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Zai-fang Jiang

Publications and source records attributed to Zai-fang Jiang.

15 recordsLinked to original sources
PubMed2006

[Galectin-7 is associated with bronchial epithelial cell apoptosis in asthmatic children].

OBJECTIVE: It is supposed that bronchial epithelial cells responses to the environmental stimuli are different between asthmatic and non-asthmatic individuals, which contribute to the pathogenesis of asthma. These different responses produce different mediators. If differential gene expressions are found in bronchial epithelial cells of asthmatic and non-asthmatic individuals after the same stimuli in vitro, and these genes are overexpressed in asthmatic children in vivo, then it is concluded that these genes may be associated with asthma. Therefore the authors analyzed the differential gene expressions in the bronchial epithelium cells of asthmatic and non-asthmatic children after RSV infection in vitro. Among these genes, Galectine-7 (lectin, galactoside-binding, soluble, 7, Galectin-7) was 8 times up-regulated in asthmatic children. Galectine-7 was associated with skin keratinocyte apoptosis. The authors hypothesized that Galectin-7 may also be associated with bronchial epithelial cell apoptosis in asthmatic children. The aim of this study was to understand the role of Galectine-7 in bronchial epithelial cell apoptosis in asthma. METHODS: The bronchial mucosae of one asthmatic child and one non-asthmatic child were obtained by biopsy and cultured in vitro. The bronchial epithelial cells were infected by RSV. The differential gene expressions were analyzed with micro array. Among those differentially expressed genes, Galectin-7 was 8 times up-regulated in asthmatic children. The bronchial mucosae from 10 asthmatic children and 17 non-asthma children were investigated for cell DNA break, Galectine-7 and mRNA expression, Caspase-3 expression by TUNEL, hybridization in situ and immunochemistry. Image analysis was used for quantitative assessment. RESULTS: Galectine-7 gene was 8 times up-regulated in bronchial epithelial cells from asthmatic children after RSV infection in vitro. Galectin-7 and mRNA were overexpressed in bronchial epithelial cells in asthma in vivo. Bronchial epithelial cell apoptosis increased in asthma in vivo. CONCLUSION: Galectin-7 may be associated with bronchial epithelial cell apoptosis in asthma.

Adolescent↗
PubMed2005

[Diagnosis and treatment of chronic pulmonary aspergillosis in 4 children].

OBJECTIVE: Chronic pulmonary aspergillosis is different from acute pulmonary aspergillosis in clinical picture, radiogram, diagnostic procedures and prognosis. Four patients with chronic pulmonary aspergillosis had been misdiagnosed as having pneumonia or pulmonary tuberculosis for a long time before admission to the hospital. The purpose of this report was to summarize the clinical manifestations and laboratory findings for correct diagnosis of chronic pulmonary aspergillosis. METHODS: Four patients with chronic pulmonary aspergillosis seen between October 2002 and October 2004 were retrospectively studied. Their clinical manifestations, chest radiographic feature, immune status, diagnostic procedure, therapy and prognosis were reviewed. RESULTS: The chief complaints of these patients were chronic cough and fever for 3 to 12 months. Chest wall abscess developed in the late course in case 1 and 4. Fine moist rales were heard and hepatosplenomegaly was found in case 1 and 2. No abnormal sign was found in case 3 and 4. Chest radiographic feature: lobar consolidation with adjacent pleural thickening was present in all cases. In early phase, solitary or multiple small nodules were found in 2 cases. Case 1-3 had normal IgG, IgM, IgA, IgE, T Cell subsets and NBT test. Case 4 had chronic granulomatous disease. Etiologic evidences: culture was positive for Aspergillus (A.) fulmigatus in sputum and in chest wall abscess in case 1 and 4; for A. niger in sputum and spore existing in lung tissue in case 2; for A. fulmigatus in sputum and hypha existing in lung tissue in case 3. All patients were treated with combination of amphotericin B and itraconazole. Their symptoms were controlled 10-30 d after treatment. In case 1 the disease relapsed 6 months later and the patient died at last due to giving up treatment by his parents. Case 2 was free of symptom for 12 months and his chest radiographic lesion disappeared completely 6 months later. Treatment of case 4 was given up. Case 3 continued to receive treatment and observation. CONCLUSION: Chronic pulmonary aspergillosis should be considered in children with long period fever and cough and lobar consolidation associated with adjacent pleural thickening or with nodular infiltration. The diagnosis of chronic pulmonary aspergillosis depended on identification of aspergillus from sputum or lung tissue. Combined amphotericin B and itraconazole might control the disease.

Amphotericin B↗
PubMed2005

[Demonstration of a mechanism of anti-inflammatory effect of erythromycin on allergic airway inflammation in rat].

