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T R Ulich

Publications and source records attributed to T R Ulich.

At least 91 records · Page 5Linked to original sources
PubMed1987

Purified native and recombinant human alpha lymphotoxin [tumor necrosis factor (TNF)-beta] induces inflammatory reactions in normal skin.

These studies report findings that demonstrate that human alpha lymphotoxin (LT) induces local, visible, and microscopic inflammatory reactions in normal skin. Skin sites in rabbits, when inoculated with a single injection of native or recombinant human alpha lymphotoxin, demonstrated erythema, swelling, and warmth within 5 hr. Erythema peaked between 24 and 48 hr had resolved by 72 hr. Histologic studies of skin sites injected with native LT revealed polymorphonuclear neutrophil (PMN) infiltration and edema beginning as early as 3 hr posttreatment. Individual skin sites that received three daily injections of native LT exhibited persistent erythema and swelling. Palpable induration was evident 24 hr after the second injection in the series. Histologic examination revealed the presence of many PMNs with associated focal dermal destruction, in the form of microabscesses, and scattered mononuclear cells. In contrast, control materials and recombinant human tumor necrosis factor (TNF-alpha) did not induce visible skin reactions in the rabbit. Several additional controls excluded endotoxin as being the agent responsible for the inflammatory skin reactions observed. The ability of LT to induce inflammation may have a role in its antitumor activity and it may be an important endogenous mediator in other immunologic reactions.

Animals↗
PubMed1987

Inhibition of the neutrophilic infiltrate of experimental tubulointerstitial nephritis in the Brown-Norway rat by decomplementation.

Anti-tubular basement membrane (TBM) antibody-associated tubulointerstitial nephritis (TIN) in Brown-Norway rats is induced by immunization with bovine TBM antigens and adjuvants. The lesion is characterized by linear deposition of IgG and C3 along the TBM with sequential neutrophil (Days 8-9)- and mononuclear (Day 10 and after)-dominated inflammatory infiltrates. To study the complement dependence of the infiltrative process, immunized rats were decomplemented with cobra venom factor (CVF). The CVF treatment did not affect the production or renal deposition of anti-TBM antibodies. CVF markedly reduced the neutrophilic inflammatory infiltrate. In rats immunized with suboptimal doses of soluble bovine TBM antigens to produce a mild lesion, decomplementation also decreased the mononuclear inflammatory infiltrates on Days 10-13. In rats immunized optimally with particulate TBM to induce maximally severe TIN, decomplementation did not affect the mild mononuclear cell infiltrate on Days 8 and 9 but did somewhat reduce the subsequent mononuclear infiltrate on Days 10 and 12. These results demonstrate that the anti-TBM antibody- and C3-associated neutrophilic inflammatory infiltrate is largely complement dependent. The early mononuclear cell infiltrate that was unmodified by CVF treatment may be dependent on complement-independent humoral events or related to cell-mediated immune events. A portion of the later mononuclear inflammatory infiltrate could be dependent on the preceding neutrophilic inflammatory phase.

Animals↗
PubMed1987

Induction, characterization, and cell transfer of autoimmune tubulointerstitial nephritis.

Autoimmune tubulointerstitial nephritis (TIN) was induced in Lewis (LEW) rats by immunization with homologous Brown-Norway (BN) rat renal basement membrane (RBM), complete Freund's adjuvant and Bordetella pertussis vaccine. The BN strain has a tubular basement membrane (TBM) antigen (Ag+) detectable by immunofluorescence which is lacking in unmodified LEW rat TBM. Development of TIN in LEW rats correlated with TBM Ag+ immunogens from homologous and heterologous RBM preparations. By day 14 after immunization TIN developed characterized by elevated serum creatinine levels and by tubular destruction with focal, circumscribed lesions containing epithelioid cells, giant cells and mononuclear cell infiltrates. Approximately 60% of the mononuclear cells bore T cell antigens with most cells expressing Ia markers. Immunofluorescence and elution studies revealed no selective IgG fixation to TBM at day 14 despite high titers of circulating alloantibody reactive with the immunizing TBM. Intravenous transfer of LNC and/or splenic cells (3.5 to 7 X 10(8)) to naive LEW rats resulted in less severe but histologically identical TIN in seven days with T cell subpopulations similar to those seen in the active model. This model strongly suggests an initiating role for cell-mediated immunity in TIN in the rat and may provide a parallel to human TIN.

