Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There have been reports of chemical attacks in which sulfur mustard might have been used (a) on Iranian soldiers and civilians during the Gulf War in 1984 and 1985 and (b) in an Iraqi chemical attack on the Iranian-occupied village of Halbja in 1988, resulting in many civilian casualties. Heavy use of chemical warfare in Afghanistan by the Soviet military is a recent innovation in military tactics that has been highly successful and may ensure further use of chemical agents in future military conflicts and terrorist attacks as a profitable adjunct to conventional military arms. Mustard is a poisonous chemical agent that exerts a local action on the eyes, skin, and respiratory tissue, with subsequent systemic action on the nervous, cardiac, and digestive systems in humans and laboratory animals, causing lacrimation, malaise, anorexia, salivation, respiratory distress, vomiting, hyperexcitability, and cardiac distress. Under extreme circumstances, dependent upon the dose and length of exposure to the agent, necrosis of the skin and mucous membranes of the respiratory system, bronchitis, bronchopneumonia, intestinal lesions, hemoconcentration, leucopenia, convulsions with systemic distress, and death occur. Severe mustard poisoning in humans is associated with systemic injury, which is manifested as headache, epigastric distresses, anorexia, diarrhea, and cachexia and is usually observed at mustard doses of 1000 mg/min/m3 with damage to hematopoietic tissues and progressive leucopenia. Sulfur mustard is a cell poison that causes disruption and impairment of a variety of cellular activities that are dependent upon a very specific integral relationship. These cytotoxic effects are manifested in widespread metabolic disturbances whose variable characteristics are observed in enzymatic deficiencies, vesicant action, abnormal mitotic activity and cell division, bone marrow disruption, disturbances in hematopoietic activity, and systemic poisoning. Indeed, mustard gas readily combines with various components of the cell such as amino acids, amines, and proteins. Although evidence of an association between lung cancer and mustard gas encountered on the battlefields of World War I is at best suggestive if not problematical (Case and Lea, 1955; Beebe, 1960; Norman, 1975), the epidemiological data accumulated from the poison gas factories in Japan (Yamada et al., 1953; Wada et al., 1968; Inada et al., 1978; Shigenobu, 1980; Nishimoto et al., 1983; Hirono et al., 1984; Takuoka et al., 1986), in Germany (Weiss, 1958; Hellmann, 1970a; Weiss and Weiss, 1975; Klehr, 1984) and in England (Manning et al., 1981; Easton et al., 1988) are substantial (International Agency for Research on Cancer, 1975). Unfortunately, attempts to seek confirmatory and substantial evidence in laboratory animals such as mice (Boyland and Horning, 1949; Heston, 1950; Heston, 1953a; McNamara et al., 1975) and rats (Griffin et al., 1951; McNamara et al., 1975; Sasser et al., 1996) have not been consistent. Sulfur mustard has been shown to be mutagenic in a variety of different species using many different laboratory techniques from fruit flies, microorganisms and mammalian cell cultures (Fox and Scott, 1980). Evidence is slowly accumulating from human data (Hellmann, 1970a; Lohs, 1975; Wulf et al., 1985). Evidence for the teratogenicity of mustard has been negative in assessment of fetotoxicity and adverse effects of mustard on the reproductive potential of both human and animal studies. Indeed, investigations of women adversely affected by mustard are minimal because most of the studies have been performed on former men employees of poison gas factories and have been negative or questionable. We have recently emphasized the need to assess the affect of a suspected teratogen on maternal toxicity in laboratory animals before any conclusions can be made.(ABSTRACT TRUNCATED)
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PMID:Toxicology and pharmacology of the chemical warfare agent sulfur mustard. 880 7

