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Biomedical subjects

F Cohen

Publications and source records attributed to F Cohen.

At least 55 records · Page 3Linked to original sources
PubMed1983

[Oxacillin and gentamicin-resistant Staphylococcus aureus: surveillance and development over a period of 6 months].

An outbreak of nosocomial infections caused by oxacillin and gentamicin-resistant Staphylococcus aureus occurred over a 3 month period in the intensive care unit of a 371-bed hospital. Four patients were infected. S. aureus isolates were resistant to multiple antibiotics beside oxacillin and gentamicin. They exhibited identical antibiotic susceptibility pattern and identical phage type (47/54/75/77/84/85). A subsequent survey of oxacillin-resistant S. aureus was conducted in the hospital during a 6 month period. Bacteriophage typing was performed on 52 isolates of oxacillin-resistant S. aureus. Seventeen were non typeable . Fourteen had the same phage type (or a minor variant +/- 2 numbers) as that of the previously isolated S. aureus. The antibiotic susceptibility pattern of 10 of the 14 isolates was identical to that of the epidemic strain. The antibiotic susceptibility patterns of 2 isolates differed from it with respect to the resistance to one antibiotic among those tested (these two isolates were obtained from patients that received the particular antibiotic before the isolation of the Staphylococcus). The 7 patients from whom these 12 S. aureus were isolated were staying in the intensive care unit except one who was hospitalized in this unit several months ago. Among the personnel screened, two intensive care unit nurses were found to be nasal carriers of oxacillin resistant S. aureus. One strain had the same phage type as that of the epidemic strain but its antibiotic susceptibility pattern was different. Room-mate to room-mate spread within the intensive care unit may be responsible for the perpetuation of the epidemic strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacteriophage Typing↗
PubMed1983

Rotavirus infection in Black and White newborns.

Rotavirus infection in asymptomatic Black and White newborns in maternity hospitals was studied by electron microscopy of stools. None of the 37 White and 30 (49%) of the 61 Black babies excreted rotavirus (P less than 0.0005). The high incidence of neonatal infection in Blacks, who have a low incidence of rotavirus diarrhea in infancy, suggests that neonatal infection might result in immunity.

Black or African American↗
PubMed1982

Variance in rotavirus infection rates in different urban population groups in South Africa.

Rotavirus infection in black infants contrasts markedly with that of white infants in being much less common and showing no seasonal variation. In this multicentre study in Johannesburg, the aetiology of winter infantile gastroenteritis in black, coloured, and white infants was investigated. Stools were examined by electron microscopy and also by enzyme-immunoassay to detect subparticular antigen which may be missed by electron microscopy in patients presenting late in the course of the illness. Stools were also examined bacteriologically by conventional techniques. Rotavirus was the most common pathogen in all three population groups with bacteria playing a relatively minor role. Striking differences were observed in the rotavirus rates between the three groups. Infection in the whites was five times more common than in the blacks (60% versus 12%) with the coloureds intermediate at 40%. The hypothesis was put forward that the relative protection of the black population may be due to a greater degree of colonization of neonates, thus inducing protection against symptomatic infection at the target age of 6 to 24 months. This may well have important implications in immunoprophylaxis. The reason for the lack of seasonal variation in the black population is still unclear.

Animals↗
PubMed1981

First component of complement and thrombosis.

The previous demonstration of an association between the collagen-like region of C1q (subcomponent of the first component of complement) and human platelets and of the inhibitory properties of C1q on platelet adhesion and aggregation to or by collagen has led us to consider the first component of complement as a possible modulator of the platelet-collagen interaction. Since collagen represents a major component of the vessel wall, the modification of C1 could play a role in the development of thrombosis. We have therefore studied two patients with abnormalities of complement (low or undetectable C1, C4, C2 and deficiency in C1 inhibitor) who presented with acquired angioneurotic oedema. Both patients had a history of multiple episodes of arterial and/or venous thrombosis. Platelet associated C1q was decreased or undetectable, and this condition was associated with a specific increase of collagen induced aggregation thereby suggesting a possible mechanism for the recurrent thromboembolic episodes.

Adult↗
PubMed1981

Enhanced thromboxane A2 and prostacyclin production by cultured rectal mucosa in ulcerative colitis and its inhibition by steroids and sulfasalazine.

Accumulation of 6-ketoprostaglandin F1 alpha and thromboxane B2, the stable metabolites of prostacyclin I2 and thromboxane A2 respectively, by cultured rectal mucosa obtained from patients with active ulcerative colitis was significantly higher than their respective accumulation by cultured biopsy specimens obtained from normal subjects. Accumulation of prostacyclin I2 and thromboxane A2 by rectal mucosa obtained from ulcerative colitis patients in remission was not enhanced. Prostacyclin I2, thromboxane A2, and prostaglandin E2 accumulation was significantly inhibited by the addition to the culture medium of 5-aminosalicylic acid, flufenamic acid, aspirin, azathioprine, and methylprednisolone. Sulfapyridine inhibited significantly only prostaglandin E2 and prostacyclin I2 while sulfasalazine inhibited thromboxane A2, prostaglandin E2, and prostacyclin I2 accumulation. Flufenamic acid potentiated the inhibition of prostaglandin E2 accumulation induced by methylprednisolone when administered alone. These results suggest that in addition to the mediation by prostaglandin E2, thromboxane A2 and prostacylin I2 may also be involved in the inflammatory response in ulcerative colitis. Moreover, the therapeutic effects of steroid hormones and sulfasalazine may be partially related to their inhibition of colonic prostaglandin E2, prostacyclin I2, and thromboxane A2 synthesis.

Colitis, Ulcerative↗
PubMed1980

Does sex make a difference? Gender, age, and stimulus realism in perception and evaluation of aggression.

Judged aggressiveness and its justifiability were examined with caricature cartoons and films of people doing comparable things. Effects of viewer gender, interactant gender, and facial expression were examined. Facial expression strongly affected both types of judgment, viewer gender had no influence, and interactant gender contributed slightly. Real-cartoon differences were significant, but accounted for little variance. Major response patterns were similar for films of people and cartoons. In two developmental studies, only facial expression influenced judgments of friendliness-hostility in cartoons, but condemnation of aggression decreased as viewer age increased. Results with films of real children followed those for cartoons. Facial expression influenced judged aggressiveness, but only viewer age affected judged justifiability. Cross-experiment comparisons revealed that facial expression and the facial expression X real-cartoon interaction yielded major differences on both dependent variables. Subject and interactant gender were not significant for major dependent variables. Results of the developmental studies were similar to adults' suggesting that for judgments of simple aggressive acts, sex makes no difference, but facial expression does make a difference.

Adolescent↗
PubMed1976

Familial partial trisomy 6q syndromes resulting from inherited ins (5;6) (q33;q15q27).

Two cases are reported of familial partial trisomy 6q syndrome due to segregation of ins(5;6) (q33;q15q27) in three generations. The common clinical features include growth and mental retardation, feeding difficulty during infancy, microcephaly with downward slanting palpebral fissures, flattened nasal bridge with anteverted and flared nares, long philtrum, high arched palate, partially opened and protruding mouth with receding chin, deep transverse creases of the ears, three creases on the 4th fingers, clinodactyly of the 5th fingers with a single crease, and other dermatoglyphic findings. These characteristic features of two patients appear to make partial trisomy 6q a clinically recognizable syndrome.

Abnormalities, Multiple↗