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Biomedical subjects

H Gong

Publications and source records attributed to H Gong.

At least 181 records · Page 10Linked to original sources
PubMed1978

Decision to enter pulmonology: motives and implications.

A study was undertaken to determine at what time American-trained pulmonary disease specialists in two California counties made their subspecialty choices and the factors which influenced their decision. Responses to 281 questionnaires were received and analyzed from 171 fellows, faculty members, and practitioners (60.8 percent). Subspecialty decisions for pulmonology were usually made during residency, motivated by pulmonary rotations and exposure to stimulating faculty members. Although this subspecialty has recently developed into an established, growing field, the survey data confirmed that the amount of pulmonary interaction during medical school remains minimal.

Adult↗
PubMed1977

Fat embolism syndrome: a puzzling phenomenon.

Fat emboli are a life-threatening source of respiratory insufficiency. Whether they are of mechanical or chemical origin remains a subject of controversy. Fat embolism syndrome is most often seen after fracture of long bones, and immobilization of the fracture site may decrease risk of its development. Adequate oxygenation is the most important aspect of therapy; most patients given vigorous supportive treatment recover with no residual lung injury.

Embolism, Fat↗
PubMed1973

Alterations in distribution of blood flow to the lung's diffusion surfaces during exercise.

We measured simultaneously, by single breath methods, pulmonary capillary blood flow (Q(c)), carbon monoxide diffusing capacity (DL(CO)), and isotopic oxygen ((18)O(18)O) diffusing capacity (DL(18) (O2)) in five normal males during conditions of rest and moderate exercise at mixed venous O(2) tensions (PO(2) 33-44 mm Hg). During moderate exercise at a work load of 100 W. pulmonary capillary blood flow increased from 6.9+/-1.5 to 12.9+/-3.4 min(-1) and DL(18) (O2) increased from 25+/-4 to 43+/-3 ml.min(-1).mm Hg(-1), whereas DL(CO) showed no significant change (45+/-5 to 49+/-10 ml.min(-1).mm Hg(-1)). DL(18) (O2) increased proportionally to Q(c) (r = 0.74), where DL(CO) did not (r = 0.08). The greater increase in DL(18) (O2) during exercise can be explained by a more homogeneous diffusion/perfusion (DL(O2)/Q(c)) distribution in the individual respiratory exchange units during exercise. This improved distribution of DL(O2)/Q(c) acts to help prevent an increase in alveolar-arterial O(2) tension difference from developing despite the decrease in pulmonary erythrocyte transit times that occur during exercise. The insignificant rise in DL(CO) with exercise under these hypoxic breathholding conditions may result from pulmonary vasomotor responses to short-term hypoxia or from relative insensitivity of DL(CO) to moderate levels of exercise.

Adult↗
PubMedDate not supplied

Inhaled albuterol does not protect against ozone toxicity in nonasthmatic athletes.

We evaluated the acute prophylactic efficacy of albuterol aerosol in protecting nonasthmatic athletes from the untoward effects of 0.21 ppm ozone (O3) on symptoms, pulmonary function, exercise performance, and post-exposure histamine bronchoprovocation. Fifteen trained competitive cyclists participated in a randomized crossover study consisting of double-blinded inhalations of albuterol (180 micrograms) and placebo approximately 30 min prior to heavy continuous exercise (minute ventilation, [VE] greater than or equal to 80 L/min) for 60 min, followed by a maximal sprint (peak VE greater than 140 L/min) until exhaustion. Each subject was exposed randomly to either 0.21 ppm O3 or filtered air (FA) during the four single-blinded exposure sessions. Albuterol pretreatment resulted in modest but significant bronchodilation as compared to placebo. However, albuterol did not prevent O3-induced respiratory symptoms, decrements in forced vital capacity (FVC), forced expired volume in one second (FEV1.0), and maximum midexpiratory flow rate (FEF25-75%), and positive histamine challenges as compared to that with placebo/O3. There were no statistically significant differences in the metabolic data or ride times across all drugs and exposures, although the peak VE was significantly lower with O3 than FA (142.3 vs. 150.7 L/min, respectively) regardless of drug. The results indicate that acute pretreatment with inhaled albuterol is unable to prevent or ameliorate O3-induced symptoms and alterations in pulmonary function and exercise performance. The contribution of beta-adrenergic mechanisms in the acute airway responses to O3 appears to be minimal.

