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Biomedical subjects

D Martinez

Publications and source records attributed to D Martinez.

At least 163 records · Page 9Linked to original sources
PubMed1982

[Immunohistochemical localization of pituitary peptides in the rat pyloric antrum mucosa].

Several peptides normally produced in the anterior pituitary lobe were searched in rat antral mucosa by immunocytochemistry. Peptides derived from pro-opiomelanocortin were tested: some endocrine cells were immunoreactive with ACTH 17-39 antiserum, and only a few elements were stained with ACTH 1-24 and beta LPH antisera. No immunoreactive cells were observed using alpha MSH, beta MSH and beta endorphine antisera. Using an antiserum against beta endorphin, a few cells and nerve fibres were immunostained. The other pituitary hormones were also tested: numerous antral cells contained immunoreactive GH, and some cells immunoreactive PRL or compounds chemically related to these hormones. No cells were stained with antisera directed against glycoproteic hormones. This work showed that several peptides previously localized in the pituitary gland were found in the antral mucosa. Further studies are needed to identify the cell types containing these peptides and to determine their origin.

Adrenocorticotropic Hormone↗
PubMed1981

Immune responses in mice against herpes simplex virus: mechanisms of protection against facial and ganglionic infections.

We performed experiments with mice to determine the nature of the immune response(s) that prevents primary infections of the skin and the trigeminal ganglia with herpes simplex virus. Immunization with infectious herpes simplex virus, inactivated virus, or material enriched for viral glycoproteins protected hairless mice against primary facial and ganglionic infections. Live and inactivated viruses induced neutralizing antibodies, whereas glycoprotein material did not. Instead, glycoprotein material induced antibodies that were largely directed against two glycopolypeptides with molecular weights of 120,000 to 130,000. Hairless mice immunized with glycoprotein material responded faster than control mice in the synthesis of neutralizing antibodies after challenge with infectious virus. Congenital athymic BALB/c (nu/nu) mice were protected against primary facial infections after immunization with glycoprotein material, but glycoprotein-specific antibodies were not induced.

Animals↗
PubMed1981

[Histological study of the action of propranolol on the genital tract of the male rat].

Increasing doses of propranolol were injected intraperitoneally to four series of adult male rats in order to study the effect of this beta-blocking agent on various organs (testis, epididymis, prostate and seminal vesicle) and endocrine glands (adrenals, pancreas, thyroid, pituitary). Histological damage was observed only in testes: i.e., necrosis and desquamation of germinal cells in the seminiferous tubules associated with light arterial vasoconstriction. Pelviperitoneal fibrosis was observed as well. These lesions seem to be of pharmacological vascular origin and appear to occur in combination with an elective toxic effect of propranolol on the germinal cells.

Animals↗
PubMed1980

Identification of lactate dehydrogenase-elevating virus as the etiological agent of genetically restricted, age-dependent polioencephalomyelitis of mice.

The etiological agent of genetically restricted, age-dependent polioencephalomyelitis of mice (the ADPE agent) and several isolates of lactate dehydrogenase-elevating virus (LDV) were compared by biological, physical-chemical and antigenic criteria. The data indicate that the ADPE agent is a strain of LDV. Like LDV, the ADPE agent induced a selective elevation of plasma enzymes and splenomegaly in mice. The enzyme-elevating activity and the paralytogenic activity of the ADPE agent preparations were shown to belong to the same virus. The ADPE agent demonstrated LDV-like replication kinetics in vivo and in vitro. Moreover, the ADPE agent required primary mouse macrophages for in vitro replication, as does LDV. In turn, the LDV isolates induced a paralytic disease with ADPE-like lesions in the spinal cords of immunosuppressed C58 mice. However, the LDV isolates showed a stronger dependence on strain and age of mouse for the induction of paralysis than did the ADPE agent. The LDV isolates and the ADPE agent exhibited indistinguishable morphologies, buoyant densities, structural protein patterns, and virion ribonucleic acid sedimentation rates. Furthermore, they displayed strong antigenic cross-reactivity, as determined by cross-protection in vivo and by radioimmunoassay.

Aging↗
PubMed1980

Macrophage dependence of polyriboinosinic acid-polyribocytidylic acid-induced resistance to herpes simplex virus infection in mice.

