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Biomedical subjects

P Schultheiss

Publications and source records attributed to P Schultheiss.

13 recordsLinked to original sources
PubMed2001

Growth factor treatment enhances vestibular hair cell renewal and results in improved vestibular function.

The vestibules of adult guinea pigs were lesioned with gentamicin and then treated with perilymphatic infusion of either of two growth factor mixtures (i.e., GF I or GF II). GF I contained transforming growth factor alpha (TGFalpha), insulin-like growth factor type one (IGF-1), and retinoic acid (RA), whereas GF II contained those three factors and brain-derived neurotrophic factor. Treatment with GF I significantly enhanced vestibular hair cell renewal in ototoxin-damaged utricles and the maturation of stereociliary bundle morphology. The addition of brain-derived neurotrophic factor to the GF II infusion mixture resulted in the return of type 1 vestibular hair cells in ototoxin-damaged cristae, and improved vestibular function. These results suggest that growth factor therapy may be an effective treatment for balance disorders that are the result of hair cell dysfunction and/or loss.

Animals↗
PubMed2001

Zinc-responsive dermatosis in dogs: 41 cases and literature review.

Forty-one cases of zinc-responsive dermatosis in the dog are described. The Siberian husky was the predominant breed affected. Periocular crusts were the most common clinical sign and parakeratosis was noted in the skin biopsy specimens of all dogs. Treatment with oral zinc ameliorated the clinical signs in most dogs, but cases necessitating other treatments such as parenteral zinc or retinoids are reported. The authors recommend a starting dose of 2-3 mg kg-1 elemental zinc per day in the treatment of this disorder.

Administration, Oral↗
PubMed1996

NYVAC-Pf7: a poxvirus-vectored, multiantigen, multistage vaccine candidate for Plasmodium falciparum malaria.

The highly attenuated NYVAC vaccinia virus strain has been utilized to develop a multiantigen, multistage vaccine candidate for malaria, a disease that remains a serious global health problem and for which no highly effective vaccine exists. Genes encoding seven Plasmodium falciparum antigens derived from the sporozoite (circumsporozoite protein and sporozoite surface protein 2), liver (liver stage antigen 1), blood (merozoite surface protein 1, serine repeat antigen, and apical membrane antigen 1), and sexual (25-kDa sexual-stage antigen) stages of the parasite life cycle were inserted into a single NYVAC genome to generate NYVAC-Pf7. Each of the seven antigens was expressed in NYVAC-Pf7-infected culture cells, and the genotypic and phenotypic stability of the recombinant virus was demonstrated. When inoculated into rhesus monkeys, NYVAC-Pf7 was safe and well tolerated. Antibodies that recognize sporozoites, liver, blood, and sexual stages of P. falciparum were elicited. Specific antibody responses against four of the P.falciparum antigens (circumsporozoite protein, sporozoite surface protein 2, merozoite surface protein 1, and 25-kDa sexual-stage antigen) were characterized. The results demonstrate that NYVAC-Pf7 is an appropriate candidate vaccine for further evaluation in human clinical trials.

Amino Acid Sequence↗
PubMed1994

Augmentation of pathogenesis of coxsackievirus B3 infections in mice by exogenous administration of interleukin-1 and interleukin-2.

Two variants of coxsackievirus B3 (CVB3) which differ dramatically in the ability to induce myocarditis in BALB/c mice were studied. H3 virus infection of murine monocytes in vitro resulted in release of concentrations of interleukin 1 (IL-1) and alpha/beta interferon that were high compared with those of cells infected with the H310A1 virus variant. In vivo, H3 virus infection caused substantial inflammatory cell infiltration of the myocardium, and lymphocytes from these animals gave predominantly Th1-cell responses to either whole H3 virus or overlapping peptides of the CVB3 vp1 capsid protein, as determined by IL-2 production. In contrast, H310A1 virus infection produced minimal myocarditis and Th1-cell responses, but Th2-cell activation was more pronounced than in H3 virus-infected mice (as determined by IL-4 concentrations). Exogenous treatment of H310A1 virus-infected mice with either IL-1 or IL-2 restored both myocarditis susceptibility and Th1-cell responses to whole virus and vp1 peptides. Furthermore, H310A1 virus-infected mice given exogenous IL-1 showed substantial in situ IL-2 deposition in the myocardium. These results indicate that CVB3-induced myocarditis may depend upon release of specific cytokines during infection and that activation of Th1 cells may be an important factor in pathogenesis.

