Cutaneous leishmaniasis: Clinical report of two cases and review of the recent literature

With 1–1.5 million cases reported every year cutaneous leishmaniasis represents an increasing health problem. The course of cutaneous leishmaniasis varies from a single self‐healing ulcer to a persistent ulcer or progressive mucosal disease with nasopharyngeal destruction. An enormous array of topical and systemic treatment modalities has been endorsed. The response to treatment depends on the species of parasite as well as the host's immunological and genetic status. Species‐specific treatment guidelines based on evidence from controlled studies are highly desirable. We present two cases of cutaneous leishmaniasis, one in a child and one during pregnancy, reviewing various diagnostic and therapeutic measures with special attention to problems in young and pregnant patients.     

Zur Ätiologie und Prophylaxe des Ernte- bzw. Feldfiebers in Südbayern

Zusammenfassung Aufgabe der vorstehenden epidemiologischen Untersuchung war es, die Tatsachen des örtlichen und zeitlichen Auftretens des Erntefiebers bzw. Felfdiebers in das Licht derPettenkoferschen Auffassung von der örtlich-zeitlichen Bedingtheit der Seuchenentstehung zu stellen.Dabei ist zugleich ein klärendes Licht gefallen auf die Zusammenhänge, in welchen dieses Ernte- oder Feldfieber zur Hepatitis epidemica, zurWeilschen Krankheit, zum epidemischen Wasserfieber und zum Sumpfoder Schlammfieber steht. Zugleich haben wir gesehen, daß es sich bei allen diesen verwandten Krankheitszuständen umeine Endemizität der Krankheitsursachen handelt, welche in einer Reihe der Fälle eine Übertragung von Person zu Person vortäuscht. Damit wäre auch der soviel umstrittene infektiöse Charakter dieser Krankheitszustände geklärt.So haben wir gesehen, daß auf diesem vonPettenkofer gewiesenen Forschungswege doch eine gewisse Klärung der Ätiologie zu gewinnen ist, die auf dem bakteriologischen bzw. parasitologischen Forschungswege nicht erreicht ist. Auch haben sich gewisse Anhaltspunkte für eine Verhütung dieser neuen endemischen Krankheit ergeben, die, wenn sich ihre Beachtung als erfolgreich erweisen sollte, für die Durchführung des Vierjahresplanes, soweit dieselbe auf der Erntearbeit beruht, von Wichtigkeit sein würden.     

Rolle der Winkelstabilität bei der intramedullären Stabilisierung

Zusammenfassung Winkelstabile Plattenfixateur-interne-Systeme haben in den letzten 20 Jahren zunehmend an Bedeutung gewonnen. Die aus der Winkelstabilität resultierende flächenhafte Krafteinleitung und gleichmäßigere Kraftverteilung führen zu einer besseren Knochenbruchheilung insbesondere im metaphysischen Bereich und bei Osteoporose. Bei Marknagelsystemen ist die Winkelstabilität bislang nur partiell verwirklicht. Der vorgestellte winkelstabile Tibiamarknagel realisiert an jedem einzelnen Bolzen eine Winkelstabilität mit dem einliegenden intramedullären Kraftträger. Von Februar 2002–August 2004 wurden 21 Patienten mit ihm behandelt. In 13 Fällen wurden Frakturen stabilisiert, 6 Patienten hatten Fehlstellungen, 2 Patienten Pseudarthrosen. Zum Nachuntersuchungszeitpunkt waren alle Behandlungen abgeschlossen. Postoperative Komplikationen traten nicht auf. In allen Fällen wurde eine vollständige Durchbauung erreicht. In 6 Fällen fand sich radiologisch eine verzögerte Knochenbruchheilung. Die ersten klinischen Erfahrungen mit dem winkelstabilen Tibiamarknagel zeigen, dass dieser aufgrund der höheren Primärstabilität insbesondere im metaphysären Knochenbereich mit kurzen Fragmenten sowie bei Osteoporose Vorteile gegenüber anderen nichtwinkelstabilen oder nur partiell winkelstabilen Marknagelsystemen erbringt. Die verzögerten Knochenbruchheilungen bedürfen weiterer klinischer und biomechanischer Untersuchungen.     

