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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two sources of variability in rat caries experiments have been investigated: infection with two S mutans strains and two types of caging. Results indicated that strain 6715 was more virulent than was strain 10449 when 24-day-old rats were orally infected with the organism under standardized conditions. Caging of rats (2 per cage) in stainless steel, raised bottom cages resulted in higher level of caries than in plastic tubs (3 per cage) with hardwood bedding. Infection and caging conditions are two of the factors which may contribute to variability in caries pattern and severity in experimental rats.
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PMID:Sources of variability in rat caries studies: microbial infection and caging procedure. 27 35

Knowledge of the pathogenesis of pneumonia due to Mycoplasma pneumoniae has been derived primarily from experimental infection of rodents. As part of an effort to establish a model with a closer resemblance to man, three seronegative, young, adult rhesus monkeys (Macaca mulatta) were inoculated with M. pneumoniae (10(7.4) cfu per animal) by oropharyngeal administration of coarse-particle aerosol. Five to six days after exposure of the animals, cultures obtained from the upper respiratory tract were positive for M. pneumoniae. Each animal subsequently developed a serologic response, as determined by complement fixation, complement-mediated killing, and tetrazolium-reduction inhibition techniques. Infection was subclinical, and serial chest roentgenograms failed to disclose pneumonia throughout the course of infection. Blood cell counts and titers of cold agglutinins remained unchanged. Althought M. pneumoniae was recovered from the upper respiratory tract of two monkeys for 50 days, there was no evidence of transmission of infection to cage-mate controls inoculated with broth.
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PMID:Experimental production of respiratory tract infection with Mycoplasma pneumoniae in rhesus monkeys. 81 46

An outbreak of lymphocytic choriomeningitis (LCM) associated with pet hamsters adquired through nationwide distributor was recognized in New York in February 1974. In upstate a New York, 57 cases occurred in a four-month period. Complete information was obtained on 49 patients ranging in age from 3 to 70 years. Characteristic findings included fever (90%), headache (85%), and severe myalgia (80%). Typically, laboratory findings consisted of a normal blood cell count and cerebrospinal fluid with mononuclear leukocyte pleocytosis and moderate hypoglycorrhacia. Al patients had contact with hamsters from one distributor. Most of the hamsters were acquired in mid to late December 1973, but some as late as March 1974. From each of eight families in which hamsters were available, at least one hamster had detectable complement-fixing antibodies for LCM. Infection rates within families varied with location and type of hamster cage; open cages and cages situated in common living areas were associated with highest infection rates (45% and 52%, respectively). Severity of illness was not associated with direct contact with hamsters. Onset of illness occurred between 8 and 90 days after initial exposure to hamsters.
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PMID:Lymphocytic choriomeningitis outbreak associated with pet hamsters. Fifty-seven cases from New York State;. 117 41

Infection of rats with sialodacryoadenitis virus (SDAV) or rat coronavirus (RCV) is acute and self-limiting, and elimination and control of either virus is based on the assumption that recovered rats are immune to reinfection. To test this hypothesis, we examined whether SDAV-immune rats could be infected with RCV or reinfected with SDAV. Sprague Dawley (SD) rats were inoculated intranasally with SDAV or with culture medium alone and serial SDAV antibody titers were obtained. Eleven months after inoculation, when antibody titers had stabilized, SDAV-immune and nonimmune rats were challenged with SDAV or RCV, and euthanatized 3 or 6 days later. SDAV-immune rats challenged with SDAV or RCV manifested acute rhinitis associated with virus antigen by 3 days after inoculation, but no lesions or antigen were subsequently found in the lower respiratory tract, salivary glands or lacrimal glands. There was also a marked anamnestic increase in antibody titer by 6 days after challenge. SDAV-immune rats challenged with SDAV or RCV also transmitted infection to nonimmune cage mates. This study indicates that 11 months after primary infection with SDAV, rats can be infected with SDAV or RCV, but that the severity of disease is significantly reduced.
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PMID:Infection of SDAV-immune rats with SDAV and rat coronavirus. 216 61

Sporulated oocysts of Eimeria acervulina were administered orally to cage-housed broilers at a dose of 3.5 X 10(5) resulted in mild subclinical coccidiosis. Clostridium perfringens incorporated in feed at a level of 2.5 X 10(8) organisms/g. produced lesions characteristic of necrotic enteritis. Mortality of 8% (7/80) occurred in birds fed a ration inoculated with Cl. perfringens alone. Mortality of 35% (28/80) was observed in birds which received an oral dose of E. acervulina and which were fed simultaneously with a ration containing Cl. perfringens. Birds which were fed an inoculated ration two days after an oral dose of E. acervulina showed 41% (33/80) mortality. Birds which received an inoculated ration for two days before administration of an oral dose of E. acervulina demonstrated 18% mortality (15/80). Birds which were fed an inoculated ration four days after an oral dose of E. acervulina showed 10% mortality. Infection with E. acervulina reduced the pH of intestinal contents with a simultaneous depression in serum protein. A 39% increase in intestinal passage time from 178 to 248 minutes occurred on the fifth day after infection with E. acervulina. These experiments suggest that necrotic enteritis, attributed to proliferation of a toxigenic strain of Cl. perfringens, followed intestinal stasis and minimal lesions induced by mild intestinal coccidiosis.
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PMID:Etiology and pathogenesis of necrotic enteritis. 286 8