Amino Acid Sequence↗
PubMed1993

T lymphocyte responses in CVB3-induced murine myocarditis.

Three monoclonal antibodies (mAB) to group A streptococcus M5 serotype (mAB 36.2.2, 49.8.9 and 54.2.8) cross-reactivity bind to various heart antigens (including myosin, tropomyosin and vimentin) and neutralize a myocarditic variant of coxsackievirus B-3 (Nancy) (CVB3). The existence of shared antigenic epitopes between the two distinct infectious agents and the heart implies that antigenic mimicry may form the foundation of the autoimmune response. Plaque purified variants of CVB3 were isolated with these streptococcal mAB. The wild-type virus (H3) and the virus variants made with mABs 36.2.2 (H3-36) and 54.2.8 (H3-54) caused significant myocarditis in Balb/c (H-2d) mice, but not in CBA (H-2k) animals. The virus variant made with mAB 49.8.9 (H3-49) caused myocarditis in CBA, but not in Balb/c mice. No significant differences in virus concentrations in the heart were detected with any of the virus variants. Cytolytic activity of mesenteric lymph node cells generally correlated to the severity of myocarditis in the infected animals. Using overlapping synthetic peptides of the CVB3 VP1 protein, mAB 49.8.9 was shown to bind preferentially peptides 6, 8, 11, and 12. T lymphocytes from H3 infected mice proliferated to VP1 peptides 1, 3, 9, 13, 14, and 21. To determine whether immunity to specific peptides could affect CVB3 pathogenicity, Balb/c mice were immunized with VP1 peptides 1, 3, 6, 13, 14 and 21 in complete Freund's adjuvant (CFA) then infected with 5 x 10(4) PFU CVB3 14 days later. Pre-immunization of animals with (a) peptide 1 resulted in a significant decrease in virus titers in the heart, (b) peptides 3, 13 and 21 increased animal mortality and lymphocyte mediated cytotoxicity to uninfected cardiocyte targets, and (c) peptides 3 and 21 resulted in significant increases in myocarditis compared to animals given virus without pre-immunization.

Amino Acid Sequence↗
PubMed1992

Clinical and laboratory findings associated with actual or suspected azoospermia in dogs: 18 cases (1979-1990).

Eighteen dogs were evaluated for azoospermia, 8 of which had sired pups. On the basis of history, physical examination, and various laboratory evaluations, the cause and site of azoospermia varied. Two dogs that had never sired pups had likely been azoospermic from puberty (congenital azoospermia). Two dogs were azoospermic as a result of tumors (Sertoli cell tumor and malignant astrocytoma of the pituitary gland). Deposits of IgG were observed in testicular biopsy samples, which suggested an auto-immune cause for azoospermia in 5 dogs. One of the 5 dogs with IgG deposits in testicular tissues also had evidence of immune-mediated thyroiditis. Culturing of microbes in the semen was not helpful in determining potential causes of azoospermia, and results did not correlate with organisms isolated from testicular biopsy samples or with the finding of inflammation in biopsy samples. Because 6 dogs had relatives with histories of reproductive dysfunction, inbreeding also must be considered when evaluating dogs for azoospermia.

Alkaline Phosphatase↗
PubMed1992

Plasma cell stomatitis-pharyngitis in cats: 40 cases (1973-1991).

Clinical signs, laboratory findings, and treatment results of 40 cats with the histologic diagnosis of plasma cell stomatitis-pharyngitis are discussed. Median age was 7.1 years, with no discernable sex predilection. Anorexia and difficulty prehending food were the most common clinical signs. Hyperproteinemia with associated hyperglobulinemia was the most common laboratory finding. Of various treatments, administration of corticosteroids or injectable gold (aurothioglucose) proved most effective in controlling the clinical signs.