OBJECTIVE: To investigate whether erythromycin exerts anti-inflammatory effect on allergic airway inflammation and whether erythromycin modulate allergic airway inflammation by inhibiting nuclear factor kappa B (NF-kappa B) activation. METHODS: Ovalbumin (OVA) together with aluminum hydroxide and Bordetella Pertussis was injected intraperitoneally to immunize SD rats and two weeks later 1% OVA was inhaled to challenge them for consecutive 7 days to mimic allergic airway inflammation. In treatment group, erythromycin was given orally (180 mg/kg.d) during the course of allergen exposure. WBC counts in bronchoalveolar lavage fluid (BALF) and lung specimen analysis were used to describe lung tissue inflammation. The expression of NF-kappa B subunit p65 in cell nucleus of lung tissue was measured by immunohistochemistry and NF-kappa B binding activation in lung tissue by electrophoresis mobility shift assay (EMSA). RESULTS: Lung tissue specimen analysis indicated that the severity of allergic inflammation was reduced in treatment group. The number of total WBC in BALF (x 10(8)/L) (31 +/- 22) was lower than that in model group animals (66 +/- 28), P < 0.01. The number (x 10(3)/mm(2)) of cells with nuclear staining of NF-kappa B per square millimeter of submucosal region around large bronchus (1.4 +/- 0.4) was lower than that in model group animals (2.6 +/- 0.6), P < 0.01. NF-kappa B binding activity (32 +/- 14) was lower than that of model group (46 +/- 17), P < 0.05. CONCLUSION: Erythromycin had an obvious protective role in allergic airway inflammation. Erythromycin inhibited NF-kappa B transcriptional activity to exert anti-inflammatory effect.

Animals↗
PubMed2005

[Effects of budesonide on chronic airway inflammation in guinea pigs sensitized with repeated exposure to allergen].

OBJECTIVE: Inhaled glucocorticosteroids (ICS) remains the first line controller medication for chronic airway inflammation in asthma till now. If the impact of allergen could not be eliminated, how would the improvement of airway inflammation be achieved with inhaled glucocorticosteroids therapy? What was its effect on airway remodeling? In this study, an animal model of asthma was established and the effects of budesonide on airway allergic inflammation and extracellular matrix (ECM) deposition in sensitized guinea pigs with repeated exposure to allergen were investigated. METHODS: Thirty-two male Hartley guinea pigs were randomly divided into four groups with 8 in each group: (A) Group of repeated exposure to ovalbumin (OVA), (B) Group of repeated exposure to OVA plus budesonide (BUD) intervention, (C) Group of stopping repeated exposure to OVA plus stopping BUD intervention, (D) Control group. At 24 h after the last OVA challenge (8 weeks after the first OVA challenge), bronchoalveolar lavage fluid (BALF) was collected from each animal. Total and differential leukocyte counts in BALF was performed on cell suspension smear stained with May-Grünwald-Giemsa (MGG) method. The upper lobe of right lung was removed and regularly fixed, then paraffin embedded lung tissues sections were prepared. The count of eosinophils infiltrated in the airway wall was performed on H&E stained lung tissue sections with LEICA Q500IW computerized image analysis system. Fibronectin and collagen type III (Col-III) deposited in the airway wall were detected by immunohistochemical staining on the paraffin embedded lung tissues sections. The intensity of positive reaction of fibronectin or Col-III deposited in the airway wall was analyzed with LEICA Q500IW computerized image analysis system. RESULTS: The count of eosinophils in BALF (x 10(5)/ml) of group A and B were higher than that of group C and D (35.70 +/- 25.22, 11.49 +/- 5.51 vs. 1.00 +/- 0.90, 1.02 +/- 0.78, P < 0.01), the difference between group A and B, group B and C was significant. The count of eosinophils infiltrated at each level of airway wall in group A and B were higher than that of group C and D (large airway: 6.95 +/- 2.28, 1.54 +/- 1.09 vs. 0.76 +/- 0.45, 0.88 +/- 0.25; medial airway: 9.22 +/- 3.89, 3.99 +/- 2.3 vs. 1.25 +/- 1.20, 0.64 +/- 0.36; small airway: 11.56 +/- 4.02, 2.67 +/- 1.15 vs. 1.32 +/- 0.83, 0.43 +/- 0.24, P < 0.01), the difference between group A and B, group B and C was significant. The gray values of fibronectin deposited in medial and small airway of group A and B were lower than those of group C and D (medial airway 122 +/- 22, 174 +/- 23 vs. 219 +/- 34, 229 +/- 20; small airway 135 +/- 29, 165 +/- 41 vs. 236 +/- 20, 220 +/- 16, P < 0.05), the difference between group A and B, group B and C was significant. The gray values of Col-III deposited in medial and small airway of group A and B were lower than those of group C and D (medial airway 153 +/- 21, 174 +/- 22 vs. 189 +/- 14, 200 +/- 18; small airway 133 +/- 23, 176 +/- 20 vs. 191 +/- 14, 198 +/- 20, P < 0.05), the difference between group A and B was significant. CONCLUSION: Inhaled budesonide could partially inhibit allergic inflammation and ECM deposition in airway wall in guinea pig chronic asthma model with repeated exposure to allergen. Early inhaled budesonide combined with avoidance of OVA exposure could completely inhibit allergic inflammation and ECM deposition. These results suggest that the inhibitory effect on airway allergic inflammation and airway remodeling of inhaled glucocorticosteroids would be limited when the allergen factor could not be avoided.

