Use of applied fields in biological treatment of toxic substances, wastewater, and sludges.
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Biomedical subjects
Publications and source records attributed to T G Akers.
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We describe computer programs that predict the most energetically favorable secondary structures in growing RNA sequences, generate a sequential display of the growing structures, and monitor the predicted participation of intramolecular sites in secondary structure. These programs may provide insight into the relationships between messenger RNA secondary structure and expressibility.
The integration of software into special-purpose systems (e.g. for gene sequence analysis) can be a difficult task. We describe a general-purpose software integration tool, the BCE program, that facilitates assembly of VAX-based software into application systems and provides an easy-to-use, intuitive user interface. We describe the use of BCE to integrate a heterogeneous collection of sequence analysis tools. Many BCE design features are generally applicable and can be implemented in other language or hardware environments.
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Secalonic acid D (SAD), a hepatotoxic, teratogenic, and slightly mutagenic metabolite of Penicillium oxalicum has been identified as a natural contaminant of grain dust. Secalonic acid D was administered intraperitoneally to male ICR mice that were exposed to influenza virus aerosols 5 days earlier. The mortality rate was significantly higher (p less than 0.001) in mice subjected to both influenza and SAD than those subjected to influenza alone. Virus titers in lung tissue samples at selected time intervals appeared similar for both influenza and influenza-SAD treated groups of mice for 9 days after exposure to the virus. After 9 days, influenza-SAD treated mice appeared to have higher virus titers. No difference in the pathological progression of pneumonia was discernible between these two groups of mice. The influenza-SAD group, in addition to pneumonia, exhibited severe hepatic necrosis characteristic of SAD administration. Mice infected with influenza virus followed by administration of SAD responded with significantly lower (p less than 0.05) antibody titers to influenza virus than mice exposed to influenza virus alone.
A new serotype of calicivirus, designated as San Miguel sea lion virus type 6 (SMSV-6), was isolated from vesicular lesions on the flipper of a California sea lion pup. Serologic studies show that SMSV-6 neutralizing antibodies (SN) occur frequently among California sea lions and occasionally among northern fur seals. Feral swine, 1- to 6-week elephant seal pups and grey whales tested negative for SMSV-6 antibody.
In a 5-year study (1972-1977) of microbial agents isolated from both clinically normal and diseased marine mammals, it was shown that certain disease agents are widespread in a diversity of ocean populations and that some are also transmissible to a number of terrestrial mammal species. Leptospira interrogans serovar pomona has been isolated repeatedly from 2 species of pinnipeds (Zalophus californianus califonianus and Callorhinus ursinus). Some of the more important bacterial pathogens for land mammals that were isolated from wild marine mammals are Pseudomonas mallei, Clostridium chauvoei, C novyi, Neisseria mucosa var heidelbergensis, Klebsiella pneumoniae, Salmonella spp, and Pasteurella multocida. Numerous serotypes of viruses classified as caliciviruses were isolated from a variety of marine mammals. Some of these are known to infect several land mammal species including swine horses, and primates. For this reason., precautions should be taken to ensure that disease agents shed by captive marine mammals are not transmitted to susceptible terrestrial mammals, including animal handlers and other human beings.
Vesicular exanthema of swine (VES) was first recognized in 1932. At the time, eradication measures and, later, quarantine procedures were instituted and extension of the disease to surrounding farms appeared to have been prevented. Between 1932 and 1936, however, seemingly unrelated epizootics continued among swine herds being fed raw garbage. In 1936, VES disappeared only to reappear in 1939. The disease was contained within California until 1952, at which time it spread to all the major swine producing areas of the United States. The disease was eradicated in 1959, through the enforcement of laws prohibiting the feeding of raw garbage to swine. Other than the association with raw garbage, a reservoir for VES virus (VESV) was never found. In 1972, a virus isolated from California sea lions--and thus named the San Miguel sea lion virus (SMSV)--proved to be distinguishable from VESV. When SMSV was injected into swine, clinical signs of vesicular exanthema developed, leading to the conclusion that, for all practical purposes, SMSV and VESV were the same. To date, 5 species of marine mammals and 2 species of terrestrial mammals, including feral swine, have been shown to possess antibodies to 1 or more of the 4 distinct SMSV serotypes. Current evidence suggests that SMSV infections occur among both terrestrial and marine mammals inhabiting the California coastal zones. This and the practice of shipping frozen meats known to contain SMSV to mink ranches in Utah point to the possibility that domestic swine in the United States are occasionally being exposed to SMSV. Although marine mammals are a source of SMSV, the primary virus reservoir is thought to be 1 or more submammalian marine species common to the southern California coastline. Such a primary reservoir presumably is the source of a new SMSV serotypes infecting marine mammals and may have been the original source of the VESV serotypes that infected swine through the intermediary of raw garbage.
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An interaction between sarcoma-180/TG cells and vesicular stomatitis virus in adult mice resulted in the rapid onset of extensive mortality. This interaction, termed lethal synergy, occurred only at early stages of ascites induction in animals with no prior virus contact. A significant sparing effect conferred by the serotonin antagonist dibenamine was reversed by the administration of serotonin. The cause of death was not determined, but a mechanism involving hypersensitivity is indicated.
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The influence of relative humidity on the airborne survival of simian virus 40 (SV40) was studied by allowing virus aerosols to age in rotating drums at 21 or 32 C and at a relative humidity (RH) value ranging from 22 to 88%. Airborne SV40 virus was stable at every RH tested at 21 C, but aerosols maintained at 32 C were inactivated within 60 min at mid-range RH values. The unusual stability at 21 C over a broad RH range indicates that potentially biohazardous situations may occur under laboratory conditions if this virus becomes accidentally airborne.
A reduction in pulmonary anti-bacterial activity due to a preceding viral illness has been suggested as the mechanism responsible for some meningococcal infections of the lung. We investigated this proposed pathogenesis by infecting mice with airborne encephalomyocarditis virus (EMC) and then challenging them 1, 4, and 7 days later with aerosols of Neisseria meningitidis. Meningococcal clearance was assessed by comparing the numbers of bacteria present immediately after inhaling the aerosols with the numbers present 3 hr later. To insure that EMC virus adequately depressed murine defense mechanisms, we also determined staphylococcal killing rates at 4 hr by using radiophosphorus-labeled staphylococcal aerosols. Viral infection depressed murine pulmonary antimeningococcal activity at 1 and 4 days (P < 0.01) but not at 7 days. Intrapulmonary staphylococcal killing was impaired on day 4 (P < 0.01) but not on days 1 or 7. Pulmonary viral titers decreased rapidly from 10(7) to 10(3) plaque-forming units/ml of lung during the experimental period. According to these data viral disease transiently depresses resistance to meningococcal infection. This impairment in host resistance is present while the viral titer is decreasing and follows a relatively similar pattern to the transient decrease noted for staphylococci.
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The effect of relative humidity (RH) on the airborne stability of two small bacterial viruses, S-13 and MS-2, was studied. Poorest recovery of S-13 was obtained at 50% RH. Humidification prior to aerosol sampling significantly increased the recovery of S-13 at RH deleterious to the airborne virus. A commercial preparation of MS-2 suspended in a buffered saline solution showed a rapid loss of viability at RH above 30%, whereas a laboratory preparation containing 1.3% tryptone showed high recoveries at all RH studied. Dilution of the commercial MS-2 into tryptone broth conferred stability on the airborne virus. Humidification prior to sampling significantly reduced the viable recovery from aerosols of commercial MS-2, whereas the laboratory preparation was unaffected.