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Background Despite the burgeoning literature describing preoperative and postoperative risks of a myasthenic crisis after thymectomy (MCAT) in patients with myasthenia gravis, substantial differences exist in the risk factors identified by previous studies. We conducted a meta-analysis to assess the reported risk factors and MCAT risk. Methods We collected relevant studies on the risk factors for MCAT by searching the PubMed, Embase, The Cochrane Library, China Biology Medicine (CBM), WanFang Data, VIP and CNKI databases. The search period ranged from the establishment of the database to November 2019. Results Twenty-five of the 458 identified studies were eligible for the meta-analysis. Seven retrospective cohort studies and 18 case-control studies were included, and 14 risk factors for MCAT were extracted. Meta-analyses of the association between MCAT and risk factors related to the patient’s preoperative condition included a preoperative history of MC, preoperative bulbar symptoms, IIa + IIb + III + VI, IIb + III + VI, VI + V, dosage of pyridostigmine bromide prior to the operation, a preoperative AchR-Ab level > 100 (nm/L), preoperative pulmonary function, preoperative complications, and preoperative disease course. Meta-analyses of the association between MCAT and surgery-related risk factors included intraoperative blood loss > 1000 mL and the mode of operation. Meta-analyses of the association between MCAT and postoperative risk factors included postoperative lung infection, thymoma and the WHO classification. The operation time was not an independent risk factor for MCAT. Conclusions The independent risk factors for MCAT were a preoperative history of MC, preoperative bulbar symptoms, preoperative MG Osserman stage, preoperative dosage of pyridostigmine bromide, preoperative serum AchR-Ab level, lung function, major postoperative complications, disease duration before thymectomy, blood loss, thoracotomy, postoperative lung infection, thymoma, and WHO classification.

To explore the mechanisms of angiogenesis in chronic myeloid leukemia (CML) through detecting the levels of angiogenesis-related factors secreted from K562 cells after overexpression and interference of HIF-1α gene in K562 cells.The K562 cells were transfected by lentiviruses carried and interfered HIF-1α gene, then the transtected K562 cells with carried and interfered with HIF-1α gene were enrolled in overexpression and interference groups respectively, at the same time the K562 cells transfected by the empty virus were enrolled in control group. The cells were harvested after culture for 72 hours under normoxid condition. The transfection efficient in 3 groups was detected by fluorescence microscopy; the mRNA expression of HIF-1α gene and angiogenesis-related factors was detected by RT-PCR; the concentration of angiogenesis-related factors in the caltured supernatant was detected by ELISA.The optimal MOI of K562 cells transfected with lentivirus was 10 and the transfection efficiency was about 50%. The positive rate of transfection after screening by puromycin was more than 90%. The mRNA expression of ANG-I, ANG-II, TGF-α and VEGF in the interference group was lower than that in the over-expression group, and the TGF-β1 mRNA expression in the interference group was higher than in the over-expression group. The mRNA expression of ANG-I and VEGF in the interference group was lower than that in the control group. TGF-αdid not could be detected, and the culture supernatant concentration of ANG-I and TNF-α in the interference group was lower than in the over-expression group, while the VEGF concentration in the interference group was higher than that in the over-expression group. All of the above-mentioned differences were statistically significant (P＜0.05).The positive K562 cells transfected with leutivirus have been harvested by screening with puromycin. The HIF-1α mRNA positively regulates the mRNA expression of ