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Biomedical subjects

C Terai

Publications and source records attributed to C Terai.

At least 55 records · Page 3Linked to original sources
PubMed1995

Effects of mild Trendelenburg on central hemodynamics and internal jugular vein velocity, cross-sectional area, and flow.

Despite widespread use of the Trendelenburg position, its autotransfusion effect remains controversial. Additionally, its adverse effect on cerebral circulation is not generally appreciated. The effects of a 10 degrees head-down tilt on central hemodynamics and flow through the internal jugular vein (IJV) were examined in ten healthy volunteers. Left ventricular end-diastolic volume (LVEDV) and cardiac output (CO) were calculated from two-dimensional echocardiograms. IJV velocity and cross-sectional area were determined by the pulsed Doppler system. Measurements were made with the subjects in the supine position and at 1 minute and 10 minutes after tilting. A significant increase (16%) in CO followed by the increase in LVEDV was observed at 1 minute after tilting, although these changes disappeared after 10 minutes of tilting. Mean arterial pressure at the heart level did not change during the maneuver. The IJV velocity decreased whereas the IJV cross-sectional area increased at 1 minute after tilting, but both factors returned to control level at 10 minutes after tilting. As a result, calculated IJV blood flow was unchanged throughout the period of tilt. Therefore, the mild trendelenburg position produces a transient autotransfusion effect in normovolemic patients. Our data also suggest that the Trendelenburg produces no adverse effect on cerebral circulation in patients with normal cerebral autoregulation.

Adult↗
PubMed1995

Adenine phosphoribosyltransferase deficiency identified by urinary sediment analysis: cellular and molecular confirmation.

Adenine phosphoribosyltransferase deficiency is an autosomal recessive purine enzyme defect that causes urolithiasis and, in severe cases, renal failure. Most homozygotes with this disorder were identified by analyses of excreted or surgically removed urinary stones, but some were identified only because they were family members of symptomatic individuals. We report here the detection of adenine phosphoribosyltransferase deficiency in two cases by routine analysis of urinary sediments. 2,8-Dihydroxyadenine-like spherical crystals were observed in the urinary sediment, and a diagnosis of homozygous adenine phosphoribosyltransferase deficiency was confirmed by cellular and molecular methods. A molecular diagnostic system using the polymerase-chain reaction and single-strand conformational polymorphism analysis proved to be a rapid and sensitive method to identify the APRT*J allele, a common mutant allele among the Japanese people. These methods will facilitate identification of symptomatic and asymptomatic individuals with homozygous adenine phosphoribosyltransferase deficiency.

Adenine↗
PubMed1994

Molecular basis for the interaction between human IgM and staphylococcal protein A.

To examine the relationship between VH gene usage and reactivity of immunoglobulins, we cloned B cells from peripheral blood from adults and from human neonatal cord blood by EBV transformation. Nearly one-third of the B cell clones from both sources produced IgM reactive with staphylococcal protein A (SPA). None of such IgM reacted with other antigens, except for the crude extract of Staphylococcus aureus. All of 22 B cell clones producing IgM reactive with SPA expressed VH3 genes, while none of the control 15 clones secreting IgM nonreactive with SPA expressed VH3. The IgM proteins reactive with SPA could be clearly divided into two subjects based on the differential binding avidity to solid-phase SPA. Both kappa and lambda light chains were used in each subset of SPA-reactive IgM. Sequence analysis of the PCR products from seven VH3-IgM clones revealed that the VH3 genes were used in nearly germline configuration. The D and J gene usage was diverse. Comparison of amino acid sequences between antibodies with high and low avidity to SPA suggests that the differential avidity is related to amino acid sequence differences in the complementarity determining region 2 and framework region 3. The high frequencies of B cells committed to the production of SPA-reactive IgM in normal blood and the restricted use of VH3 heavy chain genes in nearly germline configuration in these cells support the notion that SPA behaves like a superantigen toward human B cells.

Adult↗
PubMed1994

Analysis of the genotypes for aldehyde dehydrogenase 2 in Japanese patients with primary gout.

Alcoholic ingestion is one of the major factors for increasing serum uric acid levels. Genotypes of aldehyde dehydrogenase 2 (ALDH2, E.C.1.2.1.3), which regulates the sensitivity of an individual to ethanol, were determined in Japanese patients with gout and control subjects by allele specific oligonucleotide hybridization using PCR amplified gene. The most common allele ALDH2*1 codes for normal ALDH2 activity, while the less common allele ALDH2*2 codes for a lower enzyme activity. The frequency of homozygotes of ALDH2*2 was significantly lower in patients with gout than those with rheumatoid arthritis or a normal population. Plasma and urinary hypoxanthine levels were strikingly increased after ethanol drinking in homozygotes for ALDH2*1 but not in heterozygotes for ALDH2*1/ALDH2*2, indicated extensive purine nucleotide degradation in homozygote for ALDH2*1. These data indicated that alcohol ingestion may not be the requisite factor but is deeply involved in the pathogenesis of gout and hyperuricemia.

