Medical practice: HCFA's proposed final rule for Stark II provisions.
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Centers for Medicare and Medicaid Services, U.S.↗
Biomedical subjects
B Pang
Publications and source records attributed to B Pang.
[Histopathological changes of lung and right ventricle induced by high concentration of carbon dioxide in rats].
OBJECTIVE: To evaluate if high concentration of carbon dioxide causes any histopathological changes of the lung and right ventricle in rats. METHODS: Wistar rats were divided into control group (Group A, n = 21) and hypercapnic group (Group B, n = 30). Group B received mixed gas exposure (8% CO(2), 21% O(2), 71% N(2)), 7 hours daily for 4 weeks. Arterial blood gas, superoxide dismutase (SOD), lipid peroxide (LPO) in the tissue of the lung and right ventricle were determined. Histopathological changes of the lung and right ventricle were investigated by light microscope, transmission and scanning electron microscope. RESULTS: Decompensated respiratory acidosis [pH 7.21 +/- 0.04, PaCO(2) (56 +/- 3) mm Hg] developed in Group B. SOD in the lung [(463 +/- 174) U/g protein] and ventricle tissue [(235 +/- 94) U/g protein] in Group B were significantly lower than those in Group A (P < 0.01), while LPOs [(8.1 +/- 3.2) nmol/ml and (17 +/- 5) nmol/ml] in group B were significantly higher than those in Group A (P < 0.01). The index of pulmonary capillary permeability in Group B (37 +/- 4) was also higher than that in Group A (28 +/- 4, P < 0.001). Tissue edema in the lung and heart, endothelial cell damage of the small blood vessels and severe myofibril damage of the right ventricle, pulmonary microthrombus formation and increased pulmonary capillary permeability were found in Group B. CONCLUSION: Hypercapnic rat model is successfully reproduced by exposure of 8% CO(2); high concentration of CO(2) causes severe damage of the lung and right ventricle as well as the whole body.
Animals↗
[Effect of smoking on the guanylin in the injured lung of rats].
In order to survey the influence of smoking on the level of guanylin in lung tissue in rats, a method of passive smoking was used to set up chronic bronchitis model in rats. The content of guanylin was measured by radioimmunoassay. In the smoking group, remarkable pathological changes in the lung tissue were found. There was no significant difference in the contents of guanylin in the plasma of experimental rats, compared with the control(P < 0.05). But in the lung tissue, the difference was significant(P < 0.01).
Animals↗
[A study of influence of zafirlukast to anoxic pulmonary hypertension in rats].
OBJECTIVE: To investigate possible mechanism of the influence of zafirlukast to anoxic pulmonary hypertension in rats. METHODS: Forty wistar rats were divided into four groups in random: (1) control group; (2) anoxic pulmonary hypertension group; (3) zafirlukast preventive group; (4) zafirlukast therapeutic group. Pulmonary arterial pressure was measured, naemo kinitic indexes were recorded. RESULTS: In the anoxic group and control group, the difference of mPAP was remarkable, P < 0.01. When zafirlukast preventive group and the therapeutic group compared with the control group, there was no statistical difference, P > 0.05. When the preventive group and the therapeutic group compared with the hypoxia group, P < 0.01. In the hypoxia group, the content of NO in the plasma, broncho-alveolar lavage solution, and the lung tissue showed remarkable significance compared with that of control group, P < 0.01. The content of NO2-./NO3-. in the preventive group showed remarkable significance compared with hypoxia group, P < 0.05, P < 0.01. The content of NO2-./NO3-. in the therapeutic group showed remarkable significance compared with hypoxia group, P < 0.01. The content of collagen in hypoxia group was remarkable highened compared with that of control group, P < 0.01. The content of collagen in preventive group and therapeutic group showed remarkable significance compared with hypoxia group, P < 0.01, P < 0.05. CONCLUSIONS: The results indicate that zafirlukast can lower anoxic pulmonary hypertension, one of its mechanisms may be related with its depressing the sediment of collagen on lung tissue, adjusting NO level in rats and anti-damaging effect of free radicals.
Animals↗
[The changes of guanylin in plasma and lung tissue from asthmatic guinea pigs].