Administration, Inhalation↗
PubMed2003

[Clinical feature of four cases with bronchiolitis obliterans].

OBJECTIVE: To recognize the clinical features of the bronchiolitis obliterans. METHOD: Clinical manifestation, chest X-ray, computed tomography (CT) and pulmonary function of 4 cases with bronchiolitis obliterans were retrospectively analyzed. RESULT: Two cases were after Stevens-Johnson syndrome (SJS), the other 2 were after severe pneumonia, including one suffered from adenovirus pneumonia. Cough, tachypnea and wheezing persisted in all the 4 patients. The symptoms lasted for at least 6 weeks, in one case for over one year. Crackles and wheezing were present in all the 4 cases. Hyperinflation was seen in chest radiographs in all cases. On pulmonary CT/high-resolution CT (HRCT), patchy opacity and bronchial wall thickening were seen in each patient. Areas of air trapping were seen in three cases. Bronchiectasis was seen in 2 cases, atelectasis and mosaic perfusion were seen respectively in one case. PO(2) was low in all the four cases. Wheezing was not responsive to beta(2) agonist and other bronchodilating therapy. Prednisone was used at a dose of 1 mg/(kg.d) in 3 cases. Two cases were followed up for 3 months. The clinical condition of one case was improved, whose wheezing and bronchiolar constriction disappeared, cough and dyspnea were also relieved. However, the condition of one patient was not improved, although the wheezing disappeared. The HRCT of these two cases showed no improvement. CONCLUSION: Clinical symptoms of BO were cough, tachypnea, and wheezing after acute lung injury. Crackles and wheezing were the most common signs in the BO. Chest radiographs showed hyperinflation. Pulmonary CT showed bronchial wall thickening, bronchiectasis, atelectasis, and mosaic perfusion. Pulmonary function tests suggested obstruction of small airway.

Bronchiolitis Obliterans↗
PubMed2003

[Clinical analysis of pediatric SARS cases in Beijing].

OBJECTIVE: To study clinical characteristics of pediatric SARS cases in Beijing. METHODS: Eighteen pediatric cases with SARS diagnosed on admission were analyzed. The cases were admitted to Beijing Children's Hospital and Ditan Hospital (pediatric ward) from April 8 to May 12. RESULTS: The 18 children aged 5 months to 15 years (10 male and 8 female) had epidemiologically linked findings. Fourteen cases had close contact with SARS patients. Four cases were living in the community where adult SARS patients were found. All the 18 patients but one presented with fever and cough. Most of them had high fever, 2 cases had bradycardia, 2 had diarrhea, and another 2 had tachypnea. Malaise and headache were noted only in 3 cases respectively which were much less frequently seen than in adult patients. Symptoms and signs of the children were much less severe and aggressive than adults cases. Thirteen children had chest radiographic consolidation. Of them, 9 cases had progressive changes after admission, then improved quickly. We did not find significant lower hemoglobin and platelet levels. Most patients had leukopenia and lymphopenia. Serologic test was performed for 15 cases and 8 were positive for SARS virus-IgG and 6 for IgM antibody. Of the 4 cases who had close contact with SARS adults and without chest radiograph abnormal findings, 3 were negative for SARS virus-antibodies. Part of the patients had temporary abnormality of myocardial enzyme and liver function. All these children finally had rapid improvement on chest radiograph. The patients were treated with antiviral agents and corticosteroid. Only two cases required oxygen therapy. No child needed assisted ventilation and no death, nor lung fibrosis occurred. After hospitalization, all patients were improved and discharged when this paper was being written. The average hospital stay of these patients was 14.6 days (6 - 22 days). CONCLUSION: Compared with adults, pediatric SARS patients seemed to have their own clinical characteristics. The disease in children had lower severity and infectivity than that in adults. The mechanisms of the disease in children should be studied in well-designed clinical trials. Cases like the 4 children who had close contact with SARS adult patients but without chest radiographic changes deserve further studies with the help of more reliable and sensitive etiologic tests.

Adolescent↗
PubMed2003

[Causes and diagnostic procedure of diffuse lung disease in 28 children].