Short-term administration of rifampin was evaluated as a means of preventing or eradicating infection due to foreign bodies. Tissue cages were implanted into guinea pigs and subsequently infected with 10(3) colony-forming units of Staphylococcus aureus Wood 46. Infection developed in all tissue cages. Rifampin was administered thereafter intraperitoneally at a dosage of 7.5 mg/kg every 12 hr for 48 hr, and the tissue-cage fluid was monitored for possible development of infection by quantitative bacteriologic methods for 15 days. In all cases rifampin prevented or eradicated tissue-cage infection if treatment was initiated either 3 hr before or less than or equal to 12 hr after inoculation of microorganisms but was ineffective if initiated greater than 12 hr after inoculation. In cases of failure of treatment, rifampin-resistant variants could be demonstrated. Rifampin seems to prevent or eradicate tissue-cage infection only if given early after bacterial inoculation.
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PMID:Short-term administration of rifampin in the prevention or eradication of infection due to foreign bodies. 635 79

The penetration of various aminoglycosides into uninfected and infected fluids of steel net cages, implanted subcutaneously into rabbits, was studied. The pharmacokinetics of the antibiotics tested in these fluids were characterized by a peak concentration which was delayed in relation to that in serum after both intramuscular and intravenous administration, and by a slower elimination from cage fluids than from serum. Comparing amikacin, gentamicin, netilmicin and tobramycin, the latter seemed to have a somewhat lower penetrability into uninfected cage fluids. Infection of the cage fluids with gram-negative aerobic bacteria resulted in a reduction of the measurable concentrations of amikacin, gentamicin or netilmicin in the cage fluids when compared to those obtained in uninfected fluids in the same rabbits. Elimination of the aminoglycosides from the infected cage fluids was slower than from the uninfected ones. The lower concentrations of the aminoglycosides in infected cage fluids were considered to be primarily due to a penetration barrier created by the infection. The viable counts in infected cage fluids were only marginally affected in cages where the aminoglycoside concentrations were above the minimum inhibitory concentrations (MIC's) of the aminoglycosides against the bacterial strains used for infection when tested in vitro according to standard techniques. In infected cage fluids the pO2 and pH were low, while the pCO2 was high. The number of viable bacteria was high. These factors, which in vitro increased the MIC's of the agents, and the low concentrations achieved in infected cage fluids could explain the inefficacy of aminoglycoside treatment in this experimental model.
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PMID:Studies on some variables influencing aminoglycoside efficacy in vivo and in vitro. 679 55

Fifty mycobacterial strains were isolated from freshly imported tuberculin-negative Macacus rhesus and Cercopithecus ethiops monkeys. Of these strains, 14 were identified as Mycobacterium simiae and 4, as Mycobacterium asiaticum. These two species are slow growing with a delayed photochromogenicity. M. Simiae is niacin-positive. Both species are resistant to the antituberculous chemotherapeutic compounds streptomycin, isoniazid, p-aminosalicylate, and rifampin but are sensitive to cycloserine. The two species are virulent for white mice. Infection is contagious; 25% of noninfected cage mates become infected during 12--60 days of exposure to infected animals. Intrauterine transmission of infection also occurs. Utilizing the gel-precipitation method, we have observed up to 16 antigens in each species. Four to six antigens are shared with Mycobacterium tuberculosis. Mycobacterium species strain 52 is antigenically distinct. The 14 strains of M. simiae belong to two serotypes. Mycobacterium habana belongs to M. simiae serotype 1.
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PMID:Mycobacterium simiae and related mycobacteria. 680 23

Marine parasites with special relation to Japanese fisheries and mariculture include various types of pathogens: those causing mortality, deformity, weight loss, etc.; those giving unesthetic appearances to the hosts; those which are zoonotic. Japanese mariculture typically utilizes net cage culture systems in coastal areas. Parasite invasion in such systems is more difficult to control practically than in freshwater facilities. The limited use of chemicals and drugs for treatment makes the situation even more difficult to handle. About five species of parasites from marine organisms are known to be zoonotic. This is closely associated with the Japanese tradition of eating raw fishes and invertebrates. Infection of maricultured species with zoonotic trematodes, cestodes and nematodes has not been confirmed. On a more positive side, attempts have been made to utilize parasites as biological tags to obtain information on host biology, ecology, etc. Recent trends in Japanese mariculture include technical improvement in seed production and importation of large quantities of various species of culture seedlings. Drastic increase in the supply of seedlings of selected fish species has resulted in changes in culture methods and created parasite problems on a much larger scale. International trade of live fishes and shellfishes has introduced parasites hitherto unknown to Japan. An efficient quarantine system to prevent and control introduction and spread of marine parasites urgently needs to be established.
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PMID:Marine parasitology with special reference to Japanese fisheries and mariculture. 889 67

The Fas-Fas ligand (FasL) system plays an important role in the induction of lymphoid apoptosis and has been implicated in the suppression of immune responses. Herein, we report that gene transfer of FasL inhibits tumor cell growth in vivo. Although such inhibition is expected in Fas+ tumor cell lines, marked regression was unexpectedly observed after FasL gene transfer into the CT26 colon carcinoma that does not express Fas. Infection by an adenoviral vector encoding FasL rapidly eliminated tumor masses in the Fas+ Renca tumor by inducing cell death, whereas the elimination of Fas- CT26 cells was mediated by inflammatory cells. Analysis of human malignancies revealed Fas, but not FasL, expression in a majority of tumors and susceptibility to FasL in most Fas+ cell lines. These findings suggest that gene transfer of FasL generates apoptotic responses and induces potent inflammatory reactions that can be used to induce the regression of malignancies.
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PMID:Gene transfer of Fas ligand induces tumor regression in vivo. 939 Nov 18


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