Adult↗
PubMedDate not supplied

Exposures of health-care workers to ribavirin aerosol: a pharmacokinetic study.

We assessed health risks to nurses and therapists exposed occupationally to ribavirin aerosol, a known rodent teratogen, by measuring uptake as a function of exposure concentration. During a 4-d period, healthy, nonsmoking, young adult volunteers (N = 14) were exposed 4 h/d respirable ribavirin aerosol at concentrations that exceeded occupational levels. Intermittent exercise occurred during exposure, and all activities occurred in a simulated hospital room. Ribavirin was assayed in plasma, red cells, and urine; lung function and symptoms were also measured. In 7 volunteers who were exposed to 30 mg/m3 (i.e., received approximately 10% of therapeutic dose), postexposure ribavirin concentrations in plasma and urine were similar on all 4 d, averaging (0.89 mumol/l and 131 mumol/l, respectively. These concentrations decreased after exposure, with half-times of 37-39 h. Red-cell concentrations averaged 31 mumol/l on d 4, accounting for < 5% of inhaled ribavirin mass, and they remained stable for 4 d afterward. In 7 volunteers exposed to 3 mg/m3 (i.e., approximately 1% of therapeutic dose), plasma averaged 0.075 mumol/l and red cells averaged 3 mumol/l on d 4 (i.e., near detection limits). Small variations occurred in lung function, reported symptoms, and hematologic values for exposures to both 3 and 30 microgram/m3; therefore, these effects were most likely not caused by ribavirin. Typical occupational exposures to ribavirin, without recommended protective measures, should result in undetectable or barely detectable body burdens, i.e., approximately 0.1%-1% of levels reported to be toxic to laboratory animals.

Adolescent↗
PubMedDate not supplied

Chamber exposures of children to mixed ozone, sulfur dioxide, and sulfuric acid.

To help assess acute health effects of summer air pollution in the eastern United States, we simulated ambient "acid summer haze" as closely as was practical in a laboratory chamber. We exposed young volunteers who were thought to be sensitive to this pollutant mixture on the basis of previous epidemiologic evidence. Specifically, we exposed 41 subjects aged 9-12 y to mixed ozone (0.10 ppm), sulfur dioxide (0.10 ppm), and 0.6-microm sulfuric acid aerosol (100 +/- 40 microg/m3, mean +/- standard deviation) for 4 h, during which there was intermittent exercise. Fifteen subjects were healthy, and 26 had allergy or mild asthma. The entire group responded nonsignificantly (p > .05) to pollution exposure (relative to clean air), as determined by spirometry, symptoms, and overall discomfort level during exercise. Subjects with allergy/asthma showed a positive association (p = .01) between symptoms and acid dose; in healthy subjects, that association was negative (p = .08). In these chamber-exposure studies, we noted less of an effect than was reported in previous epidemiologic studies of children exposed to ambient "acid summer haze."

Air Pollutants↗
PubMedDate not supplied

Responses of older men with and without chronic obstructive pulmonary disease to prolonged ozone exposure.

