Objective To study the changes of T lymphocyte subsets, immunoglobulin and complements in infants with bronchiolitis and explore the immunopathogenesis of bronchiolitis in in-fants. Methods Sixty-seven infants with bronchiolitis (bronchiolitis group) and forty healthy controls (control group) were enrolled in the study. T lymphocyte subsets were determined by indirected im-munofluorescent assay, and while serum levels of immunoglobulin and complements were determined by timing nephelometry. Results The percentage of CD3+ and CD8+ T cells, the concentrations of se-rum lgA and IgM showed no obvious differences between bronchiolitis group and control group (P>0.05). As compared with those of normal group, the percentage of CD4+ T cells and the ratio of CD4+ to CD8+ were significantly higher (P<0.05 or <0.01) and the levels of serum IgG, C3, C4 were significantly lower in bronchiolitis group(P<0.05 or <0.01). Conclusion Immune function disorder and abnormality occurs in infants with bronchiolitis. T lymphocyte mediated immunity may exert an important antiviral effect. The research from the point of view of cell immunity contributes to evaluation of severity of illness and more effective therapy.

Objective To study the effect of lincomycin hydrochloride on the intestinal mucosal barrier of mice. Methods A total of 24 mice were equally and randomly divided into normal control group and model group. Mice in the model group were administered with 8 mg · kg-1 · d-1 of lincomycin hydrochloride through gastric lavage for 3 days to establish the model of intestinal mucosa injury and alteration of intestinal flora in mice. The intestinal flora was tested,bacterial translocation was analyzed,and mucosa permeability was determined by measuring diamine oxidase( DAO)in plasma. Results Lincomycin hydrochloride led to alteration of intestinal flora in mice after oral administration for three days in mice. The aerobes translocation rate was 16. 7% and 52. 3% in the normal and model groups,respectively(P〈0. 01). The anaerobes translocation rate was 8. 3% and 68. 2% in the normal and model groups,respectively(P〈0. 01). The plasma concentration of diamine oxidase was increased from(2. 08±0. 05)mg·mL-1 in the normal group to(7. 18±0. 10)mg·mL-1 in the model group(P〈0. 01). Conclusion Lincomycin hydrochloride damages intestinal mucosal barrier in mice.

Obgective To investigate the clinical effect of Adenine arabinoside monophosphate (Ara-A) on the treatment of infant cytomegalovirus hepatitis.Methods One hundred cases of infants with cytomegalovirus hepatitis in the Third Affiliated Hospital of Zhengzhou University from January 2012 to October 2013 were included and divided into 2 groups:Am-A group treated with Ara-A [a course of treatment lasting for 2 months included 10 mg/(kg · d) for first 2 weeks followed by 2 weeks' interval,and then resumed],and then control group was given ganciclovir [10 mg/(kg · d) for 14 days and 5 mg/(kg · d) for 1 week after 1 week's interval,for a total treatment period of 1.5 to 2.0 months].Both groups were given conventional therapy.Both before and after treatment,liver function,time of jaundice and transaminase back to normal,quantification of viral DNA returns to negative,side effects,hospitalization time and cost were also compared.Results After 2 weeks,alanine aminotramferase(ALT) in Ara-A group was significantly lower than that of the control group,and there was significant difference (P ＜0.05).After 2 months,ALT,aspartate transaminase in Ara-A group were significantly lower than those in the control group (all P ＜ 0.05).Time of transaminase back to normal [(38.5 ± 16.7) d] was significantly reduced compared with the control group [(44.3 ±22.9) d] (F =3.845,P ＜ 0.05).Time of jaundice back to normal [(27.1 ± 10.5) d],quantification of viral DNA back to negative [(39.5 ±24.0) d],hospitalization time [(22.6 ±5.8) d] and costs [(10 521.9 ±2 662.3) yuan] in Ara-A group had no significant difference compared with those of the control group (F =1.111,2.837,0.840,2.223,all P ＞ 0.05).The negative rate of viral DNA quantification in Ara-A group (80.9％) was higher than that of the control group (62.1％),and the liver injury rate (7.1％) was lower than that of the control group (15.5％),and the difference was statistically significant (x2 =9.137,11.514,all P ＜ 0.05).Condusion Ara-A is safe and effective for infant cytomegalovirus hepatitis and it is suitable for the clinical practice.

