Biomedical subjects
Publications and source records attributed to G Colangelo.
We demonstrate that near the threshold, the pi pi scattering amplitude contains a pole with the quantum numbers of the vacuum--commonly referred to as the sigma--and determine its mass and width within small uncertainties. Our derivation does not involve models or parametrizations but relies on a straightforward calculation based on the Roy equation for the isoscalar S wave.
We show that, independently of the size of the quark condensate, chiral symmetry correlates the two S-wave pipi scattering lengths. In view of this constraint, the new precision data on K(e(4)) decay allow a remarkably accurate determination of these quantities. The result confirms the hypothesis that the quark condensate is the leading order parameter.
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In order to determine the relationship between chronic hypercapnia and anthropomorphic data, pulmonary function tests and slopes of ventilatory responses to hypercapnia (HVCR) and hypoxia (HVR), we studied 55 patients with sleep apnea-hypopna syndrome (SAHS). Patients were divided into hypercapnic, PaCO2 > or = 45 mm Hg (Group I, n = 23, PaO2 = 61 +/- 10 and PaCO2 = 50 +/- 5 mm Hg, and [HCO3-] = 30 +/- 4 mEq/l [means +/- SD]) and normocapnic (or eucapnic), PaCO2 < 45 mm Hg (Group II, n = 32, PaO2 = 76 +/- 10 and PaCO2 = 39 +/- 4 mm Hg and [HCO3-] = 25 +/- 3 mEq/l [means +/- SD]) groups. When compared to the normocapnic group, hypercapnic patients were significantly heavier (with greater body surface area) and had significantly more severe restrictive and obstructive defects and impaired HVR and HCVR. The means (+/- SD) of some of the data follow (* indicates p < 0.05 when Group I is compared to Group II): [table: see text] When subgroups of hypercapnic and eucapnic patients with similar lung functions were compared, the subgroups differed significantly in their weights; conversely, in subgroups with comparable weights, lung function tests differed significantly. These data suggest that the mechanisms of chronic hypercapnia are multifactorial, and we hypothesize that, in the face of repetitive apneas and hypopneas, increased weight and abnormal lung function tests interact and contribute to the generation and maintenance of hypercapnia.
The mechanisms of hypercapnia observed in some patients with sleep apnea-hypopnea syndrome (SAHS) are not known. In chronic obstructive lung disease (COLD), hypercapnic and hypoxic ventilatory responses (HCVR/HVR) are decreased in normal family members of hypercapnic patients compared with those of non-hypercapnic patients. This suggests a familial (presumably genetic) diminished chemosensitivity predisposing to hypercapnia. In this study we investigated the possibility of a similar mechanism in SAHS. Based on PaCO2, 29 patients with polysomnographic evidence of SAHS were divided into those with chronic hypercapnia (PaCO2 greater than or equal to 45 mm Hg, n = 13) and those with normocapnia (PaCO2 less than 45 mm Hg, n = 16). We studied healthy adult (greater than or equal to 17 yr) immediate family members of these patients. Family members were required to have normal spirometry and be on no medications. In Group I, there were 32 family members of hypercapnic patients and in Group II, 26 family members of normocapnic patients. In Group I, the mean (+/- SD) of age (yr) was 36 +/- 12, weight (kg) 82 +/- 22, FEV1 (L) 3.1 +/- 0.8, VCO2 (ml/min) 228 +/- 63, slope (L/min) of HCVR 2.0 +/- 0.8, and slope (L/min/1% saturation) of HVR -1.20 +/- 0.82. Respective values in Group II were 34 +/- 14, 83 +/- 16, 3.2 +/- 0.8, 233 +/- 63, 2.0 +/- 1.0, and -1.34 +/- 1.20. There were no statistically significant differences in measured variables between the two groups. Furthermore, there were no significant correlations between PaCO2 of patients and slopes of HCVR or HVR of their family members.(ABSTRACT TRUNCATED AT 250 WORDS)
We performed an analysis of the value of repeat bronchoalveolar lavage (BAL) at 21 days to identify patients at risk for early relapse with Pneumocystis carinii pneumonia. Patients with P. carinii pneumonia and the acquired immunodeficiency syndrome (AIDS) were asked to participate in this study. All patients had P. carinii identified on methenamine silver stain of BAL fluid. BAL fluid was also stained with a modified Wright-Giemsa technique. The Wright-Giemsa stain was done to determine the cell differential count, and the number of P. carinii clusters associated with 500 nucleated cells was used as an estimate of P. carinii burden in the BAL. Initial and follow-up lavage was performed in 56 patients. Patients were classified based on their clinical response to anti-P. carinii therapy at 21 days. Nonresponders were patients with persistent or worsening symptoms. Responders were patients who improved and had therapy discontinued. Responders were further classified as responders with relapse if P. carinii pneumonia recurred within 6 months of the initial episode or responders without relapse if they remained disease free during the follow-up period. Responders without relapse reduced P. carinii cluster counts more than 50% in 24 of 25 cases. In responders with relapse P. carinii cluster counts were unchanged. The responders as a group had a significant decrease in the percentage of neutrophils in the BAL, with only 2 of 32 still having increased neutrophils in the follow-up lavage compared to 17 of 24 nonresponders (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
We developed a technique to estimate the amount of Pneumocystis carinii found in bronchoalveolar lavage fluid. P. carinii associated with 500 nucleated cells in the bronchoalveolar lavage fluid had little between-observer and within-observer variation. Varying the technique of the lavage did not change the amount of P. carinii recovered. This technique was used in patients treated for P. carinii pneumonia. Those patients who did not respond to treatment had more P. carinii in their bronchoalveolar lavage fluid than those who responded.
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