This study examined the incidence of infectious and neoplastic diseases among 222 HIV-seronegative gay men who participated in the Natural History of AIDS Psychosocial Study. Those who concealed the expression of their homosexual identity experienced a significantly higher incidence of cancer (odds ratio = 3.18) and several infectious diseases (pneumonia, bronchitis, sinusitis, and tuberculosis; odds ratio = 2.91) over a 5-year follow-up period. These effects could not be attributed to differences in age, ethnicity, socioeconomic status, repressive coping style, health-relevant behavioral patterns (e.g., drug use, exercise), anxiety, depression, or reporting biases (e.g., negative affectivity, social desirability). Results are interpreted in the context of previous data linking concealed homosexual identity to other physical health outcomes (e.g., HIV progression and psychosomatic symptomatology) and theories linking psychological inhibition to physical illness.
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PMID:Elevated physical health risk among gay men who conceal their homosexual identity. 881 70

During the last 25 years, several hundred papers have been published on the respiratory health effects of environmental tobacco smoke (ETS). Various independent assessments have concluded that ETS causes lung cancer in adult nonsmokers and increases the risk of various noncancer effects, principally in children. The effects on children include pneumonia, bronchitis and bronchiolitis in young children; chronic middle ear effusion; increased frequency and severity of attacks among asthmatics; possible induction of asthma in previously asymptomatic individuals; small reductions in lung function; and symptoms of upper respiratory tract irritation. In nonsmoking adults, ETS exposure is associated with irritation of the eyes, nose, and throat, and with wheezing, symptoms of bronchitis, shortness of breath, and decreased lung function. The results of recent studies not only confirm and strengthen the above findings but also provide strong suggestive evidence that ETS causes sinonasal cancer and is a risk factor for sudden infant death syndrome. To mitigate such a preventable environmental health impact, public health measures to reduce involuntary ETS exposure are warranted.
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PMID:Respiratory health effects of exposure to environmental tobacco smoke. 900 Mar 1

This cohort study investigated mortality patterns in Danish commercial fishermen between 1970 and 1985, compared to all economically active men. The population census in 1970 in Denmark was the source of information on individual occupation, age and economic status. Computerised linkage with the Danish Mortality Register gave information about deceased persons' date and cause of death. Standarised mortality ratio (SMR) for all causes among crew members was 1.50; 95% confidence intervals (95% CI) 1.34-1.65) highest in the age group 20-34 years (SMR = 2.09, 95% CI 1.68-2.58). The increased SMR among fishermen was primarity due to deaths by accident other than road accidents (SMR = 5.76, 95% CI = 3.09-7.46), ischemic heart disease (SMR = 1.27, 95% CI, 1.01-1.57) and causes without information (SMR = 6.44 95% CI 4.31-9.27). SMR due to bronchitis and emphysema among 35-64 years old crew members was 1.96, 95% CI 1.01-3.45. Among skippers, the SMR for all causes was 1.12, 95% CI 1.03-1.20). The study confirms earlier findings of a high mortality among fishermen, especially due to accidents, and a slightly increased risk of dying from cancer, respiratory and cardiovascular diseases.
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PMID:Mortality in Danish fishermen. 910 Oct 46

Lung cancer is the most common malignant cancer in males and it's incidence is rapidly rising in females. Factors linked to this are associated with cigarette smoking, urbanization along with atmospheric pollution. The lack of success in the treatment of lung cancer has to do with in many cases late diagnosis at the stage when surgical treatment is not possible and radio and chemotherapy being of minimal effectiveness. The WHO has proposed the following classification of lung cancer: 1. Squamous cell carcinoma; 2. Small cell carcinoma; 3. Adenocarcinoma; 4. Giant cell carcinoma; 5. Adeno-squamous cell carcinoma 6. Carcinoid. 7. Carcinoma of mucous gland. 8. Others. Early physical signs of lung cancer are: cough (50-80% of patients), dyspnea (10-15%), chest pain (15-20%), hemoptysis (20-50%), recurrent pneumonia and bronchitis (30-50%). More serious clinical signs associated with growth of the neoplasm are hoarseness, pleural effusion, vena cava superior syndrome, and Pancoast's syndrome. The growing neoplasm secrets many biochemical substances, which are them activity passed on the bloodstream or make their way into the blood as a result of degeneration of the tumor. These substances may then be detected in the patient's plasma and act as markers of malignant disease. The characteristics of these markers is varied, e.g.: hormones, enzymes and tissue antigens. Methods used in the diagnosis of lung-cancer which should be stressed, are apart from the obvious physical examination are chest x-rays, ultrasound, CAT scans, nuclear magnetic resonance, PET scans, and scintigraphy. Fine needle aspiration in changes in the peripheral regions, cytology of sputum, bronchial lavage, cytogenetic analysis. This underlines the need for prophylaxis, particularly the cessation of cigarette smoking.
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PMID:[Current capabilities and procedures for diagnosing lung neoplasms]. 919 23