Animals↗
PubMed1987

Effect of IgG subclasses on in vivo bioavailability and metabolic fate of immune-complexed insulin in Lewis rats.

The bioavailability, distribution, and metabolic fate of 125I-labeled insulin complexed to antibodies in guinea pig antiserum, purified guinea pig IgG1, IgG2, a mixture of IgG1 and IgG2, and homologous Lou/m rat antiserum were studied in inbred Lewis rats. 125I-insulin complexed to purified guinea pig IgG2 antibodies was rapidly cleared from the blood and sequestered in increasing amounts with time in the liver. Large amounts of the 125I-insulin complexed to guinea pig IgG1 antibodies remained in the blood for at least 30 min. The bioavailability of 125I-insulin bound to IgG1 and IgG2 antibodies was inhibited for at least 30 min because significantly less was available for rapid binding to insulin receptors on hepatocytes and renal tubular cells and its subsequent rapid degradation. The bioavailability of 125I-insulin was further decreased when bound to antibodies in native guinea pig antiserum or a mixture of IgG1 and IgG2 antibodies compared with the 125I-insulin complexed to either purified IgG1 or IgG2 antibodies alone. The 125I-insulin bound to antibodies in native guinea pig antiserum or a mixture of IgG1 and IgG2 antibodies was distributed in vivo in a manner reflecting the relative concentrations of the IgG1 and IgG2 antibodies present. The bioavailability, distribution, and metabolic fate of 125I-insulin in immune complexes prepared with homologous Lou/m rat insulin antiserum was qualitatively similar to that observed with immune complexes prepared with guinea pig insulin antiserum. It appears that the Lewis rat can be used as an in vivo model to study the bioavailability,distribution,and metabolic fate of insulin bound to xenogenic or homologous insulin antibodies.

Animals↗
PubMed1987

The effects of a stable analogue of PGE1 on the IgG subclass response to particulate bovine tubular basement membrane in the brown-Norway rat.

The IgG subclass and the IgM isotype response to immunization with particulate bovine tubular basement membrane (TBM) and adjuvants was studied in Brown-Norway rats receiving daily injections of a stable analogue of PGE1 (M-PGE1). M-PGE1 slightly reduced the average quantity of circulating TBM antibody as well as the average quantity of eluted IgG per gram of renal tissue as compared to controls. However, M-PGE1 did not qualitatively affect the distribution of the IgG subclass or IgM isotype response to TBM. The IgG response, which occurred predominantly in the IgG1 and IgG2a subclasses, increased from Days 8 to 14 after immunization, while the IgM response decreased over the same time period. The percentage of TBM antibody in the IgG2b subclass was markedly decreased as compared to the percentage of IgG2b antibody in total IgG. A substantial heterogeneity in the IgG subclass response was noted among individual rats with IgG1 constituting from 46 to 82% of circulating TBM antibody. Although no correlation between the IgG subclass response and the severity of tubulointerstitial nephritis was noted, heterogeneity in the IgG subclass response to autoantigens may, nevertheless, theoretically play an important role in the pathogenesis of autoimmune inflammatory phenomena.

Alprostadil↗
PubMed1987

Human alpha lymphotoxin (LT): studies examining the mechanism(s) of LT-induced inflammation and tumor destruction in vivo.

Recent information from our laboratories indicates that human alpha lymphotoxin (LT) is a powerful mediator of tumor necrosis, and inflammation. Our studies indicate that LT induced effects in vivo are complex and involve multiple mechanisms(s). The data presented here suggests that LT induced tissue destructive and inflammatory reactions mediated by cytolytic and antigen reactive lymphocytes may have a role in a much broader variety of inflammatory processes than had been appreciated.