Alcohol Drinking↗
PubMed1993

Fatal traumatic subarachnoid hemorrhage due to rupture of the vertebral artery.

An unusual case of traumatic subarachnoid hemorrhage (SAH) due to rupture of the intracranial vertebral artery is reported. A drunk 51-year-old man received blows with a fist to the face and lost consciousness. A massive basal SAH was identified by CT-scan. Autopsy revealed a rupture of the vertebral artery but no skull fracture or cerebral contusion.

Humans↗
PubMed1991

Dependence of cell survival on DNA repair in human mononuclear phagocytes.

Mononuclear phagocytes play a central role in the pathogenesis of chronic inflammatory diseases. It is therefore important to define chemotherapeutically exploitable metabolic pathways that distinguish monocytes from other cell types. Blood monocytes do not synthesize deoxynucleotides de novo, and their transformation to macrophages occurs without cell division. Whether or not monocytes can repair DNA damage, and whether or not DNA repair is necessary for their survival, is unknown. The present experiments demonstrate that normal human monocytes, unlike neutrophils, rapidly repair DNA strand breaks induced by gamma-irradiation. Monocyte extracts contain functional immunoreactive DNA polymerase-alpha. DNA repair synthesis in normal monocytes is blocked by aphidicolin, an inhibitor of DNA polymerase-alpha with respect to dCTP. Aphidicolin is also directly toxic to normal monocytes, but has no effect on nondividing lymphocytes or fibroblasts. Compared to most other cell types, monocytes and macrophages have very low dCTP pools, but abundant deoxycytidine kinase activity. This suggests that dCTP derived from salvage pathways is important for DNA repair in these cells. Consistent with this notion, exogenous deoxycytidine could partially protect monocytes from aphidicolin killing. The unexpected toxicity of aphidicolin toward normal human monocytes may be attributable to their high rate of spontaneous DNA strand break formation, to the importance of DNA polymerase-alpha for DNA repair in these cells, and to their minute dCTP pools.

2-Chloroadenosine↗
PubMed1991

Pyrimidine nucleotide and nucleic acid synthesis in human monocytes and macrophages.

In most cell types, the production of deoxynucleotides is tightly coupled to the pace of cell division, and nearly all deoxynucleotides are used for semiconservative DNA synthesis. The capacity of peripheral blood monocytes and macrophages to proliferate is controversial. However, these cells have been reported to produce and release thymidine, which can serve as a precursor or regulator of DNA synthesis by lymphocytes and other cells. To determine to what extent de novo pyrimidine nucleotide synthesis is linked to cell division in peripheral blood monocytes and macrophages, compared to human U937 promonocytes and CEM lymphoblasts, we used a precise precursor-product labeling method. The results showed that in all three cell types, the pace of pyrimidine deoxynucleotide production, and of thymidylate synthesis, was in proportion to the rate of DNA synthesis. The human blood monocytes and macrophages, in contrast to U937 cells, had extraordinarily low deoxyribonucleotide pools (less than 1 pmol/10(6) cells) and synthesized neither thymidylate nor DNA de novo during 7 days culture. Colony-stimulating factors augmented RNA synthesis in monocyte-derived macrophages, and enhanced cell survival, without inducing either DNA or thymidylate synthesis. We conclude that the thymidine released by macrophages derives from dead or dying cells, and not from de novo synthesis.

Cell Line↗
PubMed1991

Apoptosis as a mechanism of cell death in cultured T lymphoblasts acutely infected with HIV-1.

The mechanisms by which HIV-1 infection kills T lymphocytes are not clearly established. Apoptosis is an internally programmed cell death pathway that may regulate both T cell development and senescence, and that is characterized by cleavage of DNA at internucleosomal regions. The present experiments show that acute HIV-1 infection of MT2 lymphoblasts and activated normal peripheral blood mononuclear cells induces apoptosis. The addition of anti-gp120 neutralizing antibody, after HIV-1 infection of MT2 cells, permitted sustained high levels of viral replication, but blocked apoptosis and cell death. Apoptosis may account for the direct cytopathologic effects of HIV-1 in T cells.

CD4 Antigens↗
PubMed1991

The autotransfusion effect of external leg counterpressure in simulated mild hypovolemia.