OBJECTIVE: Diffuse lung disease comprises a large, heterogeneous group of pulmonary interstitial and parenchymal disease. It is therefore difficult to some extent to make etiologic diagnosis. Little information on clinical spectrum and diagnostic evaluation of pediatric diffuse lung disease is available in our country. The purpose of this study was to explore the causes of and diagnostic approach to diffuse lung disease in children. METHODS: Twenty-eight children with diffuse lung disease aged 2 months to 14 years were studied retrospectively. Their history, physical examination, radiographic findings, final diagnosis and diagnostic processes were reviewed. RESULTS: Confirmed diagnosis was established in 25 cases and suggestive diagnosis in 3 cases. Confirmed diagnoses included: mycoplasma pneumonia in 1 case, Chlamydia trachomatis pneumonia in 2 cases, Epstein-Barr virus pneumonia in 1, CMV pneumonia in 2, hematogenous disseminated pulmonary tuberculosis in 3, pulmonary cryptococcosis in 1, invasive pulmonary aspergillosis in 2, Staphylococcus aureus sepsis in 1, diffuse bronchiectasis in 2, idiopathic pulmonary hemosiderosis in 1, idiopathic pulmonary fibrosis in 1, extrinsic allergic alveolitis in 1, HIV-related lymphocytic interstitial pneumonitis in 1, Wegner's granulomatosis in 1, Langerhan's cell histiocytosis in 2, and lymphoma in 3. Suggestive diagnoses included Nocardia pneumonia in 1, Pneumocystis carinii pneumonia in 1, and juvenile rheumatoid arthritis-associated pulmonary fibrosis in 1. The diagnostic directions of 26 patients were conducted by radiographic features. In 17 of 26 cases, the diagnostic range was confined by history. The diagnosis of 14 cases was made by noninvasive tests including antibody detection, bacterial culture, those of 8 cases by examination of biopsy material, and those of 2 cases by autopsy. CONCLUSIONS: The causes of pediatric diffuse lung disease included pulmonary infectious disease, idiopathic pulmonary disease and pulmonary lesion associated with systemic diseases. The diagnosis may be made by radiography, history, physical examination, noninvasive tests in most cases, while in some cases invasive procedures were necessary.

Adolescent↗
PubMed2003

[Association of HLA-A, B, and DR haplotypes with genotype in Chinese children with systemic lupus erythematosus].

OBJECTIVE: Development of systemic lupus erythematosus (SLE) is not only associated with single loci of HLA gene, but also possibly related to certain haplotypes and genotypes of MHC. In the present study the authors explored association of HLA-A, B, DR haplotype and genotype with SLE in Chinese children, analyzed a large family with multiple SLE patients and genetic origin of SLE patients with HLA-DRB1 * 15, to discover the influence of linkage disequilibrium of HLA gene on SLE. METHODS: HLA-A, B, DR alleles were tested in 53 patients with SLE and 40 cases with their parents, 35 patients with SLE and HLA-DRB * 15 positive and 27 cases with their parents, a large family with SLE (18 members of three generations) and also 78 normal controls and 43 cases with their parents by microlymphocytotoxicity test and polymerase chain reaction - sequence specific primers (PCR-SSP). HLA-A, B, DR haplotype and genotype of SLE patients and controls were statistically calculated. The SLE patients with HLA-DRB1 * 15 and controls were analyzed for either the gene originated from the paternal or the maternal side. RESULTS: The variety of the haplotype in patient group (64/80) was less than that in control group (74/86). Only 9 haplotypes were found common between the patient group and control group. The frequency of the haplotype HLA-A9B40DRB1 * 15 was significantly higher in patient group than that in control group (P < 0.05), RR was 10.726 0. Five members of the large family had haplotype A9B40DRB1 * 15, 2 of them were patients with SLE, 1 of them was positive for ANA and had Raynaud's phenomenon and 2 of them were normal. The rest of the family members were normal. The frequency of genotypes DRB1 * 09/DRB1 * 15 and DRB1 * 03/DRB1 * 15 in SLE group was significantly higher than that of control group (P < 0.05), RR was 7.772 7 and 14.272 7, respectively. The number of SLE children with gene HLA-DRB1 * 15 derived from their fathers was significantly higher than that of the children with the gene derived from the mothers. CONCLUSION: These findings suggested that haplotype HLA-A9B40DRB1 * 15 and genotypes HLA-DRB1 * 09/DRB1 * 15, HLA-DRB1 * 03/DRB1 * 15 were correlated with SLE. The predisposition of multiple loci seems to have an additive effect. The children with their gene HLA-DRB1 * 15 derived from their fathers might more easily suffer from SLE than those with the gene derived from their mothers, the underlying mechanism needs further studies.

Adolescent↗