Paul Gross
Western Pennsylvania Hospital
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Featured researches published by Paul Gross.
Experimental Biology and Medicine | 1937
Frank B. Cooper; Paul Gross; Ralph R. Mellon
Conclusions The oral administration of p-aminobenzenesulfonamide is capable of prolonging, and in some cases of saving, the lives of mice infected subcutaneously with approximately 10 minimal lethal doses of highly virulent Type 111 pneuniococci.†, ‡
Experimental Biology and Medicine | 1937
Paul Gross; Frank B. Cooper
Conclusions P-aminobenzenesulfonamide therapy is effective in prolonging, and in many instances saving, the lives of rats infected intrabronchially with Type I11 pneumococci suspended in mucin.
Experimental Biology and Medicine | 1937
Frank B. Cooper; Paul Gross
Conclusion P-aminobenzenesulfonamide given orally to rats suffering from experimental Type III (“420” strain) pneumococcal pneumonia reduced the mortality and increased the survival-period. The effectiveness of this treatment varied inversely with the interval Ijetween infection and initial treatment, and with the magnitude of the infecting dose. The treated rats which succumbed showed less bacteremia and a lower incidence of peritonitis than the untreated ones which succumbed. The course and extent of the pneumonia was not appreciably affected. Treatment apparently enables many of the animals to survive the associated toxemia which is commonly fatal to similarly infected, but untreated, rats.
Experimental Biology and Medicine | 1937
Frank B. Cooper; Paul Gross
Conclusion 1. Sulfanilamide was at least as effective as specific antiserum, in the doses employed, in treating Type II pneumococcal rat pneumonia. A probable clinical application to similar human pneumonia is thereby suggested. 2. The combination of sulfanilamide and serum was no more effective than sulfanilamide alone. 3. Contrary to the observations in rabbits (Locke and Mellon), in rats Vitamin C alone, or in any combination tried, is ineffective.
Experimental Biology and Medicine | 1938
Paul Gross; Frank B. Cooper; Marion Lewis
Conclusions Sulfanilamide causes a slight, almost negligible, inhibition of the hemolytic activity of streptococcal and staphylococcal hemotoxin. More marked inhibition of streptococcal hemolysin is produced by prontosil II, normal rabbit serum, rabbit Serum heated to 61°C., eosin, phenol, mercuric chloride, and sodium carbonate. The administration of sulfanilamide in vivo or its addition to serum in vitro does not enhance the inhibitory effect of rabbit serum upon streptococcal hemolysin. Prontosil I was found to have no inhibitory effect upon streptococcal hemolysin.
Experimental Biology and Medicine | 1938
Paul Gross; Frank B. Cooper; Marion Lewis
Conclusion Sulfanilamide, 4,4′-di- (acetylamino)-diphenylsulfone, and 4,4′-diaminobenzenesulfonanilide have no therapeutic value in the treatment of mice infected intraäbdominally with virulent B. pertussis.
Experimental Biology and Medicine | 1937
Paul Gross; Frank B. Cooper; M. L. Peebles
Conclusions 1. P-aminobenzenesulfonamide is capable of protecting splenectomized mice against fatal doses of highly virulent hemolytic streptococci. 2. The degree of protection observed in splenectomized mice was identical with that obtained with normal animals.
Experimental Biology and Medicine | 1941
Frank B. Cooper; Paul Gross; Marion Lewis
Conclusions 2-(Sulfanilamido)-5-ethyl-4-thiazolone (sulfaethyl-thiazolone) has less antistreptococcic activity and approximately the same antipneumococcic activity as sulfapyridine. Its antistaphylococcic activity is of the same order as that of sulfathiazole and sulfadiazine. Sulfadiazine produces urolithiasis medicamentosa capable of causing death by acute suppression of urine in mice and rats, whereas sulfaethylthiazolone is free of this defect, but may cause fatal anemia.
Experimental Biology and Medicine | 1938
Frank B. Cooper; Paul Gross; Marion Lewis
Conclusions A cerebro-spinal meningitis due to a Type II pneumococcus has been produced in the rat. Oral treatment with sulfanilamide, instituted after this disease was well established, resulted in 73.3% cures; with 4,4-di-(acetylamino)-diphenylsulfone, 40% cures, and with no treatment, 100% fatality. It is quite evident that the sulfone compound was not as effective against this pneumococcal strain as sulfanilamide.
Experimental Biology and Medicine | 1939
Frank B. Cooper; Paul Gross; Marion Lewis
Conclusions The above experiments, more rigorous than those previously reported∗ because treatment was purposely withheld until infection was established and then conducted with equal doses of the 2 drugs, show 2-(sulfanilamido)-pyridine slightly superior to sulfanilamide in combatting Type II pneumococcal infections of less than 100 fatal doses in mice and rats.∗ These conclusions are based on survival values only.