We examined the cardiovascular response of external leg counterpressure in healthy volunteers at 100 mm Hg compression pressure. To stimulate mild hypovolemia, measurements were made with the subjects in a 60 degrees head-up tilt position. Left ventricular end-diastolic volume (LVEDV) and cardiac output (CO) were calculated from two-dimensional echocardiography. Flow through the inferior vena cava (IVC) below the origin of the hepatic veins was determined by the Doppler ultrasound technique. The application of counterpressure significantly increased LVEDV, CO, and arterial blood pressure over that seen with tilting without the device. These responses were accompanied by a small but significant increase in IVC flow. We therefore concluded that external leg counterpressure transferred blood to the central circulation by compression of the venous capacitance vessels (an autotransfusion effect) in mild hypovolemia, but such an effect may not benefit patients in a hypovolemic shock state because of the small amount of translocated blood.

Adult↗
PubMed1990

Potent toxicity of 2-chlorodeoxyadenosine toward human monocytes in vitro and in vivo. A novel approach to immunosuppressive therapy.

Lymphoid cells were thought to be uniquely susceptible to excess 2'-deoxyadenosine (dAdo), when exposed to inhibitors of adenosine deaminase (ADA). However, we now find that human monocytes are as sensitive as lymphocytes to dAdo or to the ADA-resistant congener 2-chloro-2'-deoxyadenosine (CldAdo). Monocytes exposed in vitro to CldAdo, or to dAdo plus deoxycoformycin rapidly developed DNA strand breaks. Both the DNA damage and the toxicity of CldAdo or dAdo toward monocytes were blocked by deoxycytidine, but not by inhibitors of poly(ADP-ribose) polymerase. A partial decrease in RNA synthesis and a gradual decline of cellular NAD were early biochemical events associated with monocyte DNA damage. Low CldAdo concentrations (5-20 nM) inhibited monocyte phagocytosis and reduced the release of interleukin 6. Higher CldAdo concentrations led to a dose- and time-dependent loss of monocyte viability. Circulating monocytes disappeared within 1 wk in patients with cutaneous T cell lymphoma or with rheumatoid arthritis during continuous CldAdo infusion. The marked sensitivity of human monocyte function and survival to CldAdo in vitro, together with the monocyte depletion in patients receiving CldAdo chemotherapy, suggests that CldAdo or other dAdo analogues offer a novel therapeutic strategy for chronic inflammatory and autoimmune diseases characterized by inappropriate monocyte deployment or function.

2-Chloroadenosine↗
PubMed1989

Detection of an amino acid substitution in the mutant enzyme for a special type of adenine phosphoribosyltransferase (APRT) deficiency by sequence-specific protein cleavage.

Generally, if mutant and normal proteins have similar molecular weights and electric charges, they cannot easily be distinguished from one another. We have developed a unique method by which a mutant enzyme of adenine phosphoribosyltransferase (APRT) can easily be distinguished from normal enzyme with nearly identical molecular weight and electric charge. DNA sequencing data have suggested that in this special type of disease (Japanese-type APRT deficiency) there is an amino acid substitution from Met to Thr at position 136 of APRT. Since normal APRT has only one Met residue, the Japanese-type mutant APRT should be a methionine-free protein. Using both an amino acid sequence-specific antiserum against APRT, and specific cleavage of peptide at the methionine residue with BrCN, we could distinguish between normal and mutant proteins. Thus, normal but not mutant APRT was cleaved with BrCN, indicating that the mutant APRT is a methionine-free protein. All tested patients with the Japanese-type APRT deficiency were found to synthesize exclusively methionine-free APRT. Usefulness of this method is not restricted to a single family, as 79% of all the patients with this disease among Japanese, and more than half of all the patients with this disease reported in the world, are likely to have this unique mutation. Thus, not only sequence-specific cleavage of DNA with restriction endonucleases but also that of protein with a chemical agent has been shown to be sometimes useful for the diagnosis and analysis of a genetic disease by careful examination of normal and mutant amino acid sequences.

Adenine Phosphoribosyltransferase↗
PubMed1988

Tracheobronchial rupture caused by blunt chest trauma: acute respiratory management.

The clinical management of 12 patients with major intrathoracic tracheobronchial rupture (complete, 3; incomplete, 9) due to blunt trauma has been reviewed and compared with that of two groups of patients with chest injuries not involving the tracheobronchial tree, 17 patients with multiple rib fractures and 17 with chest injuries requiring thoracotomy for control of pneumothorax and hemothorax. The effect of injury on ventilatory function was significantly greater in the patients with tracheobronchial injury in whom an elevated PCO2 at the time of admission was associated with a poor prognosis. Conventional ventilatory management with endotracheal intubation and positive pressure ventilation causing increased air leakage produced further deterioration of pulmonary function in four of the patients with tracheobronchial disruption. The use of a double-lumen endobronchial tube in two patients with tracheobronchial rupture facilitated ventilatory support and subsequent operative management.

Adolescent↗