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Biomedical subjects

B Mock

Publications and source records attributed to B Mock.

At least 19 recordsLinked to original sources
PubMed2003

[Interferon-alpha treatment of the Churg-Strauss syndrome].

HISTORY: Two patients, 60 (pat. 1; female) and 30 years of age (pat. 2; male), respectively, suffering from a histologically confirmed Churg-Strauss-syndrome and receiving immunosuppressive therapy were treated with Interferon-alpha. INVESTIGATIONS: Clinical complaints, disease activity, blood eosinophil counts, and lung function were monitored. In patient 1 the differential cell counts and immunocytology of bronchoalveolar lavage cells were assessed using flow cytometry. TREATMENT AND COURSE: Both patients were treated with interferon-alpha in dosages of 3 million units of IFN-alpha 2b or an equivalent dosage of interferon-acon thrice weekly subcutaneously. The patients were observed for a period of up to 24 months. Interferon-alpha induced remission of disease and allowed discontinuation of oral glucocorticoid therapy in both patients. Treatment also improved the peripheral polyneuropathia in patient 1 as well as the hemorrhagic cystitis and reduction of the Cushing syndrome (weight reduction of 19 kg) in patient 2. In addition, blood eosinophil counts normalised. After 12 months of treatment, the number of bronchoalveolar eosinophils decreased from 61,5% (5.7 x 106 cells/ml) to 7% (1.1 x 106 cells/ml). In addition, the proportion of CD4+ T-lymphocytes and B-cells increased, while CD8+ T-cells and NK cells decreased (pat. 1). CONCLUSION: Interferon-alpha may represent an effective alternative to the current treatment of Churg-Strauss syndrome consisting of corticosteroids and immunosuppressives.

Administration, Oral↗
PubMed2001

[Asthmatic airway inflammation].

Asthma is an inflammatory disease of the airways even in its clinically mildest manifestation. The pathogenesis is based on complex interactions between inflammatory cells, soluble signal molecules (mediators) and structural cells as well as extracellular components of the airways. Bronchial inflammation is closely associated with bronchial hyperreactivity, airways obstruction and asthmatic symptoms. Airways inflammation causes airflow limitation via (1) acute muscular bronchoconstriction, (2) formation of mucous plugs, (3) thickening of the airway wall, and (4) fibrotic remodelling of the airways ("Remodelling"). The insights into bronchial inflammation as the basis of asthma is of principle significance for the diagnosis, prevention, and treatment of the condition.

Asthma↗
PubMed2001

[Asthma therapy for adults].

The goal of asthma management is to achieve control of the condition. This essentially requires environmental control measures (allergen avoidance) and patient training and education. Drug treatment comprises anti-inflammatory (corticosteroids), and bronchodilatory controller therapy (long-acting beta 2-sympathomimetics, leukotriene receptor antagonists, retarded theophylline) as well as bronchodilatory medication as required (short-acting beta 2-sympathomimetics). The number and frequency of pharmacologic therapy relates to the severity of the clinical presentation. The combination of certain controller drugs (corticosteroids with long-acting beta 2-agonists, corticosteroids with leukotriene receptor antagonists, and beta 2-agonists with leukotriene receptor antagonists) yields a synergistic therapeutic effect as well as a compliance advantage.

Adult↗
PubMed2000

Bilateral symmetrical upper-lobe opacities: an unusual presentation of bronchiolitis obliterans organizing pneumonia.

A 45-year-old man was admitted with nonresolving fever, cough, and dyspnea 2 months after a common cold. His chest radiograph demonstrated bilateral symmetrical upper-lobe opacities reminiscent of tuberculosis. Transbronchial biopsy revealed inflammatory nonspecific alveolar lesions suggestive of bronchiolitis obliterans organizing pneumonia, which responded well clinically and radiologically to oral corticosteroids. Here, the case of a previously unreported radiographic manifestation of bronchiolitis obliterans organizing pneumonia is presented.

Administration, Oral↗
PubMed1998

[Recurrent panuveitis. First manifestation of Behçet disease in childhood].

