In ovo growth hormone alters growth and adipose tissue development of chickens

The effect of in ovo administration of ovine growth hormone (oGH) on growth and adipose tissue development of chickens was investigated. Unlike mammalian species, exogenous growth hormone has not been previously shown to increase growth of aves. In trial 1, fertilized eggs were injected with vehicle (.03 M NaHCO3 in .15 M NaCl, pH 8.3), 0.25, 2.5, 25 or 250 micrograms oGH on day 11 of embryogenesis. In trial 2, fertile eggs were injected with vehicle or 250 micrograms oGH. In contrast to previous studies in which GH was administered to growing birds, oGH injected in ovo in the present study increased body weights, skeletal growth and feed efficiencies of male broilers. Growth rate was not altered in females. Adipose cellularity data from both trials indicated that in ovo oGH also altered adipose tissue development of broilers. Seven-week-old male and female broilers treated with oGH during embryogenesis exhibited larger adipocytes with correspondingly less cell per gram of tissue. Additionally, adipocytes from oGH-treated broilers exhibited decreased sensitivity to glucagon, cholera toxin or theophylline-induced lipolysis responsiveness to dcAMP in ovo. Cholera toxin plus theophylline improved the lipolytic response of oGH-treated birds; thus, in broilers injected with oGH cAMP-mediated lipase activation may be reduced by a mechanism of increased phosphodiesterase activity. The results of this study indicate that growth and tissue development of chickens have been altered by mammalian GH in ovo.     

Mucus colonization as a determinant of pathogenicity in intestinal infection by Campylobacter jejuni: a mouse cecal model.

Human isolates of the intestinal pathogen Campylobacter jejuni have been shown to colonize mucus on the outer surface and deep within the intestinal crypts of gnotobiotic or germfree mice. The cecal crypts are preferentially colonized. A model of mucus colonization by C. jejuni in the mouse cecum has been developed, using antibiotic- and magnesium sulfate-treated specific-pathogen-free animals. These spiral-shaped bacteria colonize the mucus in a similar manner to the normal spiral-shaped microbiota. No evidence of adhesion to the intestinal surface was found with a wide variety of microscopic techniques. The campylobacters were seen to be highly motile in living preparations of gut tissue and rapidly tracked along intestinal mucus. Just as many of the normal spiral-shaped bacteria of intestinal surfaces can achieve close association with the epithelium through mucus association and do not adhere to the surface, C. jejuni colonizes the intestinal mucosa via mucus colonization. Thus, a major determinant of pathogenicity in intestinal infection with C. jejuni is proposed to be an ability to colonize intestinal mucus. The possession of specific adhesins is unlikely to be a significant determinant of pathogenicity. Better understanding of the mechanism of mucus association and the properties of the bacterium that are responsible will provide a basis for the rational selection of preventative measures. The model of mucus association in adult antibiotic-treated mice provides an opportunity for colonization studies with variant organisms and immunization studies.     

Suppression of IgE antibody production in sensitized mice and rats by tolerogenic conjugates of synthetic hydrophilic polymers with antigen or hapten: effect on antigen-induced histamine release from peritoneal mast cells

IgE antibodies were produced in mice and rats by immunization with ragweed pollen extract (RAG) or dinitrophenylated ovalbumin (DNP3-OA). Treatment of these animals with tolerogenic conjugates of (i) the antigen (RAG or OA) with monomethoxypolyethylene glycol (mPEG), or (ii) DNP with polyvinyl alcohol (DNP-PVA) resulted, within 7-14 days, in a fall in circulating IgE antibodies and in mast cell sensitivity, as assessed by the radioallergosorbent test (RAST) and in the in vitro antigen-induced histamine release (HR) test, respectively. The reduction in responsiveness was more marked in mice than rats; 10 days after a booster immunization, the IgE antibody titres in the RAG-mPEG-treated group of mice were approximately 10-fold lower than in the saline-treated group, with a 100-fold difference in cell sensitivity. DNP-PVA treatment of mice produced a more than 10-fold reduction in IgE anti-DNP titres with a substantial reduction in histamine release.     

Airway obstruction due to massive lingual oedema following cleft palate surgery

The Pierre Robin syndrome consists of micrognathia, pseudo-macroglossia, glossoptosis and a high arched or cleft palate. Difficult intubation of the trachea and associated abnormalities such as congenital heart disease are well known complications of this syndrome. Intraoral surgery (such as cleft palate repair and palatoplasty) can also be technically difficult for the surgeon resulting in prolonged retraction on the tongue with a mouth gag to provide adequate surgical exposure. We report a case where massive lingual oedema following a cleft palate repair resulted in life-threatening airway obstruction.     