Data from nationwide registry-based cohorts of patients hospitalized for silicosis in Sweden from 1965 to 1983 and Denmark from 1977 to 1989 were linked to national cancer registries in both countries and to mortality data in Sweden to evaluate the risk of cancer and other disorders among hospitalized silicotic patients. The overall cancer standardized incidence ratio (SIR) was 1.5 (95% confidence interval [CI], 1.3 to 1.7) in Sweden and 1.7 (95% CI, 1.2 to 2.3) in Denmark, primarily because of elevations in primary lung cancer in both Sweden (SIR, 3.1; CI, 2.1 to 4.2) and Denmark (SIR, 2.9; CI, 1.5 to 5.2). For Sweden, the all-causes standardized mortality ratio (SMR) was 2.0 (1.9 to 2.2). The SMR for all malignancies was 1.5 (1.2 to 1.7), primarily because of excesses of lung cancer (SMR, 2.9; CI, 2.1 to 3.9). The significant increase in mortality for all infectious and parasitic conditions (SMR, 11.2) was primarily due to tuberculosis (SMR, 21.8). Significant excesses in mortality from silicosis (SMR, 523), bronchitis (SMR, 2.6) and emphysema (SMR, 6.7) contributed to the elevation in nonmalignant respiratory deaths (SMR, 8.8), whereas excess mortality from musculoskeletal disorders (SMR, 5.9) was due to six deaths from autoimmune diseases. Despite limitations of the available data, our findings are consistent with previous reports indicating that silicotic patients are at elevated risk of lung cancer, nonmalignant respiratory diseases, tuberculosis, and certain autoimmune disorders.
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PMID:Cancer risk and mortality patterns among silicotic men in Sweden and Denmark. 925 24

47 patients were stained by using methylene blue in fiberoptic bronchoscopy. Of these, 35 had central lung cancer, and 12 bronchitis. 40 patients with central lung cancer were detected by general fibreoptic endoscopy. The results demonstrated that normal bronchial mucosa was not stained, 97.14% central malignant bronchial tumors stained, and 8.33% bronchitis stained. X2test showed the marked difference. Positive diagnosis was 97.06% in biopsy specimens stained, it was higher than 77.05% in the general investigated (P < 0.05). Using methylene blue in fiberoptic bronchoscopy would help diagnose central lung cancer, determine tumors limits, permit accurate biopsy. The stain was not related to the pathological classification, differentiation of cancer cells, and classification of clinical pathology (P > 0.05).
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PMID:[Methylene blue staining in fiberoptic bronchoscopy in the diagnosis of bronchial tumors]. 938 72

We prospectively assessed the frequency of pulmonary complications and the natural course of lung function after bone marrow transplantation (BMT), as well as the effect of several risk factors in a homogeneous group of 39 children who underwent allogeneic or autologous BMT for haematological malignancies between 1992 and 1995. Four patients developed pneumonia within the first 3 months and three 3-6 months after BMT. A considerable percentage of acute bronchitis was recorded throughout the follow-up. Three patients died after the 6 month visit because of pneumonia (two patients) and pulmonary aspergillosis (one patient). No patients had obstructive lung disease syndrome. At 3 months after BMT, forced vital capacity (FVC), forced expiratory volume in one second (FEV1) and transfer factor of the lung for carbon monoxide (TL,CO) significantly decreased, but FEV1/FVC ratio and maximal expiratory flow at 25% of FVC remained unchanged, suggesting a restrictive defect with diffusion impairment. At 18 months, there was a progressive recovery in lung function, although only 11 patients had normalized. Seropositivity for cytomegalovirus had a significant effect on lung function whereas graft-versus-host disease also had an effect, although it was not statistically significant. Baseline respiratory function, type of transplant, type of conditioning regimen and respiratory infections did not significantly affect the outcome of BMT. The high frequency of severe lung function abnormalities found in this study, suggests a careful functional monitoring in all subjects undergoing bone marrow transplantation, even in the absence of respiratory symptoms.
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PMID:Pulmonary complications and respiratory function changes after bone marrow transplantation in children. 938 57

