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Objective:To explore the etiology and characteristics of chronic wet cough in children in Qingdao.Methods:Patients with chronic wet cough treated at respiratory clinic of the Women and Children′s Hospital Affiliated to Qingdao University from July 2018 to June 2019 were included in this study.After three-month follow-up, the etiological data was analyzed.Results:(1)A total of 213 children were included, ranging in age from 1 month to 14 years old, including 38 cases of 1 month~1 year old, 47 cases of 1~3 years old, 87 cases of 3~6 years old, and 41 cases of 6~14 years old.The median age was 4.7 years.The top four causes of chronic wet cough in children were upper airway cough syndrome(33.8%), protracted bacterial bronchitis(20.7%), asthma with upper airway cough syndrome(15.5%), and asthma with infection(10.8%). Other causes were postinfection cough, pertussis syndrome, bronchiectasis, gastroesophageal reflux, bronchial foreign body, abnormal airway development, cystic fibrosis and so on.(2)The first cause of chronic wet cough in different age groups: 1 month to 3 years old group was protracted bacterial bronchitis; 3 to 14 years old group was upper airway cough syndrome.(3)The causes of chronic wet cough showed seasonal differences.Upper airway cough syndrome and cough after infection had a more balanced incidence throughout the year; protracted bacterial bronchitis and pertussis syndrome were common in winter; asthma with upper airway cough syndrome and asthma with infection were common in spring and autumn.Conclusion:Upper airway cough syndrome, protracted bacterial bronchitis, asthma with upper airway cough syndrome, and asthma with infection are the 4 leading causes for children with chronic wet cough in Qingdao.The causes of chronic wet cough have age and seasonal differences.
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Objective To observe the effect of methylprednisolone on the expression levels of aquaporin-4 (AQP-4) and S100 protein in brain tissue of hypertensive intracerebral hemorrhage in rats and to investigate the treatment timing and the possible neuroprotective mechanism of methylprednisolone for hypertensive intracerebral hemorrhage. Methods Sixty-four rats were randomly divided into 3 groups:a sham operation group ( n= 8 ), a control group ( n= 8 ), and a methylprednisolone group ( n= 48 ). The methylprednisolone group was redivided into 2, 4, 8, 12, 24, and 48 hsubgroups (n=8 in each subgroup) according to the modeling to the time intervals of methylprednisolone treatment. Methylprednisolone was administered intraperitoneal y (30 mg/kg fol owed by 15 mg/kg every 6 hours for 3 d) at the corresponding time points in the methylprednisolone group, and the equal volume normal saline was administered intraperitoneal y in the control group. Neurological behavior score was conducted at 24 and 72 h after methylprednisolone treatment. The dry-wet weight method was used to measure hemispheric water content. In situ hybridization and immunohistochemical staining were used to detect the expression changes of AQP-4 mRNA and AQP-4 protein respectively. Double staining immunohistochemistry was used to detect AQP-4 and S100 protein. Results Compared with the sham operation group, the expression level of AQP-4 and brain water content in the control group were significantly increased (al P<0. 05). Compared with the control group, the neurological scores, expression levels of AQP-4 mRNA and protein, as wel as the brain water content in early methylprednisolone subgroups (2 h, 4 h and 8 hsubgroups) were significantly decreased (al P<0. 05). Double staining immunohistochemistry showed that expression levels of AQP-4 and S100 protein in early methylprednisolone subgroups (2 h, 4 h and 8 hsubgroups) were significantly decreased than those in the control group (al P<0. 05). Conclusions Early methylprednisolone may downregulate the expression levels of AQP-4 and S100 protein in the brain tissue after hypertensive intracerebral hemorrhage in rats, and thus attenuate brain edema after intracerebral hemorrhage.
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Objective To study the effects of Schwann cell-derived neurotrophic factor(SDNF) on myoblast stem cells(called satellite cells,SCs) in vitro. Methods After setting up SCs culture system in vitro, SCs which treated with various SDNF concentrations culture medium were dynamically evaluated by cell morphology,MTT growth curve and fusion rate. Results The ability of SCs preceding their participation in muscle repair include proliferation and differentiation, 200 ng/ml SDNF stimulated cell proliferation more than the other medium,but 50 ng/ml,100 ng/ml,200 ng/ml,400 ng/ml SDNF made SCs differentiation significantly for their high myotube fusion rate. Conclusion SDNF can regulate the proliferation and differentiation of rat skeletal satellite cellsin vitro,but in differentiation significantly.SDNF might play a role in slowing down denervated muscle atrophy.
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ObjectiveTo investigate the molecular mechanism of prostaglandins E2 ( PGE2 ) in promoting bone formation by detecting the changes of gene expression profiles of MC3T3-E1 osteoblasts treated with PGE2. MethodsThe genes with differential expression in MC3T3-E1 osteoblasts treated with 10 μmol/L PGE2 for 30 minutes were performed by gene chip technology. Several major genes during bone regeneration were selected for Western blot analysis. ResultsAfter co-culture of MC3T3-E1 cells with PGE2 at concentration of 10 μmol/L for 30 min, 276 genes were up-regulated, including bone regeneration related MMD (monocyte to macrophage differentiation associated), NR4A2 (nuclear receptor subfamily 4, group A, member 2), BMP-7 ( bone morphogenetic protein-7), POSTN ( periostin, osteoblast specific factor) and catenin (cadherin-associated protein) genes; and 168 genes were down-regulated,including bone regeneration related Idl ,2,3 ( inhibitor of DNA binding 1,2,3 ) genes. Western blot analysis indicated that the expressions of nuclear factor (NF)-κB p65 and BMP-7 protein in the osteoblasts treated with 10 μmol/l PGE2 were apparently higher ( P ＜ 0. Ol ) than that of the controls, whereas the ld2 expression decreased (P ＜0. O1 ) under the same conditions, which was almost the same as the results of gene chip technology. ConclusionsWith the results of gene chip and Western blot, it can be speculated that the PGE 2 firstly activates the nuclear receptor NR4A2 and then the nuclear transcription factor NF-κB, induces the changes of the downstream gene BMP-7 and Id2 expression and finally results in the differentiation of the osteoblasts and promote the bone regeneration.
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AIM: To explore the histocompatibility of pinealocyte microencapsules in vivo. METHODS: The pineal glands of neonatal rats were removed under operating microscope and pinealocytes were isolated through collagenase and trypsin digestion. Pinealocytes were cultured for one week in vitro and collected immediately after digesting was encapsulated in APA microencapsules. The cells and empty capsules were transplanted into abdominal cavity or intermuscular space respectively and retrieved at the 15th or 30th day after operation. Morphological observation, HE staining, cell counting, and HPLC technique were used to analyze the shape, proliferation and function, the degree of inflammation fibrosis of retrieved microencapsules. RESULTS: The retrieve rate of cell capsule from abdominal cavity was about 85 % . The retrieved capsules had integrated profile mostly although some were damaged. The amount of macrophages attached to capsule wall and the thickness of wall increased gradually following the period of transplantation. However, the retrieve rate, wall thickness had no difference between retrieved cell and empty capsules at the same time. Secretion ability of pinealocytes in capsule retrieved at 15th day after operation decreased rapidly and those retrieved at 30th day after operation lossed secretion function. CONCLUSION: APA microencapsules had histocompatibility relatively in vivo and protected pinealocytes in capsule from immunologic rejection of the host. The survival time was about 20 days. During this period cells in capsule maintained activity and MT secretion ability.