Simultaneous occurrence of human herpesvirus 6 infection and intussusception in three infants.
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Biomedical subjects
Publications and source records attributed to Y Asano.
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A 75-year-old female was admitted to our hospital because of shortness of breath and palpitations. Chest roentgenogram together with a CT scan showed multiple nodular shadows in both lung fields, with hilar lymphadenopathy. The cervical lymph nodes were enlarged, and were biopsied to reveal diffuse large T-cell non-Hodgkin's lymphoma. Extensive pulmonary involvement was suspected and treatment with a modified CHOP regimen was begun. Following therapy, pulmonary symptoms were remarkably improved, and chest roentgenogram revealed virtually complete clearance of lung lesions. No severe side effects were observed as a result of the therapy.
Metastases to the adrenal glands are common in patients with cancer, but among those affected, hyperreninemic hypoaldosteronism is noted very rarely. A case of hyperreninemic hypoaldosteronism secondary to metastatic hepatocellular carcinoma is reported. Laboratory data revealed selective aldosterone deficiency with hyperreninemia. Biopsy documented replacement of the adrenal glands with metastatic hepatocellular carcinoma. A review of the literature disclosed that the present case was an extremely rare one of its kind.
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)
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A membrane protein fraction was obtained from rat liver rough microsomes by affinity chromatography on a concanavalin A-Sepharose column and then a chelating-Sepharose column. This protein fraction comprised about 2% of the total membrane proteins of rough microsomes and the ribosome-binding activity of ribosome-stripped rough microsomes was predominantly found in this protein fraction, as determined with a liposome assay system. To identify the essential components responsible for the ribosome binding, two approaches were employed. Trypsin treatment of liposomes reconstituted with this protein fraction resulted in the loss of the ribosome-binding activity in parallel with the loss of a dominant band, estimated Mr 34,000, in SDS-polyacrylamide gels. Next, the direct interaction between the binding sites on the membrane of reconstituted liposomes and 60S ribosomal subunits was investigated by photocrosslinking using sulfosuccinimidyl 2-(m-azido-o-nitrobenzamido)-ethyl-1,3'-dithiopropionate (SAND). The photocrosslinked complex was formed between 60S ribosomal subunits pretreated with SAND and binding-site proteins on the membrane of the liposomes. Then, after the liposomes were solubilized, the complex was isolated by sucrose gradient centrifugation of the binding mixture. The crosslinked proteins were released from 60S ribosomal subunits by cleavage of of crosslinks with beta-ME and analyzed by SDS-polyacrylamide gel electrophoresis and 125I-autoradiography. The 34-kDa protein (p34) was the predominant component that crosslinked to the 60S ribosomal subunits and was found in proportion to the amount of 60S ribosomal subunits added to the system. The p34 was distinguishable by immunoblot analysis from urate oxidase, which is the 34-kDa protein of peroxisomal cores contaminating rough microsomes. These results suggest that the present p34 is a likely candidate molecule for the ribosome-binding activity of rough microsomes.
A CD8+ Ts clone 13G2 was established from lymph node cells of bovine alpha s1-casein-primed C57BL/6 mice by in vitro antigenic stimulation followed by maintenance with IL-2-containing medium. The clone suppressed the Ag-induced proliferative responses of CD4+ Th cell clones without detectable cytotoxicity for both APC and responding T cells. The clone was able to suppress the in vitro proliferative response and antibody formation of Ag-primed lymph node cells. The suppression was Ag-nonspecific and not restricted to the MHC. The clone was able to suppress the proliferation of Th clones induced by an immobilized anti-TCR antibody in which APC was absent. The clone was, however, unable to suppress the proliferation of Th clones induced by anti-CD3 or IL-2. Thus, the mechanism of suppression by 13G2 was found to be due to a direct action on Th by inhibiting a consequence of signal transduction initiated through the TCR.
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APC activity of spleen cells from C57BL/10 (B10) mice infected with LP-BM5 murine leukemia virus (MuLV), which is known as a murine acquired immunodeficiency syndrome (MAIDS) virus, was investigated. The ability of splenic APC from LP-BM5 MuLV-inoculated B10 mice to induce soluble Ag-specific proliferation of cloned Th cells was decreased progressively during the infection. The APC defect was found to be due neither to the decreased expression of Ia Ag nor to the insufficient production of IL-1. It was demonstrated that cloned Th stimulated with virus-infected splenic APC displayed the increased [Ca2+]i with severely decreased inositol phospholipid metabolism, which probably led to the defect of Th proliferative responses. These results suggested that the failure of Th to respond to soluble Ag in MAIDS is at least in part due to a selective defect in signal transduction caused by abnormal APC.
Antibody to human herpesvirus-6 (HHV-6) was measured in cord blood mononuclear cell cultures by a neutralization (NT) test, in which the presence or absence of characteristic large cell formation in cells infected with HHV-6 was used as an indicator for neutralization of the virus. The NT test could measure antibodies during and just after the appearance of the skin rash in patients with exanthem subitum. The levels of antibodies measured by the NT test was generally higher than that by an indirect immunofluorescence assay.
Two infants (4 and 5 months of age) with a febrile episode for 3 and 5 days, respectively, developed skin rashes after the fever subsided and were diagnosed as exanthem subitum. The rash continued for 5 days followed by mild-to-moderate pigmentation. Human herpesvirus-6 and measles virus, which were confirmed by a specific immunofluorescence assay and by electron microscopy, were isolated simultaneously from blood in the acute stage of the disease but not from the convalescent stage. The titer of the herpesvirus-6 in blood was greater than that of measles. Specific serologic assays showed marked seroconversion against human herpesvirus-6 but not to measles virus. The results suggest that dual infection with human herpesvirus-6 and measles virus results in atypical exanthem subitum or modified measles with unique immunologic responses.
A lysate of human herpesvirus 6 (HHV-6)-infected cord blood mononuclear cells was used as antigen for enzyme-linked immunosorbent assay for the detection of IgG antibody to HHV-6. Antibody responses after exanthem subitum were well correlated with clinical recovery from the disease and the level of antibody activities was well correlated with indirect immunofluorescence assay and the neutralization test. Seroconversion to other human herpesvirus, including cytomegalovirus, was not observed in infants with exanthem subitum. All of the infants had by the age of 1 month antibodies to HHV-6, which decreased with age to the lowest level at the age of 3 to 6 months and then increased and reached the maximum level by 1 to 2 years of age. After 3 years of age, the prevalence was almost stable.
To elucidate the ionic mechanisms underlying prolongation of the action potential by OPC-8490, a novel positive inotropic agent, we examined effects of the drug on the membrane currents in isolated atrial myocytes of guinea-pig heart. The tight-seal whole cell clamp technique was used. In the current clamp condition, OPC-8490 prolonged the atrial action potential in a concentration-dependent fashion. In the voltage clamp condition, OPC-8490 affected neither the conventional L type Ca current nor the outward IK1 current significantly. The drug blocked the delayed outward K current (IK) in a concentration-dependent fashion. At a constant concentration of the drug, inhibition of IK became more marked as the membrane potential became more negative. The tail current of IK could be fitted by a sum of two exponentials (fast and slow components). OPC-8490 blocked the fast component more prominently than the slow one. Time constants of both components were not affected significantly by the drug. In conclusion, OPC-8490 prolongs the cardiac action potential mainly by blocking IK in a voltage-dependent and time-dependent fashion.
We studied clinical and biological features of five cases of hybrid leukemia. Three of the five patients were classified as biphenotypic leukemia because of the coexpression of myeloid/B lymphoid markers in patients 1 (FAB M2) and 2 (FAB CMMoL) and myeloid/T lymphoid markers in patient 3 (FAB M4). Patient 4 was identified as bilineal-biphenotypic leukemia because acute myelogenous leukemia (AML) (FAB M4) and acute lymphoblastic leukemia (ALL) (FAB L1) coexisted and each population coexpressed myeloid and T lymphoid markers. Patient 5 was identified as bilineal leukemia due to the conversion from AML (FAB M1) to ALL (FAB L1) at an interval of 3 months. The Philadelphia (Ph1) chromosome was negative in all cases. A leukemic blast colony formation using cell line 5637 conditioned medium as a stimulator was obtained in all four patients examined. Three of the five patients had been suffering from so-called stem cell disorders such as aplastic anemia in patient 2, trilineage myelodysplasia in patient 4 and refractory anemia with excess of blasts in transformation in patient 5. The pre-existing impairment of pluripotent stem cell was probably the background of these hybrid leukemia. Hybrid leukemia appears to have an inferior prognosis: an AML-directed chemotherapy resulted in a low remission rate (2/5) with a short duration of relapse free survival (1/2) and an ALL-directed chemotherapy produced no remission (0/3). Chronological phenotypic analysis revealed that hybrid features of leukemic blasts disappeared at the time of relapse in patient 1 and progression to AML in patient 2. Monitoring of lineage-associated markers should be required for the management of hybrid leukemia.
L-[13N]Tyrosine and L-[13N]phenylalanine were synthesized using immobilized enzymes by two methods. In method 1, [13N]ammonia is converted to L-[13N]glutamate; transamination with p-hydroxyphenylpyruvate yields L-[13N]tyrosine. [13N]Tyrosine is separated from other labeled intermediates on a Poropak Q column. In method 2, phenylalanine dehydrogenase catalyzes the reversible reductive [13N]amination of either phenylpyruvate or p-hydroxyphenylpyruvate to form L-[13N]phenylalanine or L-[13N]tyrosine, respectively. The feasibility of labeling DOPA and tryptophan with 13N was also demonstrated.
The number of varicella zoster virus-infected mononuclear cells in blood samples obtained during 3 days before appearance of vesicular skin rashes could be estimated in 13 of 21 immunocompetent children with varicella and viremia (range, 1-83 per 10(7) mononuclear cells). The virus was isolated from 5% of adherent cells (1/21), 71% of nonadherent cells (12/17), 43% of T lymphocytes (9/21), and 33% of B lymphocytes (7/21). The number of vesicles on the body correlated with the maximum body temperature, duration of fever, and number of infected cells in the blood. These results indicate that varicella zoster virus infection in immunocompetent children is disseminated by circulating T and B lymphocytes and the severity of the viremia is reflected in the severity of the disease.