Designing matrix models for fluorescence energy transfer between moving donors and acceptors.

A recipe is given for designing theoretical models for donor-acceptor systems in which fluorescence energy transfer and motion takes place simultaneously. This recipe is based on the idea that a system exhibiting both motion and fluorescence energy transfer can be modeled by specifying a number of "states" and the rates of transitions between them. A state in this context is a set of specific coordinates and conditions that describe the system at a certain moment in time. As time goes on, the coordinates and conditions for the system change, and this evolution can be described as a series of transitions from one state to the next. The recipe is applied to a number of example systems in which the donors and/or acceptors undergo either rotational or translational motion. In each example, fluorescence intensities and anisotropies for the donor and acceptor are calculated from solutions of eigensystems. The proposed method allows for analyzing time-resolved fluorescence energy transfer data without restrictive assumptions for motional averaging regimes and the orientation factor. It is shown that the fluorescence quantities depend on the size of the motional step (i.e., on the number of states), only if fluorescence energy transfer occurs. This finding indicates that fluorescence energy transfer studies may reveal whether the dynamics of a system (e.g., a protein) is better described in terms of transitions between a relatively small number of discrete states (jumping) or a large number of dense states (diffusion).

Smoking is a factor in causing acute chest syndrome in sickle cell anemia.

A link between cigarette smoking and "acute chest syndrome" in sickle cell anemia is suggested. Acute chest syndrome in the patient with sickle cell anemia is characterized by fever, leukocytosis, cough, chest pain, and pulmonary infiltrates in the chest radiograph. This article describes the results of a study of 69 adolescent and young adult sickle cell anemia patients. Twenty-nine of these patients were smokers, three were former smokers, and 37 were nonsmokers. Patients completed respiratory questionnaires that focused on smoking habits and included a history of chest syndrome. Information obtained was confirmed by review of clinical records. The chi-square test demonstrated a strong relationship between cigarette smoking and chest syndrome in sickle cell anemia. All 29 smokers had a history of chest syndrome, but only 24 of 37 nonsmokers had such a history. Although the exact mechanism of the relationship between smoking and the development of acute chest syndrome remains speculative, cigarette smoking joins infection, hypoxia, acidosis, infarction, dehydration, and analgesics as a causative factor in adolescent and adult patients with sickle cell anemia. Behavioral modification of the smoking habit in patients with sickle cell anemia may decrease the frequency of acute chest syndrome and sequelae of sickle cell lung disease.

Pneumocystis carinii pneumonia complicated by lymphadenopathy and pneumothorax.

A case of generalized Pneumocystis carinii infection presented as hilar and mediastinal lymphadenopathy and was complicated by spontaneous pneumothorax. Extrapulmonary P carinii infection in patients with acquired immunodeficiency syndrome is rare, and pneumothorax is even rarer. The purpose of this report is to call attention to these atypical features of P carinii infection in patients with the acquired immunodeficiency syndrome.

Lung function in sickle cell hemoglobinopathy patients compared with healthy subjects.

Previous studies of lung function tests performed on patients with sickle cell disease have shown a restrictive ventilatory defect, usually a diffusion defect, and mild hypoxia at rest. The present study was undertaken to explain the pathophysiology of these changes and to extend these studies to include functional measurements not reported previously.Lung function studies were performed at rest and during treadmill walking on 66 patients with sickle cell anemia and on 16 healthy control subjects. Patients had restrictive ventilatory defects, decreased lung compliance, and uneven ventilation-perfusion ratios. These abnormalities caused an increased alveolar-arterial oxygen tension difference that caused hypoxemia. The diffusion defects were because of the sickle cell disease.Carboxyhemoglobin levels were increased in patients with sickle cell disease. This increase may be caused by a combination of factors, including increased cigarette smoking, hemolysis, and preferential survival of red blood cells that contain carbon monoxide and which do not sickle. During treadmill walking, the patients with sickle cell disease showed a decreased work tolerance caused by impaired oxygen delivery. The anaerobic threshold is reached sooner in patients with sickle cell disease and may also account for the limitations in work capacity of these patients.

Sarcoidosis of the testis: a case report.

A left testicular mass was found in a 34-year-old black man with a history of multisystem sarcoidosis of 7½ years duration. Microscopic examination of the excised testicle revealed noncaseating granulomas throughout, as well as a few such lesions in the epididymis. This is the seventh reported, microscopically proven case of sarcoidosis of the testis without significant epididymal involvement occurring in a living individual.A review of the other cases of testicular sarcoidosis in the literature reveals that most of them had a number of organs involved with this disease, similar to the subject of this report. Over one half of these patients had skin lesions with or without bone or joint manifestations, suggesting that the testis should be evaluated with particular care when any of these areas are involved. If there is a consistent association of skin, bone, and testicular lesions in this disease, genital sarcoidosis may be more common than presently thought.