Adrenal Cortex Hormones↗
PubMed1991

An attenuated variant of Coxsackievirus B3 preferentially induces immunoregulatory T cells in vivo.

BALB/c mice infected with the Woodruff variant of coxsackievirus group B type 3 (CVB3W) develop myocarditis mediated by autoimmune cytolytic T lymphocytes. A variant of CVB3W (designated H3-10A1) which infects the myocardium but induces minimal mortality of myocarditis compared to the parental virus was selected. Although H3-10A1 infections stimulate normal CTL responses to CVB3-infected myocytes, the autoimmune response to myocardial antigens is absent. Treatment of H3-10A1-infected mice with 50 mg of cyclophosphamide per kg of body weight, a treatment which preferentially eliminates suppressor cells, allows both the development of the autoimmune cytotoxic T-lymphocyte response and the expression of myocarditis. Similar treatment of CVB3W-infected mice had no effect on the disease. The presence of the immunoregulatory cells was confirmed by adoptive transfer of T lymphocytes from either H3-10A1 or CVB3W-infected donor mice into syngeneic CVB3W-infected recipients. Animals given H3-10A1-immune cells had minimal myocardial inflammation, while animals given CVB3W-immune lymphocytes developed enhanced cardiac disease. Elimination of the T-lymphocyte population from the donor cells prior to transfer abrogated suppression with the H3-10A1-immune population, showing that immunoregulation depended upon T lymphocytes. Both H3-10A1 and CVB3W have cross-reactive epitopes between the adenine translocator protein and the virion which are indicative of antigenic mimicry and may be the basis for the autoimmunity to cardiac antigens. These results suggest that immunoregulatory T cells may be primarily responsible for the nonpathogenicity of the H3-10A1 variant.

Animals↗
PubMed1983

Action of 12-O-tetradecanoylphorbol-13-acetate on Y1 adrenal cells apparently requires the regulatory subunit of type 1 cyclic AMP dependent protein kinase.

Y1 mouse adrenal tumor cells and mutants of Y1 cells (Kin 2 and Kin 8), with defects in regulatory subunit of type 1 protein kinase (R1), were assayed for steroid, growth, and plasminogen activator after application of the tumor promoter 12-O-Tetradecanoylphorbol-13-acetate (TPA). TPA, like ACTH, caused an increase in steroid production and a decrease in growth in Y1 cells. The effects on steroidogenesis were diminished in Kin 2 and markedly diminished in Kin 8. TPA induced plasminogen activator in Y1 but not Kin 2 or Kin 8 while ACTH induced the enzyme in both Y1 and Kin 2 but not Kin 8. TPA did not produce a measurable increase in cyclic nucleotides in Y1 cells. Unlike Cytochalasin E, another agent that causes steroidogenesis without changes in cyclic AMP concentration, TPA and ACTH did not require serum for its effect on steroid production. Cytochalasin E also caused induction of plasminogen activation in Y1, but not in Kin 2 or Kin 8 cells. TPA however produced growth inhibition in both mutant cell types while ACTH produced a progressively diminishing growth inhibitory effect in Kin 2 and Kin 8. The results suggest that a portion of TPA action on Y1 cells requires R1.

Adrenal Cortex Hormones↗
PubMed1978

Immunological results in myocardial diseases.

Immunological studies have shown new diagnostically important changes in alcoholic and viral myocarditis, as well as in congestive cardiomyopathy. Increased heart size correlated with the degree of congestive heart failure, as well as with negative immunofluorescence and an increased IgA concentration in the serum. These findings may serve as a diagnostic aid in patients with myocardial disease due to alcohol abuse. Viral heart disease is characterized by a variety of symptoms and nuclear antibodies (IgM) can be of help in the differential diagnosis. Heart muscle tissue of patients with congestive cardiomyopathy preferentially binds IgG and IgA. In addition to the other changes these findings are of diagnostic importance. It seems likely that results similar to those obtained for humoral antibodies in congestive cardiomyopathy will apply in the correlation of the haemodynamic status of the patients. The pathophysiological implication of these findings is not clear at present, but the evolution of congestive cardiomyopathy appears to be associated with binding of immunoglobulin to the myocardium, as well as with humoral antiheart antibodies.

Adult↗