We report on two patients, 74 and 73 years old, each of whom had had biopsy of the bronchial mucosa elsewhere. Histologically, normal mucosa and mild bronchitis was seen, respectively. In both patients a second biopsy specimen from the same site was taken, 4 and 7 days after the first biopsy. Now the diagnosis was carcinoma in situ (not excluding early squamous carcinoma) and squamous carcinoma, respectively. One of the patients came to our lung clinic for operation on the basis of the mentioned diagnosis. A third biopsy was performed for control purposes. It revealed just a perforation of a lymph node in the bronchial wall and some epithelioid granulomas without evidence of acid-fast bacilli. There was no evidence of malignancy in this specimen. Because of the discrepancy, the pathologist at the first institution was asked to send us the previous slides. On review of these slides, the described findings were seen, but they were interpreted as regenerative-atypical. In this way, an unnecessary surgical intervention was avoided. After a follow-up of 3 1/2 years the patient is healthy. In the other patient, because of the diagnosis of squamous carcinoma a lobectomy was undertaken by a surgeon elsewhere. The pathologist could not find any carcinoma in the surgical specimen. The biopsy material was reviewed in our department, the findings being interpreted as atypical, originating in reparative changes. Like the postoperative pathologist, we did not find any carcinoma in the surgical specimen. In both cases, therefore, regenerative-atypical changes after re-biopsy were first misinterpreted as a malignant process.
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PMID:[Regeneration of bronchial mucosa after short-term repetition of biopsy versus bronchial carcinoma]. 945 41

Leukemia inhibitory factor (LIF) exhibits multiple biological activities in various tissues, and we have shown that LIF activates POMC gene transcription in response to immune signals. As higher serum levels of LIF have been reported in septicemia, we measured LIF values in biological fluids by RIA. Immunoreactive LIF was detected in 303 of 428 human serum samples. Circulating LIF detection rates were 69% in acute inflammatory diseases, 83% in chronic inflammatory diseases, 61% in noninflammatory diseases, and 90% in cancer patients. Serum concentrations of human LIF was higher in patients with inflammatory disease than in noninflammatory disease (0.80 +/- 0.10 vs. 0.53 +/- 0.02 ng/mL; P < 0.05) or in cancer patients (0.44 +/- 0.06; P < 0.05). Higher serum human LIF levels were found in septicemia (0.78 +/- 0.14 ng/mL), pneumonia (0.80 +/- 0.10 ng/mL), acute bronchitis (0.88 +/- 0.09 ng/mL), other infections (1.01 +/- 0.17 ng/mL), and systemic lupus erythematosus (SLE; 0.79 +/- 0.06 ng/mL). In 7 septicemia patients, Gram-negative infection was associated with higher LIF levels (1.06 +/- 0.16 ng/mL) than was Gram-positive infection (0.58 +/- 0.14 ng/mL). In patients with acute inflammatory disease, serum LIF levels decreased within several days after hospitalization. To test circulating mouse (m) LIF changes in response to inflammatory stress, lipopolysaccharide (LPS) was injected ip to mice. LPS increased serum mLIF values concordantly with ACTH levels. After i.p. injection of 80 microg LPS, serum mLIF increased by 144% (P < 0.05), 173% (P < 0.05), and 134% at 30, 90, and 120 min respectively. In vitro, however, LPS did not increase ACTH and mLIF secretion from dispersed mouse primary pituitary cells. These results suggest that LIF is an important participant in the pathogenesis of the acute inflammatory response. The elevated serum LIF levels observed in inflammation do not appear to originate from the pituitary.
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PMID:Measurement of leukemia inhibitory factor in biological fluids by radioimmunoassay. 954 56


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