BACKGROUND: Behçet's disease is a rare systemic vasculitis of unknown etiology. The typical symptoms include recurrent oral and/or genital aphthous lesions, iridocyclitis (historically with hypopyon) and various skin lessions. The number of young adults and children which are diagnosed with Behçet-syndrome is increasing in recent years and the mean age of manifestation has decreased to 25 years in German patients. The disease is generally diagnosed later in German (48.5 months) than in Turkish patients (25.5 months). Ocular manifestation has been confirmed as a marker of severe prognosis. In 15-25% of affected patients it leads to blindness. PATIENT: We describe a 19-year-old Caucasian woman who has suffered from the typical symptoms (oral aphthous lesions, recurrent uveitis posterior, various skin lesions) since the 16th year of age. RESULTS: After three years the patient was finally be diagnosed with Behçet's disease (using the criteria of the "International Study Group for Behçet's Disease"). Visual acuity was stabilized with an immunosuppressive therapy, although there was no complete remission in disease activity. In addition a cerebral vasculitis was manifested. CONCLUSIONS: Ophthalmologists should be familiar with Behçet's disease. In cases of recurrent uveitis Behçet's disease should be included in the differential diagnosis because timely immunosuppressive therapy can prevent irrevocable changes in the corpus vitreum and retina and preserve complete visual acuity.

Adolescent↗
PubMed1998

Ecstasy pimples - a new facial dermatosis.

Ecstasy (XTC) has become a popular drug in the rave, dance and techno scene. Several severe disorders due to drug addiction have been described but no dermatological symptoms. We report on 2 patients (20-year-old female, 21-year-old male) with medical problems after taking XTC. Both developed a facial rash with reddish pimples after oral intake of XTC. The distribution resembled either periorificial dermatosis or acneiform rash without white- or blackheads. The lesions cleared without specific treatment. We suggest that XTC pimples represent an acneiform dermatosis in young people taking designer drugs. Though the dermatosis itself seems to be mild, it may be a cutaneous marker for drug abuse.

Adult↗
PubMed1998

Basic concepts of functional arteriovenous MR imaging malformations.

This article reviews the technical features of functional MR imaging. Examples are presented demonstrating how MR imaging may be used to identify primary cortical regions adjacent to AVMs. Preliminary results suggest that cortical functions may undergo translocation when the AVM involves eloquent cortex. This finding underscores the importance of cortical mapping prior to surgical excision.

Brain Mapping↗
PubMed1998

Basic concepts of functional magnetic resonance imaging and arteriovenous malformations

Cortical mapping is an important adjunct to the workup of patients with arteriovenous malformation (AVMs) near eloquent cortical regions. Task activation imaging can be performed that clearly identifies primary cortical regions. Although current methods require considerable postprocessing, advances in hardware and software will likely make functional MR imaging a routing examination before surgical resection of AVMs in the near future.

Journal Article↗
PubMed1997

[Still's syndrome in the adult. A report of 8 cases with special reference to diagnostic value of ferritin].

BACKGROUND: Adult onset Still's disease (AOSD) is an uncommon, systemic, inflammatory disorder of unknown etiology, characterized by the triad of fever, arthritis and rash. PATIENTS AND RESULTS: We describe 8 cases of AOSD (3 male, 5 female) diagnosed and treated in the Department of Rheumatology from 1980 to 1996. The delay in reaching a firm diagnosis was between 2 and 86 months, due to both lack of specific serum markers and the abundance of possible differential diagnoses. Our therapeutic strategies and results are presented and the value of obtaining serum ferritin levels for both diagnosis and follow-up studies is discussed. The patients data are compared to those of the world's literature on AOSD. CONCLUSION: The differential diagnosis of fever of unknown origin should always include AOSD, because these patients could be spared from invasive and unnecessary diagnostic measures. Increased serum ferritin levels are of particular value in the diagnosis of acute AOSD and the normalization of the serum ferritin value is a reliable indicator of therapeutic success.

Adolescent↗
PubMed1997

New strains of inbred SENCAR mice with increased susceptibility to induction of papillomas and squamous cell carcinomas in skin.

