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Biomedical subjects

C Gulotta

Publications and source records attributed to C Gulotta.

6 recordsLinked to original sources
PubMed1994

Thyroid function and attention-deficit hyperactivity disorder.

OBJECTIVE: To examine thyroid indices in a community referred sample of boys with attention-deficit hyperactivity disorder (ADHD) for evidence of generalized resistance to thyroid hormone (GRTH). METHOD: TSH, T3, and T4 values were gathered prospectively in 53 physician, school, and/or parent referred ADHD subjects, and in 41 age and gender-matched normal controls. RESULTS: None were in the range suggestive of global or pituitary thyroid hormone resistance. CONCLUSIONS: GRTH is rare, and thyroid function should not be measured routinely in nonfamilial ADHD.

Attention Deficit Disorder with Hyperactivity↗
PubMed1993

Rapid identification of mycobacteria from culture using acridinium-ester-labelled DNA probes.

OBJECTIVES: Our study used newly developed acridinium-ester-labelled DNA (AE-DNA) probes on 183 mycobacterial isolates, performing the tests on 12B Bactec vials and Loewenstein-Jensen (LJ) slants. METHODS: The probe results were verified using the conventional method as a reference. RESULTS: The probe for M. tuberculosis complex correctly identified 131 of 133 M. tuberculosis isolates, with two false negatives and no false positives, for a sensitivity of 98.5% and a specificity of 100%. The M. gordonae probe correctly identified 27 out of 27 M. gordonae isolates, with no false negatives and one false positive, for a sensitivity of 100% and a specificity of 90.9%. One hundred sixty-eight of the 183 isolates were screened in accordance with an algorithm, designed primarily for the rapid detection and identification of M. tuberculosis. CONCLUSION: The use of the algorithm considerably reduced detection time: M. tuberculosis strains were identified within 16.2 +/- 2.3 days, while identification by conventional method required 35.7 +/- 5.5 days. Probe testing resulted in a cost increase of 67.8%.

Algorithms↗
PubMed1993

Classification of chest wall diseases.

Several disorders of the thoracic cage are known to cause respiratory failure, by means of relatively simple mechanisms, such as the increased work of breathing, which results in alveolar hypoventilation. A variety of pathogenic mechanisms may be considered, as functions of the types of thoracic disorders present. As causes of these additional potential mechanisms, we considered the following: 1) ventilation-perfusion (V/Q) inhomogeneity; 2) inability to cough; 3) malformation or acquired defect of the respiratory centres; and 4) excess blood volume and fluid retention, which aggravate work of breathing and V/Q inhomogeneity. All of these disorders can be grouped into two major categories (which nevertheless have some of the pathophysiology in common): the mechanical syndrome and the neuromuscular or paralytic syndrome. In this paper we discuss chest wall diseases falling into the first category; namely, kyphoscoliosis, fibrothorax, thoracoplasty, ankylosing spondylitis and obesity-hypoventilation. Congenital deformities of the thoracic cage, which do not have important effects on ventilatory apparatus (e.g. pectus excavatum and pectus carinatum), were also considered.

Humans↗
PubMed1991

Effects of oral lacidipine on cardiopulmonary function at rest and during exercise in normal subjects.

A randomized, double-blind, crossover, placebo-controlled study was carried out to evaluate the effects of a single oral 4-mg dose of lacidipine vs. placebo on cardiopulmonary circulation at rest and during exercise. Twelve healthy volunteers were randomized to receive either placebo or 4 mg of lacidipine once daily for 2 days, followed by a 3-day washout period, after which they received alternate treatment. Patients were assessed before and at 60, 90, and 180 min after dosing. At 120 min, a maximum exercise test with a treadmill was performed according to the Bruce protocol. No relevant changes with placebo or lacidipine were observed in the respiratory function tests whereas 4 mg of lacidipine increased pulmonary effective blood flow (Qp. eff.) and stroke volume index (SVI) at 60 min, reaching a peak at 90 min; at 180 min, these effects, although diminished, were still present. The arteriovenous oxygen difference [C(a-v)O2] decreased, but reverted to normal values by 180 min. No differences in maximum attained Qp. eff. and oxygen consumption (VO2) during exercise were observed. Only the heart rate was higher both before and after treatment with lacidipine. Lacidipine increased Qp. eff. in these normal subjects without relevant effects on respiratory function. Performance on exercise testing after dosing was normal, although drug-induced vasodilation was present.

Adult↗