ATP-Binding Cassette Transporters ; genetics ; metabolism ; Animals ; Biological Transport ; Child ; DNA Mutational Analysis ; Humans ; Hypertension, Pulmonary ; genetics ; metabolism ; Lung Diseases, Interstitial ; genetics ; metabolism ; Molecular Sequence Data ; Mutation ; Polymerase Chain Reaction ; Protein Conformation ; Pulmonary Surfactant-Associated Proteins ; genetics ; metabolism ; Respiratory Distress Syndrome, Newborn ; genetics ; metabolism

Objective To investigate the expressions of glial fibrilary acidic protein (GFAP) in the prefrontal cortex, hippocampus and amygdala in post-stroke depression (PSD) in rats. Methods Healthy adult SD rats w ere randomly divided into a normal group, a depression group, a stroke group, and a PSD group ( n=5 in each group). A model of focal cerebral ischemia w as induced by the intraluminal suture method in the stroke group;a rat chronic stress depression model was induced by using chronic unpredicted mild stress (CUMS) combined w ith single housing in the depression group;a model of focal cerebral ischemia w as induced by the intraluminal suture method in the PSD group. A rat PSD model w as induced by CUMS and single housing at 1 week after operation. The sucrose preference test (SPT) was performed in each group at day 1, 8, 15, and 29 after the first CUMS, and the open-field test ( OFT ) w as used to evaluate the depressive behaviors. Immunofluorescence staining was used to detect the expression of GFAP in the prefrontal cortex, and hippocampus and amygdala at day 29. Results At day 29 after CUMS, the sucrose solution consumption in SPT and the scores of horizontaland vertical movement in OFT in the depression group and PSD group w ere decreased significantly compared w ith the normal group and the stroke group (al P<0.05);the numbers of GFAP immunopositive cel s in the prefrontal cortex, hippocampus, and amygdala in the PSD group w ere significantly less than those in the normal group, depression group and stroke group (al P<0.05), and there w ere no significant differences among the normal group, depression group and stroke group (al P>0.05). Conclusion The decreased expression of GFAP in the prefrontal cortex, hippocampus, and amygdale may play a certain role in the process of PSD.

Objective To explore the proliferation of microglia in the frontal cortex,hippocampus and amygdala of the post-stroke depression (PSD) in rats.To understand the role of microglia in the pathogenesis of PSD.Methods The adult female SD rats were divided into four groups(n=5 per group):normal control group,depression group,stroke group and PSD group.In the depression group,the depression model rat were established by chronic unpredictable mild stress (CUMS) combined with separately breeding.In the stroke group,focal cerebral ischemic rat models were established with thread embolization method.In the PSD group,focal cerebral ischemic models rat were established with thread embolization method firstly,and then PSD models rat were established with comprehensive chronic unpredictable mild stress(CUMS) and separately breeding on this basis.After the procedure,rats were subjected to sucrose preference test and open field test.At the postoperative eighth weekend,immunofluorescence technology was used to detect the proliferation changes of OX42 positive cells in the frontal lobe,hippocampus and amygdale.Results At the 29th day after CUMS,the sucrose solution consumption ((23.8±0.8) ％),horizontal movement distance of open field test ((63.0± 1.2) cm) and vertical movement distance ((25.0± 1.0) cm) in PSD group were significantly lower than those in normal group((31.2± 1.9) ％;(69.8±2.3) cm;(31.0± 1.6) cm) and depression group((31.0±1.4) ％;(70.2±2.4) cm;(30.8± 1.1) cm) (P＜0.05).The number of OX42 positive cells of frontal lobe,hippocampus and amygdale in PSD group((20.8±2.6);(20.2±1.3);(19.8±2.6))increased significantly compared with those of normal group((7.4±2.3);(8.0± 1.6);(9.4±2.1)),depression group((8.0±2.0);(7.8 ±2.2);(9.2±1.9))and stroke group((9.6±1.1);(9.4±2.2);(10.2±2.6)) (all P＜0.05).Conclusion The number of microglia in PSD group in the emotional disorders related brain areas(the frontal lobe,hippocampus and amygdale) increases obviously and the increased expression of microglia in the emotional disorders related brain areas may be responsible for the pathogenesis of PSD.

Objective To explore the expression of the CNPase positive oligodendrocytes in the frontal cortex,hippocampus and amygdala of the post-stroke depression (PSD) model rats,and to understand the role of oligodendrocytes in the pathogenesis of PSD.Methods Healthy adult SD rats were randomly divided into normal group,depression group,stroke group,and PSD group (n =5 in each group).In the stroke group,focal cerebral ischemic rat model was made with thread embolization method.In the depression group,the depression model rats were made by chronic unpredictable mild stress(CUMS) combined with separately breeding.In the PSD group,focal cerebral ischemic rat model was made with thread embolization method firstly,and then PSD rat model was established with comprehensive chronic unpredictable mild stress (CUMS) and separately breeding on this basis.After the procedure,rats were subjected to sucrose preference test (SPT) and open field test (OFT).Immunofluorescence staining was used to detect the expression of the CNPase positive oligodendrocytes in the frontal cortex,hippocampus and amygdala at day 29.Results On the 29th day after CUMS,comparing the sucrose solution consumption,horizontal movement distance of open field test and vertical movement distance of the each group,the depression((26.6± 1.1)％,(63.6±2.3)cm,(26.4±1.1)cm) and the PSD groups((23.8±0.8)％,(63.0± 1.2) cm,(25.0± 1.0) cm) were significantlylower than normal ((31.2± 1.9) ％,(69.8± 2.3) cm,(31.0 ± 1.6) cm) and the stroke groups ((31.0± 1.4) ％,(70.2±2.4) cm,(30.8 ± 1.1) cm) (P＜ 0.05).Comparing the expression of the CNPase positive oligodendrocytes in the frontal cortex,hippocampus and amygdala of the each group,the number of the stroke((16.60± 1.82),(14.60±1.82),(15.00±2.12)),depression((16.40±2.07),(14.80±2.17),(15.80±2.28)) and the PSD groups((12.40± 1.52),(11.20± 1.48),(10.80± 1.92)) were significantly less than that in normal group((20.40±3.51),(18.20±2.59),(19.00±2.55)),and the number of expression CNPase positive oligodendrocytes in the PSD group was significantly less than that in stroke and depression groups(all P＜0.05).Conclusion The number of the CNPase positive oligodendrocytes in PSD group in the emotional disorders related brain areas (the frontal lobe,hippocampus and amygdale) reduced obviously,and the oligodendrocytes may play an important role in the pathogenesis of PSD.