A brief review of the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is seen with increasing frequency. It is associated with a variety of conditions even in the absence of preexisting pulmonary diseases. The treatment often includes intubation, using positive-end expiratory pressure (PEEP), and other ancillary support. The mortality rate is high, and physicians caring for such patients should be on guard for disseminated intravascular coagulation, gastrointestinal hemorrhage, and infection.

Respiratory effects of a single, moderately acute, smoke inhalation episode.

Twenty-three hospital employees who suffered ill effects of smoke inhalation were pulmonary-function tested within 72 hours, after ten weeks, and again after 45 weeks of exposure. Four nonexposed control subjects were selected for comparison of data.Exposed persons commonly had restrictive lung disease which may have resulted from stimulation of irritant receptors in bronchi and/or interstitial edema of chemical injury at the level of the ventilation-perfusion unit. Airways obstruction was infrequent, despite the possibility of inhalation of di-isocyanates, an intermediary product of burning polyurethane foam that may cause chemical asthma. Eye and constitutional symptoms were also frequent.Clinical recovery was as a rule rapid and complete (within a week), but physiologic recovery was protracted (over 45 weeks in some cases). Most surprisingly, cigarette smoking and/or presence of cardiopulmonary disease did not contribute to morbidity.

Protease inhibitor profile of black Americans with and without chronic cardiopulmonary disease.

An epidemiologic study of protease inhibitor (alpha(1)-antitrypsin) was undertaken among 599 ambulatory and hospitalized black American patients with chronic cardiopulmonary disease referred for pulmonary function testing, and 115 ethnically matched, healthy control subjects. Clinical evaluation consisted of respiratory questionnaire completion, physical examination, chest radiograph, and spirography. Protease inhibitor evaluation consisted of measurement of serum trypsin inhibitory capacity in all subjects corrected by comparison with control sera, while 200 of these subjects were phenotyped for alpha(1)-antitrypsin electrophoretic variants.Results showed mean serum trypsin inhibitory capacity for all subjects was 1.56, SD ± 0.47 mg/ml, while corrected values were 111.2, SD ± 30.5 percent of control. Acute phase reactivity was present for patients with heart disease, pulmonary malignancy, p<0.01 for both, and pulmonary fibrosis, p<0.05, when compared with controls. Prevalence of protease inhibitor variants in 29 controls was two heterozygotes for the Z variant (seven percent), and one homozygote for the S variant. Among 94 patients with chronic obstructive pulmonary disease, prevalence was 1.1 percent each for ZZ and SZ phenotypes, and 2.1 percent for MZ. Suprprisingly, the sole ZZ patient had asthmatic bronchitis rather than emphysema.Computed allele frequencies for Pi M and Z were comparable to those for a random sample of black Americans in St. Louis, but differed from a sample of black infants in Brooklyn, NY.These results indicate that protease inhibitor deficiency variants are not as uncommon among black Americans as the literature suggests. Furthermore, the heterozygous state is not necessarily a risk factor in development of chronic obstructive pulmonary disease. Protease inhibitor deficiency states therefore appear to play less important a role in etiology of chronic cardiopulmonary disease in black Americans than among their Caucasian counterparts.Preliminary work was published in abstract form.(1)

Homozygous alpha1 antitrypsin deficiency with unusual associations: a case report.

The rare association of protease inhibitor deficiency (Pi(zz) genotype) in a black American with chronic, obstructive pulmonary disease due to asthmatic bronchitis, rather than basal pan lobular emphysema, is presented. The late onset of symptoms, despite environmental exposures, is also unusual in this homozygote, as is his ethnic background.

Familial sarcoidosis with multiple occurrences in eleven families: a possible mechanism of inheritance.

Among 80 Black patients with sarcoidosis, 11 families were identified as containing multiple cases. Monogenic modes of inheritance were reasonably excluded by informal inspection of pedigree patterns and by poor fit of corrected ratios within sibships to the expected ratio for all sibships at risk. The observed familial distribution conforms in several respects to properties that are descriptive of multigenic traits. Additionally, heritability based only on female probands was estimated to be between 60% and 70%. A larger sample size should permit analysis of additional multigenic properties.