

A 32-yr-old Japanese female who was suffering from Turner's syndrome associated with Hashimoto's thyroiditis and sarcoidosis is reported. It is known that Hashimoto's thyroiditis is not infrequently complicated with Turner's syndrome on the basis of an abnormal X chromosome. In this case, sarcoidosis occurred 4 months after Hashimoto's thyroiditis. This extremely interesting coincidence of Hashimoto's thyroiditis and sarcoidosis in Turner's syndrome has not been reported to date to our knowledge.

Adult↗
PubMed1992

Infiltration of helper/inducer T lymphocytes heralds central nervous system damage in human T-cell leukemia virus infection.

Cellular infiltrates in new and old lesions in two cases of human T-cell leukemia virus associated myelopathy (HAM) were analyzed with anti-CD3 antibody and OPD4 antibody recognizing CD4 + CD45RO + T lymphocytes. A subset of CD4 lymphocytes with helper/inducer function and labeled with OPD4 constitutes up to 65% of CD3 cells in new lesions in the pons and the cervical cord. In contrast, nonhelper cells and macrophages were dominant in long-standing spinal cord lesions of these HAM cases and inflammatory lesions in two cases of Japanese encephalitis. Thus, unlike in viral infections, the central nervous system (CNS) tissue damage associated with human T-cell leukemia virus (HTLV-1) infection appeared to be heralded by the infiltration of helper/inducer T cells.

Antibodies, Monoclonal↗
PubMed1992

[A case of aconitine poisoning accompanied by bidirectional ventricular tachycardia treated with lidocaine].

A rare case of aconitine poisoning accompanied by bidirectional ventricular tachycardia was reported. A 67-year-old male ate several leaves of a wild plant which had been collected in Fukushima Prefecture, Japan. About 90 minutes later, he felt numbness and weakness of the limbs and vomiting took place, and he was admitted to our hospital. The blood pressure was 80/60mmHg, and the electrocardiogram showed multiple premature ventricular contractions and bidirectional ventricular tachycardia. After bolus injection of lidocaine, continuous administration of the drug was started. Immediately after starting the treatment, the arrhythmia disappeared and hemodynamic changes improved. Thereafter the wild plant was ascertained to be a species of Aconitium. Diagnosis of aconitine poisoning was made. According to the fact that aconitine acts as a agonist of Na-channel receptor, antiarrhythmic agents which belong to Vaughan-Williams' classification I might be the first choice for the therapy of aconitine induced arrhythmias.

Aconitine↗
PubMed1991

Molecular and physiological properties of murine CD14.

We have previously cloned the murine homolog of cDNA for the human myelomonocytic differentiation antigen, CD14. We synthesized three hydrophilic peptides derived from the predicted amino acid sequence of murine CD14 (mCD14), designated MS7.1, MS7.2, and MS7.3, respectively, and raised antisera against them. Each antiserum showed specific reactivity to the same peptide used for immunization. One of the anti-mCD14 antisera directed against MS7.3 peptide (AMS7.3) demonstrated the highest titer and definitively reacted with monocytic cell lines, inflammatory polymorphonuclear cells, and macrophages. Significant cross-reactivity of AMS7.3 was observed in the human monocytic cell line, THP-1. COS-1 cells transfected with MS7 cDNA expressed an antigen recognized by AMS7.3. Resident peritoneal and alveolar macrophages both expressed mCD14. mCD14 expression in peritoneal but not alveolar macrophages increased after treatment with lipopolysaccharide. Expression of mCD14 varied among monocytic cell lines and roughly paralleled the mRNA levels except in MI cells. SDS-PAGE and isoelectric focusing analysis of immunoprecipitated mCD14 showed that mCD14 was a 53 kd disulfide-linked protein with a pI of 4.5-5.1. Reduction of molecular weight by endo F treatment demonstrated that mCD14 was an N-linked glycoprotein. Since mCD14 is shed from the cell surface membrane by phosphatidylinositol-specific phospholipase C treatment, the indication is that mCD14 is a phosphatidylinositol-linked protein. The soluble form of mCD14 was detectable. Treatment with anti-mCD14 before interferon gamma (IFN gamma) stimulation significantly enhanced IFN gamma-induced H-2 antigen expression in the macrophage cell line.

Amino Acid Sequence↗
PubMed1991

Disseminated infection of herpes simplex virus with fulminant hepatitis in a healthy adult. A case report.

An autopsy case of fulminant hepatitis caused by herpes simplex virus type 1 in a healthy adult is presented. The clinical course was characterized by hepatic failure, disseminated intravascular coagulation and acute renal failure. Many small ulcerations were present in the tongue and tonsils, and there were foci of hemorrhagic necrosis in the liver. Herpes simplex viral antigen was identified in the liver, tonsils, spleen, tongue, pharynx, larynx, esophagus, stomach, intestine, adrenal glands, and lymph nodes with immunohistochemical staining using antibodies to herpes simplex virus type 1. The electron microscopic examination revealed many virions in the hepatocytes. Herpes simplex virus was isolated from the liver, and viral DNA, which had some distinctive features of herpes simplex virus type 1, was examined. We discuss possible reasons for this opportunistic infection occurring in a healthy adult.

DNA, Viral↗