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1.  A predischarge unit in a long-stay hospital for subnormality. 
British Medical Journal  1976;2(6041):921-922.
A newly built residential ward in the grounds of a long-stay mental subnormality hospital was converted into a predischarge unit to cater for those patients who could probably be discharged after some special training. So far 31 residents have been trained over the past two years; 18 (58%) have been discharged to community residences, and five were waiting for discharge. The high success rate shows the value and usefulness of a predischage unit in a long-stay hospital, and also shows that a purpose-built building is not necessary so long as the staff have the initiative and will to succeed.
PMCID: PMC1688478  PMID: 974666
2.  Semi-microtechnique for the biochemical characterization of anaerobic bacteria. 
Journal of Clinical Microbiology  1976;4(4):315-318.
A semi-micromethod is described for characterizing anaerobic bacteria by substrate utilization. Small volumes of individual substrates were placed in the wells of plastic microtiter trays. When heavy inocula and a colorimetric indicator were used, complete results were available after 30 h of incubation. Microtiter trays containing a range of substrates can be stored at -20 degrees C. The method is accurate, economical, and convenient for use in a hospital microbiology laboratory.
PMCID: PMC274463  PMID: 789392
3.  Bacillus pumilus polysaccharide cross-reactive with meningococcal group A polysaccharide. 
Infection and Immunity  1976;13(6):1654-1662.
A polysaccharide, antigenically and structurally related to meningococcal group A polysaccharide, was isolated from Bacillus pumilus Sh-17. This enteric bacterium has been implicated as a source of natural meningococcal group A immunity (Myerowitz et al., 1973). The B. pumilus polysaccharide was composed of a homopolymer of (1-6)-N-acetyl-manosamine-1-phosphate, glycerol phosphate teichoic acid-containing N-acetylglucosamine and alkali-labile alanine esters, and a mucopeptide. The cross-reaction was due to the poly-(1-6)-N-acetyl-mannosamine-1-phosphate in the B. pumilus and the meningococcal group A polysaccharides, based on the following evidence. Both polysaccharides contained N-acetyl-mannosamine phosphate. Periodate oxidized the mannosamine phosphate residues of the polysaccharide and destroyed their precipitating activity with meningococcal group A antiserum. Mild acid treatment released phosphomonoesters and destroyed the meningococcal group A precipitating activity of both polysaccharides. N-acetyl-mannosamine-6-phosphate inhibited the precipitation reaction between strain Sh-17 and meningococcal group A antisera. Only mannosamine phosphate was detected in trichloroacetic acid extracts of Sh-17 polysaccharide and meningococcal group A antigen-antibody precipitates.
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PMCID: PMC420816  PMID: 184043
4.  Temperature-dependent inactivating factor of Pseudomonas aeruginosa exotoxin A. 
Infection and Immunity  1976;13(5):1467-1472.
The adenosine diphosphate ribosyl transferase activity of Pseudomonas aeruginosa exotoxin A(PA toxin) was found to be rapidly destroyed by heating at 45 to 60C but not by heating at 70 to 90C (for at least 30 min). This phenomenon has been previously described for other bacterial toxins (staphylococcal alpha-toxin and Vibrio parahaemolyticus hemolysin) and is termed an Arrhenius effect. In contrast, the Arrhenius effect was not seen when the PA toxin was heat-treated as above and tested for cell toxicity or mouse lethality. Although the PA toxin treated at 70C for 30 min retained a significant proportion (is greater than 70%) of its adenosine diphosphate ribosyl transferase activity, the cell toxicity and mouse lethality of the toxin were virtually abolished. A temperature-dependent inactivating factor that has proteolytic activity and is co-purified with the PA toxin was shown to be responsible for the Arrhenius effect. PA toxin separated from the factor by conventional disc gel electrophoresis or PA toxin preparations lacking the factor did not show the Arrhenius effect.
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PMCID: PMC420782  PMID: 178606
5.  Colonization of soil by Arthrobacter and Pseudomonas under varying conditions of water and nutrient availability as studied by plate counts and transmission electron microscopy. 
Arthrobacter globiformis and a Pseudomonas soil isolate were incubated separately and in combination in soil that had been presterilized by autoclaving. Growth and other responses of the cells in situ in this soil were monitored by plate counts and transmission electron microscopy examinations of cell sections. During the soil incubations, some of the samples were first allowed to dry and then were remoistened with water or with a dilute or a concentrated nutrient solution. Based on plate counts and ultrastructural analysis. Arthrobacter seemed to be in a non-multiplying coccoid-rod resting state and to be virtually immune to soil drying. Addition of a dilute nutrient solution helped maintain cell ultrastructure and prevent a low level of lysing that occurred in the absence of nutrient addition. Addition of a concentrated nutrient solution brought on cell multiplication as both coccoid-rods and long rods, but the ultimate form with further incubation was the coccoid-rod. The Pseudomonas strain suffered death and ultrastructural deterioration as water became less available. It responded by cell multiplication to an equal extent when either water or dilute nutrients were added, but possibly was able to give a growth response to nutritive amendment when a concentrated nutrient addition was made. The Arthrobacter was not affected by the presence of Pseudomonas in dual culture. The Pseudomonas, however, possibly suffered a nutritive deficiency under these conditions.
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PMCID: PMC169818  PMID: 1267449
6.  Use of Clindamycin in Patients with Liver Disease 
Hepatotoxicity has been noted by several investigators during parenteral use of clindamycin, and some have reported that drug half-life is prolonged in the presence of liver disease. We administered 300 mg of clindamycin intravenously at 12-h intervals for 2 days to patients with acute and chronic hepatitis, cirrhosis, and controls to determine whether clindamycin will exacerbate preexisting hepatic dysfunction or whether drug excretion will be delayed in patients with liver disease as compared with controls. Exacerbation of hepatotoxicity was not found in this study. There was a small, but significant, delay in drug elimination between cirrhotics and controls, even after the first dose of clindamycin (P < 0.05); however, half-lives in all categories were in the range usually considered normal. We conclude that clindamycin can be used in liver disease in some circumstances, if proper precautions are exercised.
PMCID: PMC429559  PMID: 1259404

Results 1-6 (6)