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Biomedical subjects

M Ho

Publications and source records attributed to M Ho.

At least 343 records · Page 19Linked to original sources
PubMed1978

Production of interferon and serum hyporeactivity factor in mice infected with murine cytomegalovirus.

Mice injected intraperitoneally with murine cytomegalovirus produced as many as 1,000 U of serum interferon. The response appeared biphasic, with maximum titers in the first phase detectable from 2 through 4 days after infection. A second phase peaked 10 days after infection. By carboxyhexyl-Sepharose affinity chromatography, the serum interferon behaved like lymphocyte interferon. The infected mice also produced substantial quantities of serum hyporeactivity factor (D.A. Stringfellow, E.R. Kern, D.K. Kelsey, and L.A. Glasgow, J. Infect. Dis. 135:540-551, 1977), although always in the presence of interferon. This factor was separated from the serum interferon by concanavalin A-Sepharose affinity chromatography.

Animals↗
PubMed1978

Hyporeactivity factor produced after induction of immune interferon in mice sensitized with BCG.

Sera from BCG-sensitized ICR and C57BL/10J mice challenged with BCG were examined. Two types of hyporeactive factor (HF), which produced refractoriness to induction of interferon (IF) by Newcastle disease virus in mouse embryo fibroblasts, were produced in addition to type II immune IF. One was destroyed at pH 2, and the other was not. The acid-labile HF, together with immune IF, appeared 2 h after challenge with BCG. Acid-labile HF and immune IF were not neutralized by antiserum against L-cell IF and may be one substance. On the other hand, acid-stable HF appeared later and was neutralized by antiserum against L-cell IF. Furthermore, acid-stable HF was more stable at 56 degrees C than were immune IF and pH-labile HF. Induction of IF by Newcastle disease virus was also reduced in mice 6 h after receiving one injection of BCG, irrespective of whether the animals were previously sensitized to BCG.

Animals↗
PubMed1977

Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease.

Eleven instances of a mixed acid-base disorder consisting of chronic respiratory acidosis and metabolic alkalosis were recognized in eight patients with chronic obstructive lung disease and carbon dioxide retention. Correction of the metabolic alkalosis led to substantial improvement in blood gas values and clinical symptoms. Patients with mixed chronic respiratory acidosis and metabolic alkalosis constitute a common subgroup of patients with chronic obstructive lung disease and carbon dioxide retention; these patients benefit from correction of the metabolic alkalosis.

Acetazolamide↗
PubMed1977

The adrenal medulla may mediate the increase in pineal melatonin synthesis induced by stress, but not that caused by exposure to darkness.

As previously shown (Lynch et al.: Proc. Nat. Acad. Sci. [U.S.A.] 70, 1704-1707 [1973]), the activity of the enzyme serotonin-N-acetyltransferase (NAT) in the rat pineal increases when the animal is placed in darkness or is subjected to the stress of physical immobilization; partial sympathetic denervation (i.e., pretreatment of the animal with intravenous 6-hydroxydopamine [6-OHDA]) does not block either response. The present studies explored the roles of the pineal sympathetic nerves and the adrenal medullas in mediating these responses. The stress-induced increase in pineal NAT activity was blocked by bilateral adrenalectomy, but not by bilateral superior cervical ganglionectomy or by treatment with 6-OHDA (both of which potentiate the NAT response in normal rats and restore it in adrenalectomized ones). The increase in pineal melatonin content caused by immobilization was also blocked by adrenalectomy, but potentiated by pineal sympathetic denervation. In contrast, bilateral adrenalectomy did not affect the darkness-induced rise in pineal NAT activity, although pineal sympathetic denervation (by bilateral superior cervical ganglionectomy) did block this response. 6-OHDA pretreatment neither blocked the response to darkness nor restored it in ganglionectomized animals; thus, this treatment apparently fails to produce a complete pineal denervation. The pineal response to stress has previously been shown to be blocked by beta-adrenergic blocking agents. The present studies demonstrate that alpha-adrenergic blockade (with phenoxybenzamine) potentiates this response in intact animals and restores it in adrenalectomized rats (possibly by acting presynaptically on receptors on pineal sympathetic terminals and thereby augmenting norepinephrine release). These observations show that the rat pineal organ normally receives information from two "channels", i.e., trans-synaptically (from pineal sympathetic nerves) and via the circulation (from the adrenal medullas and, perhaps, from distant sympathetic nerves).

Acetyltransferases↗
PubMed1977

Enhancement of murine cytomegalovirus infection during graft-vs.-host reaction.