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.

Objective To detect the expression of bone morphogenetic protein receptor Ⅱ ( BMPR Ⅱ ) in human focal cortical dysplasia ( FCD Ⅱ b). Methods Fourteen specimens of FCD Ⅱ b surgically removed and pathologically verified were collected from June 2008 to June 2010 and the expression of BMPR Ⅱ in the normal brain tissues and the pathological specimens was detected by means of immunohistochemistry and western blot. Results In the normal brain tissues, BMPR Ⅱ was widely expressed in the cortical neurons of the grey matter, with no positive immunostaining in the white matter. In the cortical lesion of FCD Ⅱ b, BMPR Ⅱ was strongly expressed in the misshapen cells including balloon cells (BCs) , dysmorphic neurons (DNs) and giant neurons (GNs). Positive BMPR Ⅱ expression was also observed in the reactive astroeytes and low level expression of BMPR Ⅱ was found in the normal-appearing (NA) neurons. Western-blot analysis showed that BMPR Ⅱ expression tended to be lowered in the FCD Ⅱ b specimens compared with the normal brain tissues ( P < 0. 05 ). Conclusion The expression of BMPR Ⅱ is altered and reduced in the FCD Ⅱ b, suggesting that BMP signal pathway may participate in the pathogenesis of FCD.

Catheter Ablation ; Child ; Child, Preschool ; Female ; Humans ; Hypertrophy ; Male ; Palatine Tonsil ; pathology ; surgery ; Snoring ; surgery ; Turbinates ; pathology ; surgery

[Summary] Graves'ophthalmopathy ( GO) is the most common extrathyroidal manifestation of Graves disease ( GD) . It is an organ-specific autoimmune disorder. The estimated incidence of GO in the general population is 16 women and 3 men per 100,000 population every year. Approximately 3%-5% of patients with GO are exposed to the potential of losing their sight and requiring optimized medical intervention. For the clinicians it is helpful to assess the degree of activity and severity of GO;both are important in deciding whether a patient requires intervention and which type of intervention is indicated. These interventions include management of hyperthyroidism, measures to relieve local symptoms, immunosuppressive therapies for active moderate and severe GO, and finally rehabilitative surgery for inactive patients.

Objective:To explore the relationship between the type of mutation and clinical features, prognosis, and clinical characteristics of chronic granulomatous disease (CGD) caused by compound heterozygous mutations in the NCF2 gene in children. Methods:The clinical data of 1 case of neonatal CGD caused by compound heterozygous mutations of NCF2 gene at Tianjin Children′s Hospital in August 2019 was analyzed, and domestic and international literatures were searched to summarize the clinical characteristics, gene mutation type and prognosis of CGD caused by NCF2 mutation. Results:The diagnosis of CGD was confirmed by the presence of compound heterozygous mutations c. 196_197insA (p.Arg66Glnfs23X) and c. 1180T>G (p.Tyr394Asp) in the NCF2 gene, accompanied with the clinical manifestations of fever, cough, multiple clumps and nodules in the chest CT at 25 days after birth, and the neutrophil respiratory burst test stimulation index(SI) 23.This new mutation was not reported in the Human Genetic Mutation Database.The child had a residual portion of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and was followed up until the age of 9 months with an antifungal drug without recurrent infection.A total of 101 cases of CGD patients with NCF2 gene mutation were reported in domestic and international databases.Totally, 33 cases had SI results, with 22 cases below 3, 11 cases above 3, and 8 cases of missense mutations. Conclusions:c. 196_197insA and c. 1180T>G are new mutations in NCF2 gene that can lead to CGD.CGD patients containing missense mutations in the NCF2 gene may have more residual NADPH oxidase activity.

Objective To measure the renal tissue texture or flexibility with virtual touch quantization (VTQ) and to tentatively examine its clinical application in patients with chronic kidney disease(CKD).Methods A total of 750 patients (1500 kidneys) were performed with VTQ,including 400 cases in the control group,and 350 cases in the CKD group.A conventional ultrasound examination (two-dimensional,color Doppler) were first taken,and then the shear wave velocity (Vs) was measured which reflected the textural elastic.Results In both groups the Vs was the highest in renal cortex with significant difference (P<0.05); renal cortical region Vs in CKD group was lower than those in control group (P<0.05),while Vs of renal medulla and renal sinus had no significant difference in the two groups.The severity of renal dysfunction was increased along with a Vs decrease of renal cortex.Conclusion VTQ is helpful to assess renal function of patients with CKD.