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Biomedical subjects

T J Romano

Publications and source records attributed to T J Romano.

At least 55 records · Page 3Linked to original sources
PubMed1985

Esophago-bronchial fistula in a patient with rheumatoid arthritis.

A 58-year-old woman with active rheumatoid arthritis developed an esophago-bronchial fistula in close temporal proximity to the eruption of subcutaneous nodules and a worsening of her joint symptoms. Possible mechanisms to explain the fistula formation are discussed.

Arthritis, Rheumatoid↗
PubMed1985

Pars plana lensectomy and vitrectomy by ultrasonic fragmentation: Part III--Results in eyes without other ocular pathology or an implant.

The records of 320 eyes without other ocular pathology undergoing pars plana lensectomy and vitrectomy by ultrasonic fragmentation for routine cataract extraction without an implant were reviewed retrospectively. Three hundred two (302/320-94.4%) had vision between 20/20-20/40. Reasons for vision less than 20/40 in 18/320 (5.6%) eyes included 5/320 (1.5%) with retinal detachments, 11/320 (3.4%) with clinically apparent cystoid maculopathy, 1/320 (0.3%) with a macular hole, and 1/320 (0.3%) with retained lens material. Comparison was made between 184 lensectomies performed by the original technique and 136 pars plana lensectomies performed by the modified technique. Vision between 20/20-20/40 was achieved by 168/184 (91.3%) of the original technique group versus 134/136 (98.5%) of the modified technique group. In the latter group, there was one retinal detachment (0.7%), one macular hole (0.7%) and no clinical cystoid maculopathy. Fluorescein angiography performed three months postoperatively in eyes having vision of 20/20-20/40 of the modified lensectomy group showed cystoid maculopathy in one eye which had undergone trauma-induced wound dehiscence.

Aged↗
PubMed1984

Development of suckling controls in the rat: independence from thyroxine.

Until 2 weeks of age, rat pups attach to the nipples of their dam with the same avidity regardless of whether they are fed or fasted. During the 3rd postnatal week, some mode of control of suckling appears such that fasted pups attach much more rapidly than fed pups. In this study we have investigated the effects of hyper- and hypothyroidism on the maturation of suckling controls. Surprisingly, the results indicate that this aspect of behavioral development is independent of the thyroxine status of the pup. We conclude that the maturation of suckling controls is not cued by the developmental rise of serum thyroxine that occurs during the 2nd postnatal week.

Animals↗
PubMed1984

Coexistence of systemic lupus erythematosus and parotid hypertrophy. A case report and literature review.

A patient with systemic lupus erythematosus and marked diffuse bilateral parotid swelling is described. Special staining techniques were required to demonstrate a lymphoplasmacytic infiltrate in the otherwise normal appearing acinar tissue. This finding suggests that a humoral, rather than a cellular, mediated immune process is responsible for the parotid hypertrophy in this patient.

Autoimmune Diseases↗
PubMed1982

Investigation of body temperature as a possible feeding control in the suckling rat.

Under natural conditions, rat pups are deprived of milk only when the dam leaves the nest. At this time the body temperatures of the pups will fall. In this study we have investigated the possibility that lowered body temperature of the pups stimulates behavioral changes in either the pups or the dam, leading to increased milk intake. To study behavioral changes of the pups, the milk intake of warm-fasted, cool-fasted, and fed littermates was compared to 10, 14 and 16 days of age. There was no effect of body temperature on milk intake at any age. To study behavioral changes in the dam, milk release by dams suckling entire cool litters was compared with that by dams suckling entire warm litters. Milk release was not significantly affected by the litter temperature. We conclude that lowered body temperature of suckling rat pups does not cause increased milk intake.

Animals↗
PubMed1980

Analysis of the lytic step in the herpes simplex virus antibody-dependent cellular cytotoxicity system.

An antibody-dependent cellular cytotoxicity (ADCC) system in which herpes simplex virus-infected Chang liver cells are used was assessed for its dependency on cellular energy, ribonucleic acid and protein synthesis, and cytoskeletal structures such as microfilaments and microtubules. The cytotoxic reaction was only slightly inhibited when glycolysis was blocked in a glucose-free medium containing 10(-2) M 2-deoxy-d-glucose. It was more substantially inhibited when respiration was blocked with 10(-2) M sodium azide. The reaction was totally ablated, however, only when both glycolysis and respiration were suppressed. This inhibitory effect of energy deprivation was mediated solely at the level of the effector cell. Ribonucleic acid synthesis or protein synthesis by the effector cells was not required, as shown by the fact that neither actinomycin D, cycloheximide, nor emetine significantly inhibited ADCC. The ADCC reaction was partially inhibited by cytochalasin B, whose inhibitory effect was rapidly reversible, and was completely and irreversibly inhibited by cytochalasin A. Cytochalasin A acted on the effector cells rather than the target cells. The reaction was also partially inhibited by colchicine, whose inhibitory effect was directed solely against the effector cells and was slowly reversible. The inhibitory effects of cytochalasin B and colchicine, when used in tandem at submaximal inhibitory concentrations, were slightly more than additive. The results suggest a cooperative role for effector cell microfilaments and microtubules in mediating ADCC. Kinetic studies of ongoing herpes simplex virus ADCC reactions after initial centrifugation showed that the lytic step requires expenditure of metabolic energy as well as intact function of both microfilaments and microtubules. These findings, in concert with previous data, indicate that the ADCC process against herpes simplex virus-infected Chang liver cells can be resolved into adhesion and lytic steps. The lytic step can be readily distinguished from the adhesion step by its increased sensitivity to low ambient temperature or metabolic energy deprivation, its sensitivity to thermal inactivation, its requirements for extracellular divalent cations, and its dependence on normal function of both microfilaments and microtubules.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1979

Analysis of the adhesion step in the herpes simplex virus antibody-dependent cellular cytotoxicity system.

The lysis of herpes simplex virus-infected tissue culture cells by antibody-dependent cellular cytotoxicity (ADCC) requires a preliminary step in which effector cells adhere to the immunoglobulin G antibody-coated targets. To study the adhesion step, we made use of two observations: (i) some of the mononuclear cells in human blood form rosettes with antibody-coated target cells, and (ii) most ADCC effector cells can be removed by allowing mononuclear cells to adhere to monolayers of antibody-sensitized tissue culture cells. The effect of various experimental conditions on the adhesion step was assessed in ADCC cultures both at unit gravity and after centrifugation. At unit gravity both rosette formation and monolayer adhesion were partially reduced at 4 degrees C as compared to 37 degrees C. Both were also partially inhibited in glucose-free medium containing sodium azide and 2-deoxyglucose but were unaffected in glucose-free medium containing only one of these energy inhibitors. In contrast, after centrifugation neither reaction was inhibited at 4 degrees C or in glucose-free medium with sodium azide and 2-deoxyglucose. Cytochalasin B but not colchicine suppressed both reactions. Inhibition by cytochalasin B could not be reversed by centrifugation. Both reactions were independent of extracellular Ca(2+) and Mg(2+) and were unaffected by rendering mononuclear cells cytotoxically inactive by brief heat shock. These findings indicate that the adhesion step in ADCC directed against virus-infected or uninfected tissue culture cells is only modestly dependent on effector cell energy generation, that centrifugation greatly reduces this dependence, and that microfilaments but not microtubules are necessary. The modest ambient temperature and energy requirements, independence of extracellular divalent cations, lack of sensitivity to colchicine, and relative resistance to supraphysiological temperature serve to distinguish the adhesion step from the lytic step in ADCC.

Antibodies, Viral↗
PubMed1977

Selective viral immunosuppression of the graft-versus-host reaction.

Graft-vs.-host (GVH) reactivity of parental lymph node (LN) cells was assayed by measurements of 3H-thymidine incorporation in vivo in spleens of irradiated F1 recipients. Preincubation of parental LN cells with vesicular stomatitis virus (VSV) for 2 h at 37 degrees C followed by washing resulted in an 85-90% reduction in splenic radioactivity, as did injection of VSV on days 0-2 after recipients received untreated parental LN cells. In contrast, 3H-thymidine incorporation in the spleens or irradiated F1 hosts was not affected by VSV when F1 bone marrow cells were incubated with the virus. In addition, preincubation of F1 B cells with VSV still allowed these syngeneic B cells to be recruited into proliferation by mitomycin-treated parental LN cells. The inhibitory effect of VSV, thus, seems to be specific for T-cell proliferation. These observations suggest that viral immunosuppression might be capable of being developed into a useful strategy for selective deletion of lymphocytes capable of reacting against histocompatibility antigens and initiating GVH reactions.

Animals↗
PubMed1976

Mechanisms by which hapten conjugates of pneumococcal polysaccharide interfere with the challenge of anti-hapten memory cells.

Incubation of trinitrophenylated hemocyanin (TNP-KLH)-primed spleen cells with microgram amounts of 2,4-dinitrophenyl (DNP) or 2,4,6-trinitrophenyl (TNP) conjugates of pneumococcal polysaccharide type 3 (SIII) for as little as 5 min at 4 degrees C results in a specific "block" of the 19 S and 7 S adoptive memory response to TNP-KLH. This hapten-SIII-induced block of anti-hapten memory B cell responsiveness seems to be an example of specific receptor blockade. The block is specific and can be prevented by simultaneous incubation of the primed cells with hapten-protein conjugates which presumably compete with the hapten-polysaccharide for attachment to the B cell surface via anti-hapten Ig receptors. Removal via capping of these Ig receptors by exposure of TNP-KLH-primed memory cells to rabbit anti-mouse Fab serum for 45 min at 37 degrees C renders these cells refractory to the blocking effect of hapten-SIII. Once the hapten-SIII has attached to the memory cells, these blocked cells can be "rescued" (i.e. returned to a state of responsiveness) by incubating these cells with either mouse anti-SIII at 37 degrees C or rabbit anti-DNP serum at 4 degrees C. Since a papain digest of the IgG fraction of rabbit anti-DNP did not rescue the cells while the intact IgG did, a capping off of the TNP-SIII was proposed as the mechanims for this return to responsiveness of the hitherto blocked cells. A rescue was not seen by treatment of recipient mice with such B cell mitogens as dextran sulfate, endotoxin or purified protein derivative of tuberculin.

Animals↗
PubMed1976

Graft-vs-host reactions in F1 mice induced by parental lymphoid cells: nature of recruited F1 cells.

Graft versus host (GVH) reactivity of parental lymph node (LN) cells was assayed by measurements of 3H-thymidine incorporation in vivo. Mitomycin (Mit.) treatment of parental cells abolished their proliferative activity but the combination of such Mit.-treated parental cells with F1 LN cells resulted in much higher proliferation than either one population alone. This recruitment into proliferation of F1 cells was prominent on days 3 and 4 after cell injection and amounted to 35 to 51% of the total activity seen after injection of untreated parental cells alone. The F1 cell sensitive to recruitment was resistant to anti-Thy 1.2 treatment, was not removed by carbonyl iron-magnet separation; and was not present in thymus. The parental cell inducing recruitment was, however, sensitive to anti-Thy 1.2. When spleen cells from hapten immune F1 donors were injected together with Mit.-treated parental LN cells and boosted with hapten on another carrier, a typical "allogeneic effect" was observed in the anti-hapten immune response. It was concluded that Mit.-treated parental T cells exerted a mitogenic effect on F1 B cells resulting in extensive recruitment similar to that seen in murine mixed lymphocyte reactions.

Animals↗
PubMed1975

Immunological memory function of the T and B cell types: distribution over mouse spleen and lymph nodes.

Spleens from LAF1 mice injected intravenously with sheep erythrocytes (SE) are relatively rich in memory T cells early in the immune response (1 to 3 days) and rich in memory B cells as the response progresses (2 weeks or more). Marked cooperation for the secondary immune response in vitro was obtained by combining 10(6) spleen cells from LAF1 mice, taken 2 days after intravenous priming with SE, with 10(7) spleen cells from day 14 primed mice. The results indicate relative deficiencies in the spleen for B memory cells on days 1 to 2 and for T memory cells on day 14 after priming. Day -14, but not day -2, immune lymph node (LN) cells could replace the day -2 spleen cells (anti-Thy 1.2 sensitive) in the in vitro cooperation with day -14 immune spleen cells. Immune spleen cells taken 4 to 7 days after priming contain more equivalent numbers of B and T memory cells, but 10 to 7 days after transfer of such immune spleen cells without SE into irradiated recipients the T memory cells were again more prominent in lymph node and the B memory cells in spleen as shown by in vitro cooperation studies. These results suggest that during the second week after intravenous injection of SE relatively more T than B memory cells migrate from spleen to lymph node, resulting in an imbalance in the splenic memory cell population favoring B memory cell function.

Animals↗