Synthesis of ecdyson-14C and ecdysterone-14C from cholesterol-14C in cockroaches (Periplaneta americana) without molting glands

Summary The synthesis of molting hormone of cockroaches of which the prothoracic glands had previously been extirpated was investigated after injection of cholesterol-¹⁴C. It could be proved by means of radio thin-layer chromatography of extracts that ecdysterone and in small amounts ecdysone, are synthesized in Periplaneta americana larvae without prothoracic glands. The results demonstrate that other tissues are also able to perform the molting hormone besides the molting gland itself.Supported by the Sächsische Akademie der Wissenschaften zu Leipzig.     

Biosynthesis of the bufadienolide marinobufagin in toadsBufo paracnemis from cholesterol-20-14C

Zusammenfassung Der biogenetische Ursprung des Marinobufagins in KrötenBufo paracnemis wurde durch Injektion von Cholesterol-20-¹⁴C nachgewiesen. Durch Abbau wurde festgestellt, dass die Gesamtaktivität des Produktes im C-20 des Marinobufagins enthalten ist.     

Cholestanol and chenodeoxycholic acid: Metabolites of injected cholesterol-4-14C in pigeon bile

Zusammenfassung Es gelang, in Tauben die Umwandlung von injiziertem Cholesterol-C¹⁴ in Gallen-Cholestanol nachzuweisen, wobei Chenodeoxycholinsäure als Hauptmetabolit des Cholesterols-C¹⁴ in der Galle ermittelt wurde.     

The influence of estradiol on the distribution of exogenous cholesterol-4-C14 in the rat

Zusammenfassung Vorbehandlung mit Östradiolbenzoat führte bei kastrierten männlichen Ratten zu einer verminderten Aufnahme von oral zugeführtem Cholesterin-4-C¹⁴ in die Aorta. Bei kastrierten wie auch bei intakten Tieren war nach Östrogenbehandlung die Aufnahme von markiertem Cholesterin in die Leber erhöht. Durch Analyse der Faeces liess sich nachweisen, dass Östrogenbehandlung sowie Kastration die Sterolausscheidung beschleunigt.     

Electronmicroscopic identification of type C particles in cultured murine neuroblastoma

Summary Monolayer of murine neuroblastoma were treated with dexamethasone and examined by electronmicroscopy. Most of the treated cells were morphologically differentiated and exhibited type C virus particles which were budding from the cell surface. This in vitro system may be of great value for exploring the oncogenic potential of the virus, and its possible role in cell differentiation.Acknowledgments. The authors wish to thank Dr K.N. Prasad, Department of Radiology, University of Colorado Medical Center, for providing the NBP₂ clone, and Mr P. Reimann for photographic assistance. This research was supported in part by NIH Grant NS 11650 to T.H.W.     

Anti-type 2 transglutaminase antibodies as modulators of type 2 transglutaminase functions: a possible pathological role in celiac disease

Auto-antibodies to the ubiquitous enzyme type-2 transglutaminase (TG2) are a specific hallmark of celiac disease (CD), a widely diffused, multi-factorial disease, affecting genetically predisposed subjects. In CD an inflammatory response, at the intestinal level, is triggered by diet consumption of gluten-containing cereals. Intestinal mucosa displays various degrees of atrophy and hyperplasia, with consequent global intestinal dysfunction and other relevant extra-intestinal symptoms. Through deamidation of specific glutamines of gluten-derived gliadin peptides, TG2 strongly enhances gliadin immunogenicity. In addition, TG2 cross-linking activity may generate complexes between TG2 itself and gliadin peptides, and these complexes seem to cause the auto-immune response by means of an apten-carrier-like mechanism of antigen presentation. Anti-TG2 antibodies can be early detected in the intestinal mucosa of celiac patients and are also abundantly present into the serum, thus potentially reaching other organs and tissues by blood circulation. Recently, the possible pathogenetic role of auto-antibodies to TG2 in CD has been investigated. Here, we report an overview about the genesis of these antibodies, their specificity, their modulating ability toward TG2 enzymatic or non-enzymatic activities and their biological effects exerted by interacting with extracellular TG2 or with cell-surface TG2. We also discuss the auto-immune response occurring in CD against other TG members (i.e. type 3 and type 6) and analyze the occurrence of anti-TG2 antibodies in other auto-immune CD-related diseases. Data now available let us to suppose that, even if antibodies to TG2 do not represent the triggering molecules in CD, they could be important players in disease progression and manifestations.     

Electronmicroscopic identification of type C particles in cultured murine neuroblastoma.

Monolayer of murine neuroblastoma were treated with dexamethasone and examined by electronmicroscopy. Most of the treated cells were morphologically differentiated and exhibited type C virus particles which were budding from the cell surface. This in vitro system may be of great value for exploring the oncogenic potential of the virus, and its possible role in cell differentiation.     

Current cases in which epitope mimicry is considered as a component cause of autoimmune disease: immune-mediated (type 1) diabetes

Autoimmune diseases result from a combination of genetic, immunologic, hormonal, and environmental factors. Infectious agents may induce the breakdown of immunological tolerance and the appearance of autoreactivity. However, the specific relationship between infection and autoimmunity is still unclear. One of the mechanisms responsible could be molecular mimicry between the infectious agent and self. The concept of molecular mimicry is a viable hypothesis in the investigation of the etiology, pathogenesis, treatment, and prevention of autoimmune disorders. Immune-mediated (type 1) diabetes in humans and in non-obese diabetic (NOD) mice is polygenic and characterized by autoimmune destruction of insulin-producing pancreatic beta cells in islets of Langerhans. In NOD mice, a T-helper 1 (Th1)-based autoimmune response arises spontaneously against glutamate decarboxylase (GAD) concurrently with the onset of insulitis. Subsequently. this Th1-type autoreactivity spreads intra- and intermolecularly to other beta cell autoantigens, suggesting that a Th1-type response is responsible for the progression of the disease, whereas Th2 responses when experimentally induced are protective. In humans, a homology between GAD and the P2-C protein of Coxsackie B make a cause-and-effect molecular mimicry an attractive hypothesis. Evidence to support the concept of molecular mimicry in diabetes is reviewed.     

Thixotropic effect and electro-osmosis as possible factors of membrane electrical excitability]

Cation motion under the electrical field might break the membrane structure. In the temporary wake of each cation conductivity would be increased. Thus a zone of negative resistance would occur in the intensity-voltage relation. Membrane dehydration, due to electro-osmosis, might induce repeated flip-flops of current at the limits of the negative resistance zone.     

Pathological changes in the heterologous phase of antibasement membrane antibody mediated disease in the rat

Summary The immunological and structural changes during the heterologous phase of experimental antibasement membrane antibody mediated disease was sequentially studied in the rat following single i.v. injections of rabbit antibodies to basement membrane antigens prepared from kidney, lung and salivary gland tissues. Although each of the anti-bodies bound strongly to GBM, structural changes were initially subtle accompanied by proteinuria and hematuria. More severe structural changes related to dose and duration of the disease did not appear for several weeks.