The relative contributions of macrophages and lymphocytes to the induction of resistance to primary herpes simplex virus type 1 (HSV-1) infection by polyriboinosinic-polyribocytidylic acid complex [poly (I:C)] were investigated in C58 mice. The induction of resistance was found to be strongly dependent on macrophages compared to lymphocytes. Macrophage-deficient (silica-treated) mice produced less interferon and were not as responsive to prophylactic treatment of HSV-1 infections with poly (I:C) as were either normal, lymphocyte-deficient (cyclophosphamide-treated), or T-lymphocyte-deficient (anti-thymocyte serum-treated, adult-thymectomized) mice. Silica and cyclophosphamide treatments reduced the therapeutic activity of poly (I:C), whereas T-cell depletion did not have a significant effect. Similarly, the protection of mice with exogenous interferon was markedly reduced in silica-treated mice and moderately reduced in cyclophosphamide-treated mice, but unaffected in T-cell-deficient mice. Furthermore, suppression of HSV-1 plaque formation was obtained by cocultivation of infected mouse fibroblast monolayers with peritoneal (macrophage-rich) cells, but not with splenic (lymphocyte-rich) cells, from poly (I:C)-treated mice. Peritoneal cells did not protect heterologous (human) fibroblasts, suggesting that the protection of mouse embryo fibroblasts is mediated by interferon. Collectively, the data indicate that macrophages are required for the production of poly (I:C)-induced interferon and that macrophages and perhaps B-lymphocytes are important for mediating the protection against HSV-1 infection after interferon has been produced.

Animals↗
PubMed1979

Viral etiology of age-dependent polioencephalomyelitis in C58 mice.

The etiology of immune polioencephalomyelitis (IPE) and the mechanisms of resistance to IPE induction were investigated in C58 mice. IPE was found to be induced by a lipid-solvent-sensitive, filterable replicating agent present in line Ib leukemic cell suspensions. IPE was serially transmitted in immunosuppressed mice with filtered extracts of spleens from diseased animals. The IPE-inducing activity of Ib cell extracts was abolished by chloroform or deoxycholate. Gel filtration of Ib cell extracts showed that the IPE agent has a molecular weight of at least 10(7). Electron microscopy of the active fractions from columns and of spinal cord extracts from mice with IPE revealed a virus-like particle, 40 nm in diameter, which is probably the IPE revealed a virus-like particle, 40 nm in diameter, which is probably the IPE agent. Administration of cyclophosphamide at various times after challenge increased the incidence of IPE in mice, suggesting that IPE is not autoimmune mediated. Immunosuppression resulted in maintenance of high levels of IPE agent in the central nervous system tissue, while immunization resulted in low levels. Moreover, immunized mice produced neutralizing antibodies. These data suggest that antibodies help restrict the amount of IPE agent in the nervous tissue, and that this restriction is required for resistance to IPE induction in C58 mice.

Aging↗
PubMed1979

Histocompatibility-linked genetic control of susceptibility to age-dependent polioencephalomyelitis in mice.

Susceptibility to induction of immune polioencephalomyelitis (IPE) was found to be controlled by a gene that is closely linked to the H-2 complex. Whereas mice of the AKR (H-2k) strain were susceptible to IPE induction, H-2-congenic mice, AKR.H-2b (H-2b from C57BL/6) and AKR.M (H-2m), were resistant. However, susceptibility to IPE may be under additional control by a gene(s) outside of the H-2 region, since both C57BL/6 (H-2b) mice and congenic B6.H-2k mice (H-2k from AKR) were resistant to IPE induction. F1 hybrid mice derived from AKR (susceptible) and DBA/2 (resistant) mice were susceptible to IPE induction, indicating that susceptibility is dominant in at least one gene, but susceptibility developed at a later age in the hybrid mice than in AKR mice. B6.PL-Ly-2a Ly-3a/Cy, C57BR, C57L, PL, and RF strain mice were resistant to ipe induction. Thus, of the 12 inbred strains tested so far, only two (C58 and AKR) are susceptible to IPE.

Aging↗
PubMed1979

Resistance of C58 mice to primary systemic herpes simplex virus infection: macrophage dependence and T-cell independence.

The relative contribution of thymus-derived lymphocytes (T-cells) and of macrophages to resistance to primary infection with herpes simplex virus type 1 (HSV-1) was studied in C58 mice. Resistance was dependent on macrophage competence, but was relatively independent of T-lymphocyte competence. Although aging mice became progressively more deficient in functional T-cells, as demonstrated by a decreasing resistance to transplanted line Ib leukemia and by declining responses to T-cell nitogens (concanavalin A and phytohemagglutinin), their resistance to HSV-1 increased with increasing age. Moreover, in mice that were made selectively deficient in T-cells by the combination of adult thymectomy and treatment with anti-thymocyte serum, resistance to HSV-1 did not correlate spleen and mesenteric lymph nodes. However, selective reduction of macrophages by intraperitoneal injection of silica resulted in enhanced susceptibility to HSV-1. Furthermore, in vitro suppression of HSV-1 plaque formation in mouse embryo fibroblast cells was obtained by cocultivation of infected fibroblast monolayers with peritoneal macrophages, but not with splenic lymphocytes, from adult mice. Macrophages from weanling mice failed to suppress the development of plaques, indicating that the increase in resistance to HSV-1 with age is a result of increased macrophage competence.