To develop mouse strains useful for studies of susceptibility and resistance to the induction of skin tumors, three new inbred SENCAR strains were independently derived by random inbreeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested. The F1 hybrid between SENCARA/Pt males and resistant BALB/cAnPt females was resistant to the induction of both papillomas and SCCs after initiation by 2 microg of DMBA and promotion by 20 weekly applications of 2 microg of TPA. Papillomas developed in all of the SENCARA/Pt mice, none of the BALB/cAnPt mice, and 12% of the F1 progeny. Thus, at these doses of initiator and promoter, resistance was incompletely dominant in the F1 hybrid. However, the responsiveness of the F1 mice could be increased substantially by increasing the dose of the promoter.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

MuLV-insertional mutagenesis of c-myb and Mml1 in a murine model for promonocytic leukemia.

Analysis of retroviral integration sites in MuLV-induced promonocytic leukemias has determined that two genetic loci, c-myb and Mml1, can contribute to disease development but not in the same leukemia. Recent studies aimed at understanding the function of Myb in leukemia development have focused on the consequences of ectopic Myb expression on monocytic and granulocytic differentiation in vitro. In all instances Myb was shown to block growth arrest but not commitment to differentiation, a result which is consistent with observed effects of Myb in leukemia development. No effect of Myb protein truncation was observed in these studies although similar truncations are produced as a result of insertional mutagenesis. Common integration site, Mml1, was recently identified and mapped to mouse chromosome 10 within 1cM of c-myb. Despite its linkage to c-myb, Myb mRNA and protein expression appear to be unaffected in leukemias with Mml1 integrations.

Animals↗
PubMed1996

Mml1, a new common integration site in murine leukemia virus-induced promonocytic leukemias maps to mouse chromosome 10.

MuLV-induced myeloid leukemias (MML) having promonocytic characteristics are produced with high incidence in some strains of adult mice that are undergoing chronic peritoneal inflammation. Previously we showed that many leukemias have rearrangements of the c-myb locus due to insertional mutagenesis, however, we also identified a number of leukemias that had proviral integrations in the absence of c-myb rearrangement in the present study, a new locus, Mml1, was found to be a target of insertional mutagenesis in 10 of the promonocytic leukemias that lacked c-myb alterations. Chromosomal mapping studies, performed using progeny from interspecies backcross mice generated by mating (BALB/cAn x M. spretus)F1 females to BALB/cAN males, determined that Mml1 is located on the proximal end of mouse chromosome 10. Interestingly, there were no recombinants between c-myb and Mml1 in 101 backcross progeny and Mml1 was mapped approximately 20-25 kb upsteam of c-myb. Interestingly, c-myb mRNA and Myb protein are expressed at levels similar to the levels observed in myeloid progenitor cells, but are not overexpressed. It is anticipated that future experiments will determine whether Mml1 integration prevents down regulation of c-myb expression or activates another gene on chromosome 10.

3T3 Cells↗
PubMed1996

Retroviral insertional mutagenesis in murine promonocytic leukemias: c-myb and Mml1.

Studies have focused on two genetic loci, c-myb and Mml1, whose activation by retroviral insertional mutagenesis contribute to promonocytic leukemia in our acute monocytic leukemia (AMoL) model. Multiple mechanisms of activation of c-myb by retroviral insertional mutagenesis implicate both transcriptional deregulation and protein truncation in conversion of this proto-oncogene to an oncogene. Because transformation by c-Myb can be viewed as a block to differentiation our studies moved into two in vitro systems to evaluate effects of truncated forms of c-Myb on cytokine induced maturation of myeloid progenitors to the granulocyte and macrophage lineages. Deregulated expression of truncated and full length c-Myb did not result in maintenance of the myelomonocytic progenitor state but rather a block in differentiation at intermediate to late steps in the maturation processes of myelomonocytic cells. Our results argue that inhibition of differentiation is due to c-Myb's ability to maintain the proliferative state of cells. Interestingly, the phenotype of continuously proliferating monocytic cells resembles that of the tumor cell phenotype. Recently we identified a new target of integration, Mml1, which is rearranged in ten promonocytic leukemias that do not have c-myb rearrangements. This locus which was mapped to chromosome 10 is presently being characterized.