A mouse model was used for elucidation of the role of a graft-vs-host reaction in promoting cytomegalovirus infection. F1 (DBA/2 X C3H/He) hybrid mice were infected with murine cytomegalovirus. Five weeks later, a graft-vs.-host reaction was produced in the chronically infected animals by the administration of multiple doses of DBA/2 parental splenocytes. Cytomegalovirus was recovered more often from the organs of mice undergoing graft-vs.-host reaction than from those of control animals (P less than 0.001). These results indicate that the graft-vs.-host reaction alone can enhance murine cytomegalovirus infection in a chronically infected host and may help explain the high incidence of cytomegalovirus infection after bone marrow allograft transplantation in man.

Animals↗
PubMed1977

Cellular origin of interferon induced by bacterial lipopolysaccharide.

Bacterial lipopolysaccharide (LPS) induces interferons with different properties in mouse macrophages and B lymphocytes. Macrophage interferon is labile at 56 degrees C and is neutralized by anti-mouse fibroblast interferon at a dilution of 1:6,142. B cell interferon is more heat stable and is neutralized by the same antiserum only at a dilution of 1:276. Serum obtained early (1 h) after an intravenous injection of 100 mug of LPS resembled macrophage interferon, whereas serum obtained at later times resembled more and more B cell interferon. The diverse cellular origin of LPS-induced interferon may explain the broad hyporesponsiveness produced by LPS in animals.

Animals↗
PubMed1977

Differences in mouse interferons according to cell source and mode of induction.

Mouse interferon induced by ultraviolet-irradiated Newcastle disease virus or polyriboinosinic-polyribocytidylic acid in T lymphocytes, B lymphocytes, macrophages, and primary mouse embryonic cell culture was studied. Irrespective of the inducer, interferons produced by T or B lymphocytes were relatively heat stable and of low antigenicity when reacted with antiserum against L-cell interferon (ALI), whereas interferons produced by macrophages and mouse embryo cells were heat labile and of high antigenicity against ALI. Mouse interferons induced by ultraviolet-irradiated Newcastle disease virus were separated into three components by chromatography on CH-Sepharose 4B. Interferons produced by T and B lymphocytes consisted primarily of component 1 (unbound fraction), whereas interferons produced by macrophages or mouse embryo cells consisted primarily of component 3 (eluted by 0.5 M NaCl). Component 1 was heat stable and of low antigenicity against ALI, properties characteristic of T- and B-cell interferon. Components 2 and 3 were heat labile and of high antigenicity against ALI, properties characteristic of macrophage and mouse embryo cell interferon. In contrast, interferon induced in mice sensitized with BCG differed from these interferons induced in B cells, T cells, macrophages, and fibroblasts in being extremely acid labile and nonreactive against ALI.

Animals↗
PubMed1977

Evaluation of anti-complement immunofluorescence test in cytomegalovirus infection.

The anti-complement immunofluorescence (ACIF) technique was evaluated for the diagnosis of human cytomegalovirus (CMV) infection in a group of sera derived from renal transplant recipients and donors by comparing it with the indirect immunofluorescence (FA) and complement fixation (CF) TESTS. The ACIF and FA tests yielded similar results. However, the ACIF test had a distinct advantage over the indirect FA test, since it eliminated the nonspecific cytoplasmic staining that may result in false positive readings in inexperienced hands. Both the indirect FA and ACIF tests were more sensitive than the CF test. In primary CMV infection, the FA and ACIF antibodies appeared earlier and had significantly higher titer than corresponding CF titers. This difference in titers was not seen in seropositive individuals who lacked overt infection. Our previously reported correlation between the seropositivity of the donor and CMV infection in seronegative recipients has been confirmed.

Antibodies, Viral↗
PubMed1977

Primary and secondary cytomegalovirus infection.

Forty-seven patients who underwent renal transplants were followed clinically and were examined for serologic or virologic evidence of cytomegalovirus (CMV) infection. There were 18 cases of primary infection and ten cases of secondary infection. These findings were based on whether the patient was seronegative or seropositive prior to transplantation. Thirteen patients with primary infection and only one patient with secondary infection had two or more of the following manifestations that are temporally associated with laboratory evidence of infection: fever, leukopenia, atypical lymphocytes, lymphocytosis, hepatosplenomegaly, myalgia, arthralgia, and pneumonitis. Five patients with primary infections, one of whom died with disseminated disease, were recognized by attending physicians as having CMV disease. Since primary infection is though to be largely due to virus transmitted by the kidney of a seropositive donor, it may be possible to prevent symptomatic primary infection by using only seronegative donors for seronegative recipients.

Adult↗
PubMed1977

Induction of the interferon protein in the animal: general considerations.

Serum interferon is largely produced by B and T lymphocytes and macrophages, depending on the inducer. Lymphocyte interferon is different from macrophage and fibroblast interferon. There are two alleles controlling mouse interferon production. A protein possibly related to interferon may cause hyporeactivity. Our work was supported by NIH Grant 5-RO1-02953.

