RANTES, MIP and interleukin-16 in HIV infection.
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Biomedical subjects
Publications and source records attributed to M Heino.
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Regular use of inhaled beta-agonists with steroids was not harmful in stable asthma. Morning and evening peak expiratory flow (PEF) values were recorded daily for 1 week (week 1) before regular inhalation of beta-agonists and steroids. Then beta-agonists were withdrawn and used as needed for a 2-week washout period. The PEF values of the first week (week 1) were compared with the PEF values before treatment during a further 1-week period (week 4) of as-needed use of beta-agonists. The mean evening PEF values were significantly higher (difference = 9.55 L/min; p = 0.017; 95% confidence interval [CI], 1.80 to 17.30 L/min), and the mean morning PEF values were nearly significantly higher (difference = 6.49 L/min; p = 0.088, 95% CI, -0.99 to 14.00 L/min) during regular beta-agonist use. There were significantly more patients with more symptom days, including nights with awakening, during as-needed treatment (difference in ratio of patients = 40.74%; p = 0.0001; 95% CI, 20.21% to 61.27%). When nocturnal symptoms are considered separately, there were more patients with more nights with awakening during as-needed treatment with a nearly significant difference (difference in ratio of patients = 12.96%; p = 0.0654; 95% CI, 0.92 to 25.00%). PEF monitoring should be used to distinguish the majority of patients with asthma who have higher PEF values during regular treatment from those who do better with administration of beta-agonists as needed. To deny patients with asthma regular use of small doses of beta-agonists in general is to deny individual differences among patients with asthma.
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We have compared the inflammatory changes in the bronchial mucosa and the increase in the airway hyperresponsiveness in an asthmatic patient during the deterioration of symptoms. A striking increase in the number of bronchial epithelial eosinophils was associated with an increase in both airway hyperresponsiveness and asthma symptoms. During 16 wk of treatment with the inhaled corticosteroid, budesonide, the patient's clinical status and airway hyperresponsiveness improved. This was accompanied by an improvement in the ultrastructure of bronchial mucosa and a decrease in the number of epithelial eosinophils.
A series of 41 individuals were restudied after childhood cancer with a median follow-up time of 17 years after chest irradiation or treatment with cyclophosphamide or Adriamycin (doxorubicin). Radiotherapy of the chest had been used in 21 patients, and in 13 of these irradiation was also directed at the heart. Thirty-five patients received cyclophosphamide and five received Adriamycin therapy. All patients were investigated by a pediatric cardiologist. Investigations included an electrocardiogram (ECG), a chest radiographic film, an echocardiogram, an exercise test, and a 24-hour ECG. Altogether 20 patients (49%) showed some abnormality in cardiac tests. Each additional year of follow-up was associated with a 1.3-fold (95% confidence limits, 1.04-1.66; P less than 0.05) increase in the risk for pathologic cardiac findings. The risk for an abnormal cardiac test result in the 13 patients who had received cardiac irradiation was 12.8-fold (95% confidence limits, 1.8-90.8; P less than 0.02) that of the other patients. However, abnormalities in cardiac function were mild.
We studied the ultrastructural findings in biopsies from the main carina of seven school-aged children who had had chronic cough for at least 3 months and who all had a history of early lower respiratory illness (LRI). They had their first LRI between birth and 7 yr of age (range, 5 to 11 yr). The cross-sectional area of the epithelium was quantified by point counting for the percentage area of intercellular spaces (ICS) denoting edema, and the numbers of both inflammatory cells (leukocytes, including eosinophils, and mast cells) and ciliated cells. The children (excluding the one using inhaled steroids) demonstrated nearly 17- and more than sevenfold increases in the mean area of ICS and number of inflammatory cells per epithelial area, respectively, and a nearly three-fold decrease in the mean number of ciliated cells per epithelial area compared with the biopsy specimens from the orifice of the right upper lobe bronchus of two healthy adults. In the children, the increase in inflammatory cells (greater than 91% were lymphocytes) was more prominent in the children with two LRI before the age of 1 yr. Our findings imply a close association of early LRI and later epithelial inflammation during chronic cough. Allergic mechanisms in the epithelial inflammation cannot be ruled out as six of the patients had, either alone or in combination, signs of atopia, positive family history of allergic rhinitis or asthma, and eosinophils or mast cells in the epithelium.(ABSTRACT TRUNCATED AT 250 WORDS)
A group of 40 individuals were restudied at a median follow-up time of 18 years after chest surgery, chest irradiation, or cyclophosphamide treatment. Their median age at diagnosis was 4.5 years. Nineteen subjects were operated on in the chest area. Radiotherapy of the chest had been used in 21 and cyclophosphamide in 35 patients. Chest deformity was evident in 17 subjects. Chest radiographs showed some evidence of fibrosis in eight subjects and late effects of surgery in three subjects. In nine subjects some evidence of fixed obstruction was seen in spirometry. In three subjects pulmonary diffusion capacity was abnormal. Spirometry commonly showed a restrictive pattern of findings. The incidence of abnormalities in pulmonary function was highest among the patients diagnosed before age 3 years. Spirometry was more likely to reveal abnormalities in patients who had received irradiation to the chest. However, abnormalities in pulmonary function were fewer than anticipated.