OBJECTIVE: To study the changes of guanylin in asthmatic guinea pig models. METHODS: Male guinea pigs were randomly divided into two groups: the control (n = 6) and the asthma group (n = 10). The levels of guanylin in plasma, BALF and lung tissue were measured by RIA kit. The mean thickness of airway wall and glands was determined by contour tracing, using a digitizing pad and microcomputer. RESULTS: The levels of guanylin in plasma and lung tissue from the asthma group were 56% and 183% higher than those of the control (P < 0.01). Concentrations of guanylin in BALF from the control were below the detection level in 4 guinea pigs, and 1.7 pg/ml and 1.6 pg/ml in two, respectively. The level of guanylin in BALF from asthma group was (3.1 +/- 1.2) pg/ml. The level of guanylin in the lung tissue correlated with that in plasma and BALF (r = 0.72, P < 0.01, r = 0.61, P < 0.05, respectively). The level of guanylin in plasma did not correlate with those of BALF (r = 0.32, P > 0.05). The mean thickness of airway wall and glands in asthma group were 86% and 87% greater than those of the control respectively (P < 0.01). The level of guanylin in lung tissue correlated with the thickness of glands (r = 0.95, P < 0.01). CONCLUSIONS: In the guinea pig model of asthma, guanylin in plasma, BALF and lung tissue were increased, indicating that it may play a role in the mechanism of airway hypersecretion in asthma.
Animals↗
[Lung injury caused by passive smoking and its effects on cytokines in rats].
OBJECTIVE: A rat model with chronic bronchitis was replicated by passive inhalation of cigarette smoking fume to study its long-term effects on lung injury and nitric oxide (NO), interluekin-6 (IL-6), interleukin-8 (IL-8). METHODS: Levels of nitrogen dioxide (NO(2)) and nitrogen trioxide (NO(3)) were measured with spectrophotometry in rats indicating their level of nitric oxide (NO). Levels of IL-6 and IL-8 were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Levels of NO in serum, bronchial alveolar lavage fluid (BALF) and lung tissue in the smoking group were significantly lower than those in the normal controls (P < 0.01). But, levels of IL-6 and IL-8 were higher in the smoking group than those in the controls. CONCLUSION: Long-term passive smoking could cause injury of lung tissue to certain extent, reduction in secretion of NO in endothelial cells and damage to pulmonary vessels.
Animals↗
The effects of 2-bromopropane on viability and testosterone production ability of rat Leydig cells in primary culture.
Epidemiological surveys and animal experiments have shown that 2-bromopropane induces oligozoospermia in exposed workers and inhibits spermatogensis in laboratory animals. However, the mechanism by which 2-bromopropane exerts its effects is unknown. To this end, we examined the formation of testosterone by the Leydig cells and their survival of these cells in the presence of different concentrations of 2-bromopropane in vitro. Leydig cells were isolated following vascular perfusion, enzymatic dissociation and Percoll gradient centrifugation techniques. The cells were cultured in culture dishes. After 8 h, different cultures were exposed to 2-bromopropane at concentrations of 0.01 mmol/L, 0.10 mmol/L and 1.00 mmol/L. In order to stimulate Leydig cells to secrete testosterone, human chorionic gonadotropin (hCG) was also added. Cell viability was determined using the trypan blue dye exclusion test and cell numbers were counted by hemocytometer. Testosterone secretion was detected by radioimmunoassay. The cell viability decreased after exposure to 2-bromopropane in a dose-dependent way, but no morphological change was observed. The cell number decreased in the 2-bromopropane-treated cultures. The secretion of testosterone did not manifest defectable changes in the culture treated with 0.10 mmol/L and 0.01 mmol/L of 2-bromopropane; however, it decreased significantly (P < 0.02) in the presence of 1.00 mmol/L. Therefore, our results strongly suggest that 2-bromopropane may exert its cytotoxic effects on Leydig cells in vitro. We speculate that the decrease in the numbers of Leydig cells caused by 2-bromopropane was mediated by a feedback mechanism resulting from a lower testosterone concentration.
Animals↗
[Anasarcous mechanism induced by hypercapnia in rats].