Clinical teaching is an important link in cultivating clinician,Heuristic teaching can stimulate students'activeness of learning,enlighten their thoughts,arouse their positivity and creativity,find out their inner potential,and increase teaching effect.Intractable case discussion is an important method of heuristic clinical teaching,which can help strengthening theory knowledge,exercising correct clinical thinking,creating scrupulous scientism and satisfactory medical ethics.

Objective To investigate the expressions of Occludin in brain after bacterial meningitis and to discuss possible molecular mechanism of bacterial meningitis when brain edema occurs. Methods The models of bacterial meningitis and normal control were constructed via inoculating intracisternally with strain Ⅲ streptococcus pneumoniae and the same volume of normal saline solution, respectively. The expression of Occludin in brain was detected by immunohistochemistry and Western blot methods respectively and 24 h, 48 h and 5 days after inoculation. Results (1) Loeffler neurologic deficit score (NDS) in 24 h, 48 h and 5 d decreased significantly when compared with that of control group (P < 0.05). (2) After the brain received streptococcus pneumoniae injection, expression of Occludin began to decrease at 24 h and touch the bottom at 48 h,then increase at the 5th day, but still remained lower than that in control group, which indicated statistical difference (P < 0.05). Conclusions Expression of Occludin in the models of bacterial meningitis decreased firstly and then increased regularly. It suggests that Occludin plays a protective role during the development of infectious brain edema.

Objective To investigate the protective effect of melatonin and its possible mechanism for repairing in the immature white matter damage due to brain hypoxia-ischemia (HI).Methods Forty-eight three-day SD rats after birth were randomly divided into 3 groups:sham-operated(SHAM) group,HI group and melatonin treatment(MT) group.Periventricular white matter damage (PWMD) to animal models were estabished according to Rice modeling.MT group was treated with melatonin pre-operatively,immediately postoperation,1 hour postoperation and 24 hours postoperation via intraperitoneal injection,and the other groups were injected with the same volume of dissolvent.The rats were executed by decollation after 2 days and 14 days.The histological changes in periventricular white matter were observed by HE staining and immunohistochemistry.Results For the 3 groups,the structure in ope-ration side of the white matter in the peripheral ventricles of the brain 2 days postoperation were significant different (P ＜0.05).The O4 positive cells decreased one by one/greatest in the SHAM group[(75.548 ± 7.333)/hpf] followed by MT group [(59.971 ± 3.635)/hpf],and HI group [(40.511 ± 2.848)/hpf] (P ＜ 0.05).The expression of Casepase-3 increased in the SHAM group (107.724 ± 10.266),MT group (132.289 ± 8.537),and HI group (202.168 ± 14.367),and the difference was statically significant (P ＜ 0.05).Ventricular index was greater in operation side of the white matter in the peripheral ventricles of the 14-day-brain in the SHAM group(0.928 ±0.063),MT group (1.813 ± 0.110),HI group (2.752 ± 0.201),increasingly,while absorbance value of myelin basic protein decreased one by one in sequence(39.504 ± 1.673,21.729 ± 1.614,11.344 ± 1.118).Conclusions MT plays a role in protecting the periventricular white matter via inhibiting the apoptosis of oligodendrocyte progenitor cell,and thus benefits the PWMD.

Objective To investigate the expressions of aquaporin 4 (AQP4) in the bacterial meningitis in rats and to explore the molecular mechanism for brain edema caused by bacterial meningitis.Methods Totally 40 of 3-week-old-Sprague-Dawley healthy rats,body weight 60-80 g,male or female,were divided into a normal control group(n =10),and infection groups:24 hours after injection(n =10),48 hours after injection(n =10),and 5 days after injection(n =10).The expressions of AQP4 in the brain were detected by immunohistochemistry and Western blot methods respectively after 24 hours,48 hours,5 days of inoculation.Results Mortality rate:no rats in the control group and the infection group after 24 hours were dead.Two rats in the infection group after 48 hours and 4 rats in the infection group after 5 days were dead because of serious sickness,with the mortality rates 20％ and 40％,respectively.AQP4 expression was slightly positive under light microscope,and the positive cells mainly surrounded glial cells and blood vessels,while neurons were not dyed.Immunohistochemical staining showed that AQP4 expression in the model group increased with the severity of edema;compared with the control group,the AQP4 expression in the brain tissues increased in different periods after rats were infected,and the differences between groups were statistically significant (F--91.84,P ＜ 0.01).Western blot analysis showed that after the brain received streptococcus pneumoniae injection,expression of AQP4 began to increase in 24 hours after streptococcal injection,and reached to the peak in 48 hours,but decreased in 5 days,but the expression still remained higher than that of the normal control group.Each group had statistically significant difference(F =14.23,P ＜ 0.01).Conclusions Expression of AQP4 in the models with bacterial meningitis may increase initially and decrease later.It suggests that AQP4 plays a protective role during the development of infectious brain edema.