Involvement of E-cadherin and beta-catenin in germ cell tumours and in normal male fetal germ cell development

Intercellular contacts, mediated by E-cadherin, are essential for germ cell migration and maturation. Furthermore, it has been suggested that decrease or loss of E-cadherin correlates with tumour progression and invasive behaviour. beta-catenin is involved in a number of different processes, including cell--cell interaction when bound to cadherins, and determination of cell fate in pluripotent cells when activated via the Wnt signal-transduction pathway. To shed more light on the role of these factors in normal fetal germ cell development and the pathogenesis of germ cell tumours (GCTs), the present study investigated the presence and localization of E-cadherin and beta-catenin by immunohistochemistry. E-cadherin was only weakly expressed in or absent from fetal germ cells of the second and third trimesters, and was not expressed in carcinoma in situ/intratubular germ cell neoplasia unclassified (CIS/ITGCNU) and gonadoblastoma, the precursor of an invasive GCT in dysgenetic gonads. In GCTs, it was generally not expressed in seminoma and dysgerminoma, but was found in the vast majority of non-seminoma cells. beta-catenin was found in the cytoplasm of fetal germ cells at all gestational ages and in spermatogenesis in post-pubertal testes. It was also present in CIS/ITGCNU and gonadoblastoma. Whereas seminomas and dysgerminoma were negative, non-seminoma cells were frequently found to express beta-catenin. Expression of both factors therefore reflects the degree of differentiation of these tumours. No differences for either E-cadherin or beta-catenin were observed between samples of tumours resistant or sensitive to chemotherapy, and E-cadherin expression did not correlate with vascular invasion. E-cadherin and beta-catenin therefore play a role in both normal and malignant germ cell development and differentiation that warrants further investigation, but they seem to be of limited value as predictive or prognostic factors in GCTs.     

Chronic obstructive pulmonary disease is associated with enhanced bronchial expression of FGF-1, FGF-2, and FGFR-1

An important feature of chronic obstructive pulmonary disease (COPD) is airway remodelling, the molecular mechanisms of which are poorly understood. In this study, the role of fibroblast growth factors (FGF-1 and FGF-2) and their receptor, FGFR-1, was assessed in bronchial airway wall remodelling in patients with COPD (FEV1 < 75%; n = 15) and without COPD (FEV1 > 85%; n = 16). FGF-1 and FGFR-1 were immunolocalized in bronchial epithelium, airway smooth muscle (ASM), submucosal glandular epithelium, and vascular smooth muscle. Quantitative digital image analysis revealed increased cytoplasmic expression of FGF-2 in bronchial epithelium (0.35 +/- 0.03 vs 0.20 +/- 0.04, p < 0.008) and nuclear localization in ASM (p < 0.0001) in COPD patients compared with controls. Elevated levels of FGFR-1 in ASM (p < 0.005) and of FGF-1 (p < 0.04) and FGFR-1 (p < 0.001) in bronchial epithelium were observed. In cultured human ASM cells, FGF-1 and/or FGF-2 (10 ng/ml) induced cellular proliferation, as shown by [3H]thymidine incorporation and by cell number counts. Steady-state mRNA levels of FGFR-1 were elevated in human ASM cells treated with either FGF-1 or FGF-2. The increased bronchial expression of fibroblast growth factors and their receptor in patients with COPD, and the mitogenic response of human ASM cells to FGFs in vitro suggest a potential role for the FGF/FGFR-1 system in the remodelling of bronchial airways in COPD.     

Organization and expression of genes involved in the production of the K88ab antigen

Escherichia coli K-12 minicells were used to study the expression of the genes located on plasmid pFM205, which contains the genetic determinant of the K88ab antigen. Plasmid pFM205 is composed of a 4,3-megadalton large deoxyribonucleic acid fragment derived from the wild-type K88ab plasmid pRI8801 (51 megadaltons) and the cloning vehicle pBR322. The K88ab deoxyribonucleic acid of pFM205 appeared to express six polypeptides with apparent molecular masses of 81, 30, 29, 27, 26, and 17 kilodaltons, respectively. These polypeptides account for approximately 85% of the coding capacity of the cloned deoxyribonucleic acid. The 26-kilodalton polypeptide was found to react with specific anti-K88ab antibodies and therefore represents the K88ab subunit. The K88ab subunit and at least two other polypeptides (81 and 17 kilodaltons) were translated into precursors which were about 2 kilodaltons larger than the mature proteins. Plasmid pFM205 was used to construct deletion mutants. By analyzing these mutants in minicells the genes of the six polypeptides could be located on the physical map of pFM205. It appeared that deletion of the gene of the 81-kilodalton polypeptide resulted in an altered conformation of the K88ab antigen.