OBJECTIVE: To study anasarcous pathogenesis during hypercapnia. METHODS: The mixed gases of highly concentrated carbon dioxide (8% CO2, 21% O2, 71% N2) were given to Wistar rats 7 hours a day for four weeks. The various indexes were comparatively observed between control group and hypercapnia group. RESULTS: Pulmonary arterial pressure (mPAP) in control group was (1.94 +/- 0.28) kPa and PaCO2 (4.6 +/- 0.9) kPa. T1/2 of 125I-BSA in the blood was (238 +/- 30) min, plasma lipid peroxide (LPO) level (3.08 +/- 0.69) nmol/ml, erythrocytic superoxide dismutase (SOD) activity (1,042 +/- 135) CU/g Hb. Water content was (76.2 +/- 1.0)% in lung and (74.1 +/- 2.8)% in muscular tissues. mPAP in hypercapnia group was (2.0 +/- 0.4) kPa, PaCO2 (7.4 +/- 0.4) kPa, T1/2 (150 +/- 23) min, LPO (8.8 +/- 2.0) nmol/ml, SOD (682 +/- 341) U/g Hb1 and water content was (78.8 +/- 1.8)% in lung and (76.04 +/- 1.07)% in muscular tissues. No significant differences were found in mPAP (P > 0.05). There were significant differences in PaCO2 (P < 0.01), T1/2 (P < 0.01), LPO (P < 0.001), SOD (P < 0.01), water content in lung (P < 0.01), and water content in muscular tissues (P < 0.05). CONCLUSIONS: Rat hypercapnic model can be reproduced with 8% CO2 mixed gases. Systemic water and natrium retention (edema) might occur in the model. Microvascular endothelial cell damage and its highly increased permeability induced by lipid peroxidation is the direct cause of edema. The pulmonary cause per se can produce anasarca.
Animals↗
[Nitric oxide in the treatment of COPD-induced chronic cor pulmonale: therapeutic effect and mechanism].
OBJECTIVE: To study the hemodynamic and oxygen-dynamic effects and the mechanism of nitric oxide (NO) inhalation therapy in COPD-induced chronic cor pulmonale at acute exacerbation period. METHOD: Right heart catheterization was performed in 11 cases of chronic cor pulmonale. The hemodynamic parameters and plasma endothelium-I(ET-I) level were examined and recorded before and after inhalation of 40 ppm NO for 20 minutes. The plasma level of NO and lipid peroxide Ca(2+)-Mg(2+)-ATPase(calcium pump) and Na(+)-K(+)-ATPase (natrium pump) activities of RBC membrane in 30 cases of chronic cor pulmonale and 30 healthy controls were determined synchronously. RESULTS: After NO therapy, the average pulmonary pressure (PAPM) and pulmonary vascular resistance index (PVRI) were lowered by 16.6% and 25.9% respectively (P < 0.05). Intrapulmonary shunt was lowered by 16.3% (P < 0.05). ET-I also lowered and showed a positive correlation with PAPM (r = 0.59, P < 0.05). The activities of calcium and natrium pump were lowered when NO level declined, showing a positive correlation with NO concentration and negative correlation with lipid peroxides. CONCLUSION: No inhalation therapy exerted favorable hemodynamic and oxygen-dynamic effects on COPD-induced chronic cor pulmonale in its exacerbation period. Suppression of ET-I release might be one of the important factors for pulmonary vessel relaxation. Dysfunction of calcium and natrium pump activities in the acute exacerbation period of chronic cor pulmonale were closely related to NO level.
Administration, Inhalation↗
[The correlative study on nitric oxide and cotinine nicotine metabolite in smokers' urine].
OBJECTIVE: In order to observe the changes of nitric oxide (NO) affected by smoking and their relationship in vivo. METHOD: 60 male nonsmoker as the control group, 192 male smoked as the study group which was divided into 4 subgroups (1-10, 11-20, 21-30 and > 30) according to the number of cigarettes smoked per day. The metabolite of nicotine-cotinine in urine was assayed by means of barbituric acid. Cotinine was used as an objective indicator to reflect the smoking quantity. The urinary NO (NO2.-) was determined with colorimetric estimation. RESULT: The urinary cotinine level in the 4 subgroups were 6.6 +/- 1.6, 25.1 +/- 6.2, 37.8 +/- 8.5, 53.6 +/- 8.3 (mumol/L) respectively. The urinary NO of nonsmokers were 4.43 +/- 0.97 (mumol/L), in the 4 subgroups it was 3.04 +/- 0.07, 2.75 +/- 0.05, 2.18 +/- 0.01, 1.60 +/- 0.01 (mumol/L) respectively. The results of statistical analysis between the 4 subgroups were t = 4.2894, P < 0.01; t = 2.7446, P < 0.01; t = 2.7667, P < 0.01 accordingly. As compared between the 4 subgroups of smokers and the nonsmokers, the statistical results were t = 2.7118, P < 0.01; t = 3.1826, P < 0.01; t = 3.2100, P < 0.01; t = 4.6600, P < 0.01; respectively. The statistical differences between the 4 subgroups were t = 2.9286, P < 0.01; t = 3.0357, P < 0.01; t = 3.8181, P < 0.01; t = 2.2160, P < 0.05 respectively. There was a good positive correlation between the number of cigarette smoked and urinary cotinine content (r = 0.8626, P < 0.01), also a significant negative correlation between it and urinary NO level (r = -0.6596, P < 0.05). A negative correlation could be observed between urinary cotinine and NO (r = -0.6026, P < 0.05). CONCLUSION: With the increase of quantity and duration of smoking, the NO content in vivo will decrease, suggested that the vascular endothelial cells could be damaged severely.