Pulmonary response of rats exposed to titanium dioxide (TiO2) by inhalation for two years

Rats were exposed to TiO2 by inhalation exposure to concentrations of 0, 10, 50, and 250 mg/m3 for 6 hr/day, 5 days/week for 2 years. There were no abnormal clinical signs, body weight changes, or excess mortality in any exposed group. Exposed groups showed slight increases in the incidence of pneumonia, tracheitis, and rhinitis with squamous metaplasia in the anterior nasal cavity. The pulmonary response at 10 mg/m3 satisfied the biological criteria for a "nuisance dust." The lung reaction was characterized by dust-laden macrophage (dust cell) infiltration in the alveolar ducts and adjoining alveoli with hyperplasia of Type II pneumocytes. Rats at 50 and 250 mg/m3 exposure concentrations revealed a dose-dependent dust cell accumulation, a foamy macrophage response, Type II pneumocyte hyperplasia, alveolar proteinosis, alveolar bronchiolarization, cholesterol granulomas, focal pleurisy, and dust deposition in the tracheobronchial lymph nodes. Minute collagenized fibrosis occurred in the alveolar walls enclosing large dust cell aggregates. The pulmonary lesions with massive dust accumulation appeared to be the result of an overwhelmed lung clearance mechanism at 250 mg/m3 exposure. Bronchioloalveolar adenomas and cystic keratinizing squamous cell carcinomas occurred at 250 mg/m3 exposure, while no compound-related lung tumors were found in rats exposed to either 10 or 50 mg/m3. In addition to excessive dust loading in the lungs of rats exposed chronically at 250 mg/m3, the lung tumors were different from common human lung cancers in terms of tumor type, anatomic location, tumorigenesis, and were devoid of tumor metastasis. Therefore, the biological relevance of these lung tumors and other pulmonary lesions for man is negligible.     

Comparison of arsenic-induced cell transformation, cytotoxicity, mutation and cytogenetic effects in Syrian hamster embryo cells in culture

Sodium arsenite and sodium arsenate were observed to inducemorphological transformation of Syrian hamster embryo cellsin a dose-dependent manner. A linear dose-dependence with aslope of 1 was observed with both compounds when the data wereplotted on a log-log graph. The trivalent sodium arsenite was> 10-fold more potent than the pentavalent sodium arsenate.The compounds also exhibited toxicity; however, transformationwas observed at non-toxic as well as toxic doses. At low doses,enhanced colony-forming efficiency of the cells was observed.To understand the mechanism of arsenic-induced transformation,the genetic effects of the two arsenicals were examined overthe same doses that induced transformation. No arsenic-inducedgene mutations were detected at two genetic loci. However, celltransformation and cytogenetic effects, including endoreduplication,chromosome aberrations, and sister chromatid exchanges wereinduced by the arsenicals with similar dose-responses. Theseresults support a possible role for chromosomal changes in arsenic-inducedtransformation.     

Inhibition of lens-aldose reductase activity by brazilin and haematoxylin

Brazilin and haematoxylin, plant pigments, were examined for their effects on the Bovine-Lens aldose reductase (LAR)-activity. About 50% inhibition was observed in a concentration of 10 (-4) M-brazilin and 10 (-4) M-haematoxylin, and above 95% inhibition was observed in a concentration of 10 (-3) M-brazilin and 10 (-3)M-haematoxylin. In order to determine the type of inhibition, kinetic studies were also conducted with brazilin and haematoxylin, in which both were found to be noncompetitive inhibitors.     

Dysplasia in Barrett's esophagus. A clinicopathologic study of six patients

To evaluate the consequences of dysplasia in Barrett's esophagus, six patients with esophageal mucosal biopsies showing dysplastic Barrett's mucosa in the absence of clinically evident esophageal carcinoma were identified and their clinicopathologic features reviewed. The patients, four men and two women, averaged 60 years and had long histories of gastroesophageal reflux. Four patients had high-grade dysplasia; two had low-grade. Dysplastic Barrett's mucosa appeared to arise most commonly from specialized-type Barrett's mucosa. After a mean follow-up of 29 months, four patients, all with high-grade dysplasia, had esophageal resections. Three of the four were found to have invasive adenocarcinoma, which extended through the esophageal wall in two patients. The fourth patient had a noninvasive adenomatous polyp ("Barrett's adenoma"), an infrequently described form of dysplasia in Barrett's esophagus. The two patients with low-grade dysplasia had developed no clinical indications of carcinoma. The results confirm that dysplastic Barrett's mucosa, particularly the high grade, is a morphologic marker for adenocarcinoma. Biopsy surveillance of patients with Barrett's esophagus is histologically feasible, but prospective studies are required to prove its effectiveness.     

Chronic empyema: key-point and results of our one-step operation

A new operative method named as "Extraperiosteal air plombage" against chronic empyema were performed to 80 patients and its cure rate by the first operation was 93.8% which is a good and high rate. Know-how to perform the operation without failure is (1) to complete the excoriation of the pleural debris, (2) to seal completely the leakage such as bronchiolar fistula, (3) to perform the extraperiosteal abbration rather over much to attach the lung to the muscle layer, (4) to close the chest wall completely, and (5) to wash out thoroughly the extraperiosteal cavity with brush and enough saline solution and to use the effective antibiotica.