We tested responses to ozone (O3) under simulated "worst-case" ambient exposure conditions. Subjects included 9 men who had severe chronic obstructive pulmonary disease (COPD) with subnormal carbon monoxide diffusing capacity (i.e., an emphysemic component) and 10 age-matched healthy men. Each subject was exposed to 0.24 ppm O3 and to clean air (control) in an environmentally controlled chamber at 24 degrees C and 40% relative humidity. Exposures were randomized, they occurred 1 wk apart, and they lasted 4 h. During each half-hour interval, light exercise occurred (i.e., average ventilation 20 l/min) for 15 min. During both control and O3 exposures, group mean symptom intensity and specific airway resistance (SRaw) increased, whereas forced expiratory performance decreased. The healthy subgroup's mean arterial oxygen saturation (SaO2) rose slightly, and the COPD subgroup's mean SaO2 declined slightly, during exercise. Group mean forced expiratory volume in 1 s (FEV1.0) declined significantly in O3 exposures, compared with controls (p approximately .01). Mean excess FEV1.0 loss after 4 h in O3 (relative to control) was 8% of the preexposure value in the COPD subgroup, compared with 3% in the healthy subgroup (p > .05 [nonsignificant]). Overall FEV1.0 loss during O3 exposures, including exercise effects, averaged 19% in the COPD subgroup, compared with 2% in the healthy subgroup (p < .001). Symptoms, SRaw, and SaO2 responses, as well as healthy subjects' postexposure bronchial reactivity, differed little between O3-exposed and control subjects. We therefore concluded that in older men with or without severe COPD, O3 causes lung dysfunction under "worst-case" ambient exposure conditions, despite older subjects' comparative unresponsiveness to O3. The combined effect of O3 and exercise on lung dysfunction is markedly greater with COPD. It is still unclear whether COPD causes an increased response to O3 per se.

Aged↗
PubMedDate not supplied

Attenuated response to repeated daily ozone exposures in asthmatic subjects.

The development of attenuated response ("tolerance") to daily ozone (O3) exposures in the laboratory is well established in healthy adult volunteers. However, the capability of asthmatics to develop tolerance during multiday ozone exposures is unclear. We exposed 10 adult volunteers with mild asthma to 0.4 ppm O3 in filtered air for 3 h/d on 5 consecutive d. Two similar filtered-air exposures during the preceding week served as controls. Follow-up O3 exposures were performed 4 and 7 d after the most recent consecutive exposure. All exposures were performed in an environmental chamber at 31 degrees C and 35% relative humidity. The subjects performed moderate exercise (mean ventilation rate of 32 l/min) for 15 min of each half-hour. Responses were measured with spirometry and symptom evaluations before and after each exposure, and a bronchial reactivity test (methacholine challenge) was conducted after each exposure. All response measurements showed clinically and statistically significant day-to-day variation. Symptom and forced-expiratory-volume-in-1-s responses were similarly large on the 1st and 2nd O3 exposure days, after which they diminished progressively, approaching filtered air response levels by the 5th consecutive O3 day. This tolerance was partially lost 4 and 7 d later. Bronchial reactivity peaked after the first O3 exposure and remained somewhat elevated after all subsequent O3 exposures, relative to its control level following filtered-air exposures. Individual responses varied widely; more severe initial responses to O3 predicted less rapid attenuation. We concluded that asthmatics can develop tolerance to frequent high-level O3 exposures in much the same manner as normal subjects, although the process may be slower and less fully effective in asthmatics.

Adult↗
PubMedDate not supplied

Relationship between acute ozone responsiveness and chronic loss of lung function in residents of a high-ozone community.

We hypothesized that acute respiratory responsiveness to ozone predicts chronic lung injury from repeated exposure to ozone-containing air pollution. We tested this hypothesis in 164 middle-aged nonsmoking residents of an ozone-polluted community who underwent lung-function measurements during 1986 and 1987 (i.e., time 3). The time-3 study was a follow up of more comprehensive studies conducted in 1977-1978 (time 1) and in 1982-1983 (time 2). In contrast to the apparent rapid (i.e., approximately 60 ml/y) decline in lung-function measurements between times 1 and 2, our subjects showed little change in forced vital capacity (FVC) or forced expired volume in 1 s (FEV1.0) between times 2 and 3, and they experienced a normal decline between times 1 and 3. A subgroup (n = 45) underwent 2-h laboratory ozone exposures to 0.4 ppm ozone, accompanied by intermittent exercise, and they experienced mild acute reductions in FEV1.0 and FVC, but there was little change in bronchial responsiveness to methacholine. Individual acute responses to laboratory ozone were not correlated with individual long-term changes between times 1 and 3. In summary, the results did not support our initial hypothesis, and they did not confirm rapid function decline in nonsmokers chronically exposed to ozone-containing air pollution.

Adult↗
PubMedDate not supplied

Repeat fiberoptic bronchoscopy in patients with recurrent, unexplained hemoptysis.