Animals↗
PubMed1987

Recombinant human alpha lymphotoxin (tumor necrosis factor-beta) induces peripheral neutrophilia and lymphopenia in the rat.

Recombinant human alpha lymphotoxin (rLT) administered intravenously to Lewis rats induces peripheral neutrophilia and lymphopenia in a dose-response dependent fashion. A dose of 30,000 units of rLT induced a neutrophilia (1589 +/- 326 to 5554 +/- 1050 neutrophils/cu mm) and lymphopenia (10,368 +/- 992 to 4636 +/- 878 lymphocytes/cu mm) at 2 hours after injection that was highly significant (P less than 0.001 and P less than 0.001, respectively) in comparison with vehicle controls. The kinetics of the neutrophilia that peaked at 2 hours as well as of the lymphopenia were highly reminiscent of the neutrophilia and lymphopenia following intravenous administration of either recombinant human interleukin-1 (IL-1) alpha or beta to rats. The peripheral neutrophilia was accompanied by a significant depletion of bone marrow neutrophils (P less than 0.001), as is also known to occur after administration of IL-1. Systemic blood pressure was not affected by rLT, which suggested that the changes in circulating leukocyte subsets were not attributable to hemodynamic changes nor to the hemodynamic-change-related release of adrenal hormones. Adrenalectomy did not alter the rLT-induced neutrophilia or lymphopenia, which suggested that rLT does not mediate its hematologic effects on peripheral blood leukocytes via the release of adrenal hormones. Pretreatment of rats with dexamethasone, indomethacin, or aspirin also did not alter rLT-induced neutrophilia or lymphopenia, which suggested that rLT-induced hematologic effects were not mediated via arachidonic acid metabolites, in stark contrast to IL-1 induced neutrophilia, which is inhibited by both dexamethasone and indomethacin.

Animals↗
PubMed1987

Stable analogs of prostaglandins E1 and F2 alpha ameliorate the proteinuria of aminonucleoside-of-puromycin nephrosis in Lewis rats.

Prostaglandins have been implicated by previous investigators in the pathogenesis of the nephrotic syndrome. A single subcutaneous injection of 1 mg/kg of stable analogs of prostaglandins E1 or F2 alpha (15[S]-15-methyl -PGE1 [M-PGE1] and -PGF2 alpha [M-PGF2 alpha]) was found in the present study to dramatically decrease proteinuria on Day 10 of puromycin aminonucleoside (PAN) nephrosis in Lewis rats. The decrease in proteinuria was mediated at least in part by a decrease in glomerular filtration rate (GFR), as quantitated by inulin clearances in nephrotic control and prostaglandin-treated rats. M-PGE1, moderately, and M-PGF2 alpha, to a lesser degree, also decreased the GFR in normal rats. Interestingly, the GFR was dramatically decreased in nephrotic as compared with nonnephrotic control rats, which suggests that PAN nephrosis may not be an ideal experimental model for human minimal change nephrosis in which the GFR is usually not severely compromised. The prostaglandin-induced decrease in GFR in both nephrotic and normal rats was coincident with a drop in systemic blood pressure. Nephrotic rats, however, had a slightly higher baseline blood pressure than normals, and the hypotensive effects of both prostaglandins were much less in nephrotic than in normal rats. The decrease in proteinuria was not related to a cytoprotective effect, as indicated by the failure of daily doses of 5 micrograms/kg M-PGE1 to reduce proteinuria 6, 8, or 10 days after injection of puromycin aminonucleoside. The similar antiproteinuric effects of prostaglandin synthesis inhibitors and of pharmacologic doses of prostaglandins are somewhat paradoxical but are reminiscent of the similarly paradoxical mutual antiinflammatory effects of these agents. The high doses of prostaglandins required to reduce proteinuria as well as their reduction of blood pressure and GFR will limit their clinical usefulness in the nephrotic syndrome.