Adult↗
Toxic streptococcal syndrome.
The reappearance of more virulent strains of exotoxin-producing streptococci over the past decade has led to the re-emergence of invasive Group A streptococcal infections and the recognition of a new syndrome resembling staphylococcal toxic shock syndrome. Toxic streptococcal syndrome is characterized by fever, shock, multiorgan system failure and a desquamating scarlatiniform rash. It usually occurs in otherwise healthy young adults, often in association with a severe soft tissue infection and has a 30% mortality rate. The case of a 37-year-old obese man, who rapidly developed features of this syndrome after an antecedent pharyngitis and cellulitis, is presented. There was serological evidence of a recent Group A streptococcal infection. Intensive organ supportive measures and intravenous antibiotic therapy led to his gradual recovery.
Adolescent↗
Acupuncture combined with application of xiaoke plaster for treatment of 309 cases of diabetes mellitus.
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Acupuncture Therapy↗
Comparison of seroreactivity of rams with brucellosis in a complement fixation test, whole cell ELISA and by immunoblotting.
In rams with ovine brucellosis, a high degree of serological correlation exists between the complement fixation (CF) test which utilises antigen extracted from bacteria with hot saline, and the ELISA reactivity using methanol-fixed Brucella ovis as the assay reagent. Since the whole cell ELISA (CELISA) detects mainly antibodies against surface antigens of B. ovis, it was concluded that the similar findings of the two serological tests is due in part to the presence of membrane antigens in the CF test antigen following hot saline extraction of intact bacteria. Immunoblots with pooled sera representing different CF titres confirmed that the major immunoreactive antigens of B. ovis were located in four zones: alpha, beta, gamma 1 and 2 with corresponding apparent molecular masses of 55 and 60 kDa; 27 and 29 kDa; 18.5-20 kDa and 17-18 kDa, respectively. These zones of reactivity were consistently present in immunoblots when assayed against different B. ovis isolates even though Coomassie brilliant blue staining of SDS-PAGE gels revealed some differences in polypeptide banding patterns. However, these intensely-stained CBB bands located at 38 and 40 kDa which distinguished three of the seven B. ovis isolates were considerably less reactive in immunoblots compared to polypeptides that were located at positions equivalent to alpha, beta or gamma reactivities. Intensity of immunoblot reactivity against polypeptides located in the alpha, beta and gamma zones intensified with increasing CF titre. Sera with CF titres greater than 32 also tended to react against bands of higher apparent molecular masses located at 65, 70, 73, 78, 80 and 86 kDa.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Monoclonal antibodies against ovine IgA purified from lung lavage fluid.
Ovine secretory IgA (sIgA) has been purified to relative homogeneity by ammonium sulphate precipitation (to 40 per cent w/v) of lung lavage fluid from 3- or 12-month-old lambs, followed by molecular sieve chromatography on a Sephacryl S300 matrix. Three peaks A, B and C with molecular sizes corresponding to 550,000, 400,000 and 165,000 respectively were eluted from the column. Immunoelectrophoresis, radial immunodiffusion and enzyme-linked immunosorbent assays (ELISAs) with class specific antiserum confirmed that peak B contained only IgA. Polyacrylamide gel electrophoresis of peak B under reducing conditions resolved three subunits corresponding to secretory component, heavy and light chains. Hybridomas generated by fusing spleen cells from IgA-primed Balb/C mice with murine myeloma (Sp2/0) were screened for IgA-specific monoclonal antibodies against a panel of ovine IgG2, IgG1, IgA and IgM. One particular clone, F3-4B4, identified as murine IgG1, was monospecific against ovine IgA with no cross reactivity against bovine immunoglobulins. This hybridoma was successfully tested as a serological probe by ELISA profiling to locate IgA containing fractions in the course of immunoglobulin purification from biological fluids.
Animals↗