Objective To compare the efficacy of adrenocorticotrophic hormone (ACTH) and methylprednisolone on the rat models of infantile spasms (IS).Methods The SD rats on postnatal 10 day (P10) were divided into blank group (n =18),control group (n =18) and model group (n =110) according to the random number table method.The rats of model group were prepared by adopting prenatal stress exposure and N-methyl-D aspartate (NMDA) injection.In the model group,after inducing epileptic seizures,the rats were divided into different groups (18 rats in each group) according to the random number table method as following:model group Ⅰ (subcutaneous injection ofACTH,50 IU/kg,at P10:14:00,21:00;P11,P12:7:00,14:00,21:00;P13:7:00),model group Ⅱ (subcutaneous injection of 9 g/L saline),model group Ⅲ (intraperitoneal injection of methylprednisolone,60 mg/kg,at P11,P12,P13:9:00,once per day),model group Ⅳ (intraperitoneal injection of 9 g/L saline) and model group Ⅴ (positive control group,with no drug or saline injection).Three days later,epilepsy was induced again,and the rats of model group were intraperitoneally injected with NMDA (12 mg/kg) at P13 (10:00).The rats of control group were injected intraperitoneally with same volume of 9 g/L saline,but the rats of blank group were not treated.Behaviors of rats with epilepsy seizures were observed and epilepsy scores were given.The expression of corticotropin-releasing hormone (CRH) in the hypothalamus of each group was detected by using immunohistochemistry and fluorescence quantitative polymerase chain reaction.The learning and memorizing capacity of the rats were measured by Y-maze experiment.Results There was no death in the model group after the onset of seizure.In the model group Ⅰ,13 cases were attacked(72.22％),and 14 cases were attacked in the model group Ⅲ (78.78％).The level of attack was decreased.The buckling state was not observed in model group and Ⅲ,but the latency period of epilepsy was prolonged and the epilepsy scores were significantly decreased.There were no significant differences of onset latency [(2 369.38 ± 628.70) s vs.(1 922.93 ± 462.36) s] and epilepsy score [(2.15 ± 1.14) scores vs.(2.07 ± 0.83) scores] between the 2 groups (all P ＞ 0.005).The rats of model group Ⅱ,Ⅳ,Ⅴ were all attacked completely and presented buckling state.There was no onset or death in blank group and control group.The number of CRH positive cells and CRH mRNA relative expression of each model group were higher than those in the blank group and control group.The number of CRH positive cells and CRH mRNA expression of model group Ⅰ and Ⅲ were lower than those in model group Ⅱ,Ⅳand Ⅴ,and the differences were significant (all P ＜ 0.002 4).There was no significant difference in the number of CRH-positive cells(39.12 ± 5.98 vs.41.48 ± 7.61) and CRH mRNA relative expression (1.92 ± 0.16 vs.2.06 ± 0.39) between model group Ⅰ and Ⅲ (all P ＞ 0.002 4).No significant difference was found between blank group and control group,or among model group Ⅱ,Ⅳ and Ⅴ (all P ＞ 0.002 4).There were no significant differences in the learning capacity among all groups (F =2.196,P ＞ 0.002 4).The correct response rate after 24 hours of the model group was lower than the blank group and control group,and ACTH and methylprednisolone pretreatment did not influence the memorizing capacity (P ＞ 0.002 4).Conclusion The effect of pretreatment of ACTH is similar to that of methylprednisolone in the rat model of IS.

