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Biomedical subjects

D Buffa

Publications and source records attributed to D Buffa.

At least 37 records · Page 2Linked to original sources
PubMed1983

Myxoid degeneration with prolapse and dystrophic calcification of the annulus fibrosus of the mitral valve. Pathological and clinical survey.

Two degenerations of the mitral valve apparatus, namely myxoid degeneration of the mitral cusps and necrosis with subsequent calcification of the annulus fibrosus, are extensively reviewed and discussed. Both lesions are mainly noticed in elderly patients, with the possible exception of systemic dystrophies of the connective tissue associated with metabolic disorders. The clinicopathological correlations of several cases are reported, with special emphasis on modern diagnostic procedures and their wide anatomic spectrum.

Adult↗
PubMed1981

Murein synthesis and beta-lactam antibiotic susceptibility during rod-to-sphere transition in a pbpA(Ts) mutant of Escherichia coli.

The conditional morphology mutant of Escherichia coli SP45 grows as a rod at 30 degrees C and assumes a spherical shape after 90 min of incubation at 42 degrees C. The rod-to-sphere morphological transition has been found to be associated with the disappearance of penicillin-binding protein 2 (PBP-2), the progressive reduction (as much as 50%) of murein synthesis, as measured both in intact cells and ether-permeabilized bacteria, and alterations in the structure of the cell envelope, including detachment of the outer membrane from the underlying structures. The detachment was initially localized at the poles of the cells and then spread over the entire surface. Shape transition was also linked to increased susceptibility to beta-lactam antibiotics which preferentially bound to PBP-1A (cephalothin, cephaloridine) or to PBP-3 (furazlocillin, piperacillin). Treatment with beta-lactams possessing a high affinity for PBP-1A, although inducing a low degree of peptidoglycan synthesis inhibition (5 to 10%), was associated with a marked loss of cell viability and massive lysis. On the other hand, the simultaneous absence of PBP-2 and inhibition of PBP-3 causes a significant reduction of peptidoglycan synthesis, yet only slightly affected cell viability. Whereas PBP-1A inhibition during shape transition had no effect on morphology, addition of antibiotics binding to PBP-3 30 min after the temperature shift-up caused formation of elongated cells with a centrally located bulge, not observed in similarly treated cells grown at 30 degrees C. Inhibition of PBP-3 in round cells 90 min after temperature shift caused formation of giant cells, indicating complete loss of elongation ability. The different effects of the simultaneous inhibition of two PBPs, combining mutational loss with specific binding in vivo of another PBP by beta-lactams, provide new insight into the role of these proteins and the killing mechanisms of this class of antibiotics.

Bacterial Proteins↗
PubMedDate not supplied

A case-control study on cigarette, alcohol, and coffee consumption preceding Parkinson's disease.

OBJECTIVE: To investigate the association between cigarette smoking, alcohol drinking, coffee consumption and Parkinson's disease (PD). METHODS: We selected subjects affected by idiopathic PD, with a Mini-Mental State Examination of > or =24, and controls matched 1 to 1 with cases by age (+/- 2 years) and sex. Controls were randomly selected from the resident list of the same municipality of residence of the cases. We assessed cigarette smoking, alcohol drinking, and coffee consumption preceding the onset of PD or the corresponding time for controls using a structured questionnaire, which also evaluated the duration and dose of exposure. Using conditional logistic regression analysis, we calculated adjusted OR and 95% CI. RESULTS: We interviewed 150 PD patients and 150 matched controls. Cigarette smoking (ever vs. never smokers OR = 0.66, 95% CI = 0.41-1.05, p = 0.08) did not show a statistically significant association with PD. We observed an inverse association between alcohol drinking (ever vs. never OR = 0.61, 95% CI = 0.39-0.97, p = 0.037) and coffee consumption (ever vs. never OR = 0.16, 95% CI 0.05-0.46, p = 0.0001) and PD. These associations remained significant after adjustment for other covariates: OR for ever vs. never alcohol consumption was 0.62 (95% CI = 0.43-0.89, p = 0.009) and that for coffee drinking 0.19 (95% CI = 0.07-0.52, p = 0.001). Heavy coffee consumption confirmed the inverse association between coffee and PD (more than 81 cup/year vs. none: OR = 0.20, 95% CI = 0.08-0.47, p < or = 0.0001). CONCLUSIONS: Consistent with previous studies, our results suggest an inverse association between coffee drinking, alcohol consumption and PD. The multiple inverse association observed may indicate a complex interaction between genetic and environmental factors.

Adult↗