Aging↗
PubMed1976

Pathogenetic mechanisms in immune polioencephalomyelitis: induction of disease in immunosuppressed mice.

Immune polioencephalomyelitis (IPE) was induced by the i.p. injection of x-irradiated (10, 000 R) syngeneic line Ib malignant lymphocytes into C58 mice that were 7 or more months old and in young mice immunosuppressed by x-ray or drugs. The occurrence of IPE in young immunosuppressed C58 mice was systematically analyzed. When mice less than 2 weeks old were x-irradiated with 600 R, IPE could not be induced. The incidence in 1-month-old mice was approximately 50% and increased progressively with the age except for a drop in incidence at 3 months. An analysis of the dose effects of x-irradiation on the occurrence of IPE in mice of different ages revealed a marked increase in the incidence in 3- and 5-month-old mice beginning at dose levels of 450 R and 300 R, respectively. Considered together, these data indicated that two subpopulations of immunocytes differing in x-ray sensitivity interacted to protect mice from IPE. It appears that under natural conditions an x-ray sensitive cell population, possibly having suppressor function, decreased with age and made mice susceptible ot induction of IPE. Five-month-old mice were immunosuppressed with an LD10 of cyclophosphamide, prednisolone, or methotrexate to determine whether mice immunosuppressed with drugs also were susceptible to the induction of IPE. The incidence was 89%, 13%, and 5%, respectively. The mouse strain specificity of IPE induction also was studied. In 6- to 8-month-old mice suppressed with 600 R, IPE could not be induced in non-H-2k strains: BALB, C57BL/6, NZB. Of the H-2K strains tested (CBA/J, C3H/He, AKR/J, C58), the disease could be induced only in the C58 and AKR/J strains. Histopathologic studies showed that CNS lesions in immunosuppressed C58 and AKR/J mice did not differ significantly from those in old C58 mice with IPE. Taken together, the results of these studies indicate that IPE can be used as a model for analyzing age-dependent diseases of suspected immunopathologic etiology.

Aging↗
PubMed1976

Nursing attitudes toward oral liquid unit dose packaging.

Nurses' attitudes toward three types of oral liquid unit dose packages--glass, plastic and aluminum--were determined. Thirty nurses who previously had not used unit dose packaging on their units were asked to evaluate the three types of packaging. The nurses preferred both aluminum and plastic over the glass containers; there was no significant difference in attitude toward the plastic and aluminum packages.

Aluminum↗
PubMed1976

Pathogenetic mechanisms in immune polioencephalomyelitis: quantitative evaluation of protective and pathogenic effects of lymphoid cells.

Terminal dilution, adoptive cell transfer techniques were developed to quantify the protective effect of lymphoid cells in the pathogenesis of immune polioencephalomyelitis (IPE). The pathogenic effects of lymphoid cell populations were quantified by deleting the step of antigenic challenge. Regression curves were computer analyzed and PD50 values were compared. Immune spleen cells (ISC) from 4- to 6-week-old donors were more protective (PD50 = 4.9 +/- 1.3) than ISC from 12-month-old animals (PD50 greater than 7.0). The slopes of the regression curves also differed markedly (young mice, -0.24; old mice, -0.09). ISC were less protective in 12-month-indicator mice than in 5-month-old recipients (PD50 values of 5.2 +/- 0.8 and 3.7 +/- 0.8, respectively). When adoptive cell transfer tests were used to quantify the pathogenetic effects of donor cells it was found that ISC were pathogenetic at doses of 10(5) or less, but protective at higher doses. IPEC were pathogenetic at all test doses. When ISC were x-irradiated or sonicated the were only pathogenetic. Normal spleen or peritoneal exudate cells were neither protective nor pathogenetic. A model was developed in which mice were either thymectomized at birth (Tx), or Tx at birth and x-irradiated (500 R) 8 weeks later (Tx-XR). Sham Tx or Tx-XR mice served as controls. All of the mice were challenged with antigen (10(4) x-irradiated Ib cells). Only a portion (8/24) of the Tx mice developed IPE, indicating that resistance was T cell dependent but also involved a significant T cell independent component. The data also indicated that T cells were not pathogenetic effector cells in this model. Tx mice were not reconstituted by ISC (7/18 developed IPE), Tx-XR mice were partially reconstituted (3/12 developed IPE), but sham Tx-XR were fully restored (0/20 had IPE). Normal spleen cells did not reconstitute any of the mice.

Age Factors↗