Alprostadil↗
PubMed1987

Adenomyoma of the papilla of Vater.

An adenomyoma of the papilla of Vater that caused biliary obstruction resulted in an extensive surgical resection because of the clinical and roentgenographic suspicion of carcinoma. Benign neoplasms of the papilla and extrahepatic bile ducts are exceedingly rare, but their recognition is of clinical importance. Histologically, the adenomyoma, characterized by lobules of ducts and ductules with interlacing bundles of smooth muscle, was similar to the adenoleiomyomatous hamartoma of the intestines and to lesions of the gallbladder or extrahepatic ducts known as adenomyomas or adenomyomatous hyperplasia. The presumed rapid recent growth of the present lesion, as roentgenographically documented by the recent onset of dilatation of the common bile duct in an elderly woman, as well as the lack of gallstones or inflammatory disease of the biliary tract, might support the contention that the present lesion was neoplastic. On the other hand, the possibility that the lesion represents a hamartoma or diverticulosis of the saccules of Beale cannot be excluded.

Aged↗
PubMed1986

Endocrine and tumor differentiation markers in poorly differentiated small-cell carcinoids of the cervix and vagina.

Immunoreactivity for endocrine peptides (serotonin, gastrin, somatostatin, insulin, corticotropin, calcitonin, neurotensin, vasoactive intestinal peptide, and bombesin), cytoskeletal proteins (high and low molecular weight keratins), and tumor differentiation markers (chromogranin, neuron-specific enolase, carcinoembryonic antigen, S100 protein, and Grimelius stain) was sought on nine cervical and one vaginal poorly differentiated small-cell carcinoids. Dense-core secretory granules were ultrastructurally identified in all cases (seven of ten) in which tissue was available for electron microscopy. Immunoreactivity for endocrine secretory products was rarely noted, and only in a minority cell population (serotonin in two of ten). The majority of the tumors exhibited immunoreactivity for low molecular weight keratin (AE1/AE3 in eight of ten; CAM 5.2 in seven of nine), and three of ten tumors focally expressed high molecular weight keratin. Among the markers of neuroendocrine differentiation, neurospecific enolase was more frequently expressed (ten of ten) than chromogranin (five of ten) or argyrophilia (three of ten). Carcinoembryonic antigen was present in eight of ten tumors. S100 protein was absent in all cases. In summary, poorly differentiated small-cell carcinoids of the lower female genital tract, similarly to other small-cell endocrine tumors, occasionally exhibit focal glandular and squamoid differentiation, and only relatively infrequently or focally express immunohistochemically detectable endocrine secretory products, chromogranin, and argyrophilia.

Antigens, Neoplasm↗
PubMed1986

In vivo induction of neutrophilia, lymphopenia, and diminution of neutrophil adhesion by stable analogs of prostaglandins E1, E2, and F2 alpha.

Stable analogs of prostaglandins E1, E2, and F2 alpha (M-PGE1, DM-PGE2, and M-PGF2 alpha) were found to induce marked changes in circulating white blood cell subsets in Brown-Norway rats after subcutaneous injection. Dose-response studies demonstrated that 1000 micrograms/kg of each prostaglandin induced a maximum neutrophilia in the range of 40-70% of the total white blood cell count (normal, 5-20%) and that as little as 5 micrograms/kg of M-PGE1 induced a significant neutrophilia (P less than 0.05). Kinetic studies demonstrated that the maximum neutrophilia occurred 4-6 hours after injection of each prostaglandin and was not accompanied by the release of morphologically immature neutrophil forms from the bone marrow. Splenectomy slightly diminished the average neutrophilia at 2 hours but not at 4-6 hours after injection, which suggests that release of neutrophils from the spleen partially contributed to the early neutrophilia. Adherence experiments employing whole heparinized blood from rats given prostaglandins 6 hours prior to sacrifice demonstrated that neutrophils exposed to prostaglandins in vivo have diminished adherence to nylon wool columns, which suggests that diminished adherence of the marginated neutrophil pool may contribute to the neutrophilia. The prostaglandin-induced neutrophilia was accompanied not by a significant change in total numbers of circulating white blood cells, but, rather, by a significant decrease in circulating mononuclear white blood cells, including T-helper, T-suppressor, and B cells. The combination of neutrophilia with lymphopenia has classically been attributed to the release of adrenal hormones and suggests 1) that prostaglandins may directly or indirectly cause the release of adrenal hormones, or 2) that adrenal hormones may mediate their effects on circulating white blood cell subsets via prostaglandins, or 3) that prostaglandins activate intracellular messenger systems that are also activated by adrenal hormones.