The effect of steroids on the ciliogenesis of bronchial epithelium has not previously been studied in asthmatics. Bronchial biopsies were taken during bronchoscopy from five asthmatics before and after oral steroid treatment, and studied by transmission electron microscopy. Two untreated healthy subjects served as controls. After treatment, ciliogenesis was abundant in all patients.
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For over a hundred years Finnish sauna has been documented as a physiotherapeutic method in respiratory diseases. Physiological changes of ventilation remain small (about 10%) in the sauna. Heat load, sauna air and sympathetic stimulation generally do not cause problems to the lungs. Electron microscopic studies have not shown irreversible damages to the airway epithelium. Sauna takers should avoid bathing during acute respiratory infections. Sympathomimetic drugs may provoke tachycardia and arrhythmias in the sauna.
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We measured bronchial reactivity to inhaled histamine and prepared electron micrographs from bronchial biopsies from 8 asthmatic patients who never smoked (2 females, 6 males, 18 to 62 yr of age). Judging from their clinical histories and the need for medication and long-term follow-up of PEF values, 2 of them had mild asthma, 3 moderately severe, and 3 severe asthma. They had not experienced respiratory infections for at least 2 months prior to the study. The result, obtained from the cumulative dose-response curve, was expressed as the provocative dose (PD20) of histamine producing a 20% fall in forced expiratory volume in one second (FEV1). In 5 patients, the PD20 varied from 0.049 mg to 2.234 mg. In the sixth patient, only PD15 could be measured (5.187 mg). In 2 patients, the low initial FEV1 values, because of severe, partly irreversible obstruction, prevented the measurement of bronchial reactivity. Bronchial biopsies were taken with rigid tube bronchoscopy from 3 levels: (1) at the carina of the right upper lobe, (2) at the opening of the right middle or lower lobe, and (3) inside the right lower lobe. The specimens were prepared for both light and electron microscopy. Fresh biopsies showed that asthma patients can have epithelial destruction at all levels of the airways. The ciliated cells appeared to be the most destroyed cell type in the epithelium. Intraepithelial nerves and mast cells were seen. Epithelial destruction in the respiratory tract of the asthma patients with mild to severe bronchial hyperresponsiveness was prominent enough to expose the epithelial nerves for specific or nonspecific stimuli.
By electron-microscopy, we have shown that airway epithelial changes occur in farmer's lung, at a level which is even as high as the carina of the right upper lobe. When spores were apparent in the bronchial lumen, ciliated and goblet cells had disappeared, and in some specimens, even basal cell layers. In general, the ciliated cells were those most affected; the cell destruction is that of bronchitis, with the cilia being less affected than the rest of the ciliated cell. Ciliogenesis is stimulated but it does not keep pace with the cell destruction, which advances more rapidly. Disturbed ciliogenesis is suggested. The pathogenesis of epithelial damage is obscure. By reason of epithelial damage, it is suggested that the superficial afferent nerves in the bronchial epithelium are susceptible to irritation; degranulating mast cells in the vicinity of the epithelial nerves may also be involved in the bronchial hyperreactivity observed in some patients. Mast cells were found in the alveoli; these might influence alveolar ventilation. The alveoli presented granulomas characteristic of farmer's lung.
Adult male rats were exposed to pure oxygen at atmospheric pressure for 12 and 24 h. Electron microscopic examination indicated ciliogenesis at every respiratory tract level. For the first time this investigation has established an oxygen insult which affects the epithelium of the entire extra-pulmonary respiratory tract, viz. ciliogenesis. An alteration in muco-ciliary clearance is suggested
An investigation has been made of the effect of acute decompression sickness upon the permeability of the cerebral, iridic, and retinal vessels of the rat, with sodium-fluorescein as intravenous tracer. No permeability changes were observable during the first 15 min subsequent to decompression, following exposure to 5.1 bar for 50 min. Focal leaky areas were found in the brain parenchyma after exposures to 5.1 bar for 120 min. Although sodium-fluorescein partially permeated the pial vessels in controls, the treatment in a hyperbaric chamber seems to increase the diffusion of the tracer from the pia into the cerebral cortex. Nevertheless, both the iridic and retinal vessels remained "tight." The factors which increase the permeability of microvasculature in brain and possible reasons for the negative results obtained with the iris and retina in decompression sickness are discussed.
Paraffin-embedded kidney biopsies sent to our laboratory in 1967 were re-embedded in Epon and studied with electron and light microscopy (1-micrometer thick sections). Of 28 biopsies with enough material 18 were cases with clinical suspicion and symptoms of glomerular disease. In electron microscopy all of these were shown to be of glomerular origin by demonstrating either dark deposits in or at the basement membrane, or amyloid fibrils, or areas with retraction of the foot processes of the epithelial cells. Original light microscopy in 1967 had given proof of glomerular origin in 9 of these 18 cases. Light microscopy of plastic sections of these originally paraffin-embedded biopsies was also helpful in diagnosis and showed deposits in 9 out of 14 cases with ultrastructural deposits. The study shows that considerable benefits can be gained through re-embedding biopsies in plastic, especially in cases with minor alterations.
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