Animals↗
PubMed1976

Cytomegalovirus infection in patients receiving immunosuppressive therapy for rheumatologic disorders.

Evidence of cytomegalovirus infection was sought in 131 patients attending a rheumatology clinic, 211 blood donors, and 14 patients before and after the initiation of cytotoxic immunosuppressive therapy for a rheumatologic condition. The titer of complement-fixing antibody to cytomegalovirus was significantly related to age and sex, but not to rheumatologic disease. After adjustment for age and sex differences, the proportion of patients treated with corticosteroids who had measurable antibody was lower than that of controls (P less than 0.025). Immunosuppressive therapy with azathioprine or cyclophosphamide did not affect the proportion of patients with antibody, but there was a significantly increased titer of antibody in those who were seropositive (P = 0.04). Cytomegalovirus was isolated from the urine of 20% of patients receiving cytotoxic immunosuppressive drugs, but not from any of the patients receiving corticosteroids or neither form of therapy (P = 0.001). Eight of 14 patients followed prospectively after the initiation of therapy with immunosuppressive drugs became infected with cytomegalovirus as demonstrated by a fourfold or greater rise in complement-fixing titer, viruria, or both. Seven of the eight patients were seropositive before therapy, a finding suggesting that immunosuppression acts largely by reactivating latent infection. It is postulated that immunosuppressive agents alone may account for a large proportion of cytomegalovirus infections seen after allograft transplantation.

Adrenal Cortex Hormones↗
PubMed1976

Cellular basis of interferon formation and hyporeactivity after exposure to bacterial lipopolysaccharide.

Endotoxin apparently induces interferon in only a few types of cell, yet it produces strong hyporesponsiveness to a large number of agents. After incubation for 24 hr with endotoxin in vitro, tissue cultures of thymus, spleen, mesenteric lymph nodes, and to a lesser extent, liver and lung produced interferon. Lymphoid tissues of bone marrow-derived (B-) cells (sacculus rotundus, appendix, and Peyer's patches) and kidney did not produce interferon. Adherent spleen cells produced more interferon than nonadherent cells. Purification of spleen cells on a bovine serum albumin gradient showed that light, DNA-synthesizing cells made interferon in response to endotoxin or polyriboinosinic-polyribocytidylic acid. Mouse spleen cells produced a "late" interferon 24-48 hr after exposure to endotoxin, which, in contrast to "early" interferon (produced at 0-24 hr) from spleen and other tissues, is stable at 56 C for 60 min. It is suggested that this late interferon represents a "B-cell" interferon. Hyporeactivity was produced in vitro by endotoxin only in tissues that make endotoxin-induced interferon, a fact consistent with the theory that the interferon-inducing mechanism must be initiated before hyporeactivity results. The fact that endotoxin has been found to act on a fairly large range of cells (i.e., macrophages, thymus-derived cells, and probably B-lymphocytes) explains its ability to produce broad hyporesponsiveness.

Animals↗
PubMed1976

Viral infections in renal transplant recipients.

Cytomegalovirus (CMV) infections are common in renal transplant recipients. We studied 23 recipients prospectively to determine whether infections by other herpes-group and non-herpes-group viruses were also present. Sera, obtained at the time of surgery and periodically thereafter, were tested for antibody to CMV, herpes simplex virus (HSV), Epstein-Barr virus (EBV), parainfluenza viruses types 1, 2, and 3, and the viruses of measles and rubella. We found no evidence of an unusual incidence of primary or secondary infection by the non-herpesviruses tested. Rises to CMV, HSV, and EBV antibody titers occurred in 43, 38, and 32% of patients, respectively. All serological rises to herpes-group viruses occurred in patients seropositive at the time of transplantation, with the exception of three patients who experienced primary CMV infections. We conclude that reactivation of all herpes-group viruses tested may occur in transplant recipients. Morbidity was associated only with primarly CMV infection.

Adolescent↗
PubMed1976

Use of biological characteristics to type Herpesvirus hominis types 1 and 2 in diagnostic laboratories.

Fifty clinical isolates of Herpesvirus hominis were typed by pock size on chicken embryo chorioallantoic membranes, sensitivity to heparin, and plaque formation on chicken embryo cell cultures. Of 19 isolates that were typed serologically, there was 100% concordance with respect to plaque formation. Pock size was incorrect in one instance and indeterminate in another. Heparin sensitivity was incorrect for one. Of 31 strains that were only biologically characterized, there were four for which heparin sensitivity did not agree with the other two characteristics. Of the three biological tests, the ability to form plaques in chick cell monolayer was the most reliable indicator type.

Animals↗