Animals↗
PubMed1986

Inhibition of experimental autoimmune tubulointerstitial nephritis in Brown-Norway rats by (15S)-15-methyl prostaglandin E1. Analysis of the effect of prostaglandin E1 on the induction of the humoral immune response and the elicitation of humorally mediated inflammation.

Brown-Norway (BN) rats develop tubulointerstitial nephritis (TIN) after immunization with bovine tubular basement membrane (TBM) and adjuvants. Daily subcutaneous injections (either on Days 0-7 or Days 0-14) of (15S)-15-methyl prostaglandin E1 (M-PGE1) at a dose of 1 mg/kg/day markedly inhibited or completely abrogated the development of both the acute polymorphonuclear (Day 10) and the subsequent mononuclear (Day 14) inflammatory phases of BN rat TIN. Circulating anti-TBM antibody in Days 0-7 M-PGE1-treated rats was moderately diminished on Day 8 after immunization but not on Day 14. Circulating anti-TBM antibody in Days 0-14 M-PGE1-treated rats was only slightly diminished on Day 14. In experiments to test the effect of M-PGE1 on the elicitation phase of humorally mediated inflammation, M-PGE1 inhibited the acute inflammatory response observed 6 hours after intradermal injection of particulate TBM into TBM-sensitized BN rats. The inflammation in these skin tests was demonstrated by passive transfer experiments to be humorally mediated. The inhibition of acute humorally mediated intradermal inflammation was not attributable to neutropenia, because M-PGE1 caused a significant neutrophilia as demonstrated by peripheral blood smears. Although the inhibition of TIN in Days 0-14 M-PGE1-treated rats may have been due, in part, to dysfunction of the elicitation phase of humorally mediated inflammation, the inhibition of TIN in Days 0-7 M-PGE1-treated rats was more likely secondary to the diminished induction of either humoral or cellular immunity.

Alprostadil↗
PubMed1985

Tubulointerstitial nephritis induced in the brown Norway rat with chaotropically solubilized bovine tubular basement membrane: the model and the humoral and cellular responses.

Doses of as little as 50 micrograms of a soluble chaotropic extract of bovine tubular basement membrane (Bov-KBr-TBM) with adjuvants induced anti-TBM antibodies and tubulointerstitial nephritis (TIN) in Brown Norway (BN) rats. The lesion was shown by renal histology, by deposition of IgG and C3 along TBM, and in terms of the humoral and cellular immune responses to compare to that produced by the standard immunization (particulate bovine TBM) for this model of TIN in BN rats. More than half of the mononuclear cells in kidneys of BN rats with TIN bore various T-cell antigens (monoclonal antibodies W3-13, W3-25, and OX-8), and most of the infiltrating cells were positive for Ia (monoclonal antibody OX-6) by indirect immunofluorescence. Purified suspensions of these mononuclear infiltrates were prepared by using Ficoll-Hypaque gradients and the fluorescence-activated cell sorter (FACS) to eliminate renal tubular epithelial cells. The purified mononuclear cells, cultured for 5 days, incorporated thymidine in response to concanavalin A (Con A), Mycobacterium tuberculosis purified protein derivative, and Bov-KBr-TBM but not in response to a variety of autologous renal antigens. After culture for 5 days in Bov-KBr-TBM and Con A supernatant, lymph node cells (LNC) from Bov-KBr-TBM-immunized BN rats passively transferred TIN to naive BN rats. Although no cells reactive with autologous renal antigens were detected in the renal infiltrates, the transfer of disease with propagated LNC suggests that elements of the cellular immune system, in addition to anti-TBM antibody, contribute to the generation of this BN-TIN.