Animals↗
PubMed1995

Spacious phagosome formation within mouse macrophages correlates with Salmonella serotype pathogenicity and host susceptibility.

Light microscopic studies indicated a correlation between the virulence for mice of different Salmonella serotypes and the ability to form or maintain spacious phagosomes (SP) within mouse macrophages. Although Salmonella typhimurium induced membrane ruffling, macropinocytosis, and SP formation in macrophages from BALB/c mice, serotypes which are nonpathogenic for mice produced markedly fewer SP. SP formation correlated with both serotype survival within mouse macrophages and reported lethality for mice. Time-lapse video microscopy demonstrated that the human pathogen S. typhi induced generalized macropinocytosis and SP formation in human monocyte-derived macrophages, indicating a similar morphology for the initial phases of this host-pathogen interaction. In contrast to bone marrow-derived macrophages from BALB/c mice, macrophages from S. typhimurium-resistant outbred (CD-1) and inbred (CBA/HN) mice did not initiate generalized macropinocytosis after bacterial infection and formed markedly fewer SP. These deficiencies were not due to the Ihy resistance genotype of these mice, as macrophages from mice that were congenic except for the Ihy locus demonstrated equal SP formation in response to S. typhimurium. The observation that S. typhimurium-resistant CD-1 and CBA/HN mice are deficient in the ability to form and/or maintain SP indicates that a variable host component is important for SP formation and suggests that the ability to induce or form SP affects susceptibility to S. typhimurium. When serotypes nonpathogenic for mice were used to infect BALB/c macrophages, or when CD-1 or CBA/HN mouse macrophages were infected by S. typhimurium, some of the SP that formed shrank within seconds. This rapid shrinkage suggests that SP maintenance is also important for S. typhimurium survival within macrophages. These studies indicate that both host and bacterial factors contribute to SP formation and maintenance, which correlate with Salmonella intracellular survival and the ability to cause lethal enteric (typhoid) fever.

Animals↗
PubMed1994

Molecular cloning, sequencing, chromosomal localization and expression of mouse p21 (Waf1).

The recent discovery that expression of Waf1 (p21), an inhibitor of cyclin-dependent kinases, is induced by the tumor suppressor p53 provides an important linkage between growth suppression and the cell cycle. We report here the cloning and sequencing of a mouse p21 cDNA that contains the entire coding region. Hybridization of the mouse p21 probe in Southern blot analyses confirms that p21 is a single-copy gene and that the corresponding locus, Waf1, lies proximal to H-2 on mouse chromosome 17. In northern analyses, the expression of p21 is found in most normal mouse tissues, but a surprising lack of correlation is found between mRNA levels of p21 and p53. In order to determine which regions of p21 are most evolutionarily conserved, we have compared the cDNA sequences for the entire p21 coding region in 13 different mouse strains or species and the human p21 sequence. We conclude that two regions (corresponding to human codons 21-60 and 130-164) are strongly conserved in p21 and that these regions may represent domains that are especially critical to a functional p21 protein.

Amino Acid Sequence↗
PubMed1993

Genetic control of Leishmania major infection in congenic, recombinant inbred and F2 populations of mice.

The outcome of subcutaneous infection with L. major NIH 173 was evaluated in a series of recombinant inbred and congenic strains, as well as F2 progeny generated from a genetic linkage testing stock carrying the visible markers Ra, Os, and Pt. The disease parameters monitored were the incidence of open or necrotic lesions and footpad depths of infected feet, and the incidence and number of amastigotes in livers following infection. Regions of mouse chromosomes 2, 4, 7, 8, 12 and 15 were excluded from linkage to a gene (Scl-1) involved in the susceptibility of inbred strains of mice to cutaneous infection with L. major NIH 173 by F2 and congenic strain analyses. Strain distribution patterns generated for Scl-1 in the CXB and CXS recombinant inbred strains suggested linkage to the distal end of mouse Chromosome 11.

Animals↗