Repeat fiberoptic bronchoscopy (FB) is indicated in patients with recurrent, unexplained hemoptysis to localize and/or diagnose the source of bleeding. The results of 34 bronchoscopies in 14 patients over a 6-year period were examined. 10 patients had 2 FBs each and 1 patient had 5 procedures at varying intervals. Only early FB detected active bleeding (12/25) early FBs) and localized a bleeding site (10/25). Definitive diagnoses (6/34 FBs) occurred only in patients with lung malignancy and were not necessarily influenced by the timing or frequency of FB. Clinical diagnoses and management were infrequently altered by each FB, except for management of malignancy. Thus, early, repeat FB in this diagnostically difficult group of patients contributes limited immediate information and minimally changes therapy in patients with nonneoplastic conditions. Despite these limitations, direct bronchial visualization by FB remains the most reliable standard available for localizing and, to a lesser extent, diagnosing the etiology of recurrent hemoptysis.

Adult↗
PubMedDate not supplied

Air pollution health risks: do class and race matter?

Air pollution is not spread evenly across demographic groups. Exposures and associated health risks appear to fall disproportionately on populations that are poor and nonwhite. Although scientific evidence documenting disparities in air pollution exposures, doses, and health effects is scant, the available data strongly support the contention that disadvantaged groups, many of whom are ethnic and racial minorities, routinely encounter levels of air pollution that are higher than average. The extent to which exposure differentials contribute to observed differences in health status by class and race is unknown, but worthy of further investigation. We recommend several steps, all of them feasible and most of them relatively inexpensive, to improve our understanding and ability to address environmental health disparities.

Air Pollution↗
PubMedDate not supplied

Comparative short-term health responses to sulfur dioxide exposure and other common stresses in a panel of asthmatics.

We studied 14 unmedicated sulfur dioxide (SO2)-sensitive asthmatics to test the hypothesis that SO2 exacerbates asthma more than other everyday respiratory stressors. In Phase I, subjects underwent controlled exposures to 0.0, 0.5, and 1.0 ppm SO2 with light, medium, and heavy exercise (average ventilation 30, 36, and 43 l/min, respectively). Lung function, symptoms of asthma, and psychophysical (stamina) changes were measured. Function, symptom, and stamina responses correlated modestly. Increasing SO2 had stronger unfavorable effects than increasing exercise. In Phase II, subjects performed eight different physical tasks in SO2-free ambient air while symptoms and stamina were measured. Fast stair-climbing evoked symptoms similar to the effects of 0.5 ppm SO2/light exercise, while stamina reduction was comparable to 0.5 ppm SO2/heavy exercise. In Phase III, subjects recorded time-activity patterns, symptoms, and stamina during randomly selected intervals on a typical weekday and weekend day. Most reported activities were sedentary. Infrequent, strenuous Phase III exercise increased symptoms more than did 0.5 ppm SO2/light exercise, but with less effect on stamina. We conclude that for typical mild asthmatics, ten-minute SO2 exposures at concentrations > 0.5 ppm and ventilation > 30 l/min can cause short-term asthma manifestations more intense than those usually experienced from everyday stresses without SO2 exposure.

Activities of Daily Living↗
PubMedDate not supplied

Ultrastructural study of primary lacrimal adenocarcinoma.

PURPOSE: Primary adenocarcinoma of the lacrimal gland is a rare malignant tumor of the orbit. Up to now, there has been no presentation of its ultrastructural features. The histopathological findings and fine structures of one case of adenocarcinoma of the lacrimal gland are described in the present work. METHODS: The patient was a 59-year-old Japanese man with proptosis that had persisted for one month. A tumor was extirpated, and the tissues were prepared for light and electron microscopic examination. RESULTS: Electron microscopic examination demonstrated that the tumor cells had well-developed microvilli and lumens. These ultrastructure features are similar to those seen in adenocarcinomas at other sites. CONCLUSIONS: These observations suggest that the accurate diagnosis of rare malignant adenocarcinoma depends not only on routine techniques such as light microscopy of hematoxylin-eosin and PAS-diastase stained slides, but also on electron microscopic findings.

Adenocarcinoma↗