Objective: To investigate the changes and clinical significance of vascular endothelial (VE)-cadherin and procalcitonin (PCT) in serum and cerebrospinal fluid (CSF) of children with viral encephalitis or bacterial meningitis(BM). Methods: A total of 42 cases of children with viral encephalitis(viral encephalitis group), 36 cases of children with BM(BM group), and 20 cases of children with non-nervous system injury(control group) were selected from September 2016 to June 2018 at the Third Hospital of Zhengzhou University.The serum and CSF levels of VE-cadherin and PCT levels of the 3 groups were detected by using enzyme-linked immunosorbent assay. Results: The levels of VE-cadherin in the serum of viral encephalitis group, BM group and control group at the acute phase were (5.60±1.17) mg/L, (7.08±1.01) mg/L and (2.52±0.68) mg/L respectively, and the levels of VE-cadherin in CSF of viral encephalitis group, BM group and control group were (6.00±1.09) mg/L, (6.97±1.11) mg/L and(1.93±0.88) mg/L, respectively.The levels of PCT in the serum of viral encephalitis group, BM group and control group at the acute phase were (0.26±0.11) μg/L, (0.82±0.17) μg/L and (0.27±0.13) μg/L, respectively, and the levels of PCT in the CSF of viral encephalitis group, BM group and control group were (0.25±0.11) μg/L, (0.72±0.14) μg/L, (0.28±0.17) μg/L, respectively.As a result, the levels of VE-cadherin and PCT in the serum and CSF of BM group showed significant increase, compared with viral encephalitis group and control group in the acute phase(F=124.94, 163.21, 151.62, 127.37, all P<0.01). The levels of VE-cadherin in the serum and CSF of viral encephalitis group were also significantly higher than that of control group (all P<0.01), but there was no difference between viral encephalitis group and control group about the levels of PCT in the serum and CSF (all P>0.05). The levels of VE-cadherin in the serum of viral encephalitis group and BM group after treatment were (2.34±0.81) mg/L and (2.67±1.29) mg/L, and were(2.55±0.92) mg/L and(2.39±0.74) mg/L in the CSF.The levels of PCT in the serum of viral encephalitis group and BM group after treatment were (0.25±0.11) μg/L, (0.30±0.17) μg/L, and the levels of PCT in the CSF of viral encephalitis group and BM group were(0.22±0.10) μg/L and (0.27±0.12) μg/L.After effective treatment, the levels of VE-cadherin, PCT in serum and CSF of BM group and viral encephalitis group were almost equal, and the difference was not statistically significant(F=1.83, 0.76, 2.72, 3.89, all P>0.05). In the receiver operating characteristic (ROC) curve, the area under the ROC curve of VE-cadherin in serum and CSF was 0.896 and 0.912, and was 0.670 and 0.668 of PCT respectively. Conclusions VE-cadherin may be involved in the early stage of intracranial infection, and it may be helpful in differentiation of virus or bacterial infection with PCT.VE-cadherin has a good diagnostic value for intracranial infection.

Objective:To summarize the clinical features and PLGL gene variation characteristics of children with CHIME syndrome. Methods:The medical records of one patient who was diagnosed with CHIME syndrome in the Third Affiliated Hospital of Zhengzhou University in October 2018 were analyzed.Foreign and domestic databases were searched with " CHIME syndrome or PIGL gene" as the keywords, so as to review clinical features of CHIME syndrome and PIGL gene variation characteristics. Results:(1) The boy, 1 year old and 3 months, developed seizures at the age of 7 months, when he received rehabilitation due to developmental delay.Physical examination showed that the boy had facial dysmorphisms, including high forehead, ocular hypertelorism, low and flat nasal root, broad nose tip, full lips, overfolded helices, cleft palate, developmental delay, dry skin, erythematous papular rash on the neck, and indirect inguinal hernia. Conductive deafness was revealed by the hearing test and retinal defect was found in fundus examination.Whole exome sequencing test identified PIGL(NM_004278)gene compound hybrid variation.The frameshift variation c. 26delT was present in one allele, combined with a synonymous variation c. 333C>T in the opposite allele.(2) A total of 9 CHIME syndrome patients were retrieved from the databases.No cases were reported in China.All 9 patients had craniofacial dysmorphism, epilepsy, conductive deafness, development delay and retinal defect.Eight patients had ichthyosiform skin, 6 patients had congenital heart disease and 4 patients had renal malformation.There were 6 different kinds of PIGL gene variations in patients, including 7 missense variants, 4 frameshift variants, 3 deletion variants, 2 nonsense variants, 1 splice variant, and 1 synonymous variant. All of the missense variants were c. 500T>C (p.Leu167Pro), which was the most common site. Conclusions:CHIME syndrome is mainly manifested by nervous system and dermal system abnormalities, and often involves multiple systems. PIGL gene variation is the cause of CHIME syndrome, and c. 500T>C (p.Leu167Pro) is the most common site.