Animals↗
PubMed1985

(15S)-15-methyl prostaglandin E1-induced neutrophilia in Brown-Norway rats.

A stable analogue of prostaglandin E1, (15S)-15-methyl prostaglandin E1 (M-PGE1), induces a marked relative and absolute neutrophilia after subcutaneous injection at a pharmacologic dose of 1 mg/kg in Brown-Norway rats. The neutrophils reached a peak of 6 hours after injection at which time the absolute neutrophil count was 13,457 +/- 6,038/mm3 versus 2,451 +/- 1,298/mm3 before injection (p less than 0.001). The absolute white blood cell count/mm3 did not change significantly at 6 hours after injection, but a significant eosinopenia was noted, as has been described by previous investigators, after the administration of prostaglandins. A possible physiologic in vivo role for prostaglandin in the causation of neutrophilia remains to be elucidated.

Alprostadil↗
PubMed1985

Chronic active hepatitis of hepatitis B and non-A, non-B etiology. Immunohistochemical localization of hepatitis B core antigen in a series of needle biopsies.

Hepatitis B core antigen (HBcAg) was immunohistochemically demonstrated in 19 of 30 needle liver biopsies (63%) of chronic active hepatitis (CAH) from 15 of 24 patients (63%) whose serum contained hepatitis B surface antigen (HBsAg). The percentage of hepatocytes with nuclear and/or cytoplasmic immunoreactivity was quantified in each biopsy specimen, and these percentages were then compared with the amount of HBsAg and the degree of inflammation within the biopsy specimen. The percentage of HBcAg-positive hepatocytes in a biopsy specimen was greatest in those specimens that contained the most HBsAg, although this finding was not statistically significant. The percentage of HBcAg-positive hepatocytes was greatest in those specimens having the least inflammatory activity, and this was statistically significant (P less than .01). Also, the percentage of biopsy specimens containing HBcAg was increased in those groups with lesser inflammatory activity (P less than .01). By staining for both HBcAg and HBsAg, the detection rate of hepatitis B (HB)-related antigens rose to 27 of 30 biopsies (90%) in 22 of 24 patients (92%).

Biopsy, Needle↗
PubMed1983

A colonic adenocarcinoma with argentaffin cells. An immunoperoxidase study demonstrating the presence of numerous neuroendocrine products.

A well-differentiated colonic adenocarcinoma containing large numbers of gastrointestinal neuroendocrine cells is presented. The presence of neurosecretory granules was confirmed by electron microscopy. Immunocytochemistry showed large numbers of serotonin-containing tumor cells and lesser numbers of somatostatin, gastrin, motilin, secretin and neurotensin-containing cells. Some of these hormones are not normally present in the colon in significant numbers of cells. The presence of several cell types within a single tumor supports the concept that the normal epithelial cells of the gastrointestinal mucosa are derived from a common endodermal stem cell. There exists a spectrum of tumors ranging from the classical adenocarcinoma to the classical carcinoid, and this report identifies the position of this case within that spectrum.

Adenocarcinoma↗
PubMed1983

"Aggressive" chondroblastoma. Light and ultramicroscopic findings after en bloc resection.

A chondroblastoma of the proximal humerus in a 15-year-old boy was removed en bloc due to its very large size and locally destructive, aggressive character. This case is reported because of the rarity of chondroblastomas excised en bloc; specimens were examined in detail by correlated roentgenographic, gross inspection, histologic and electron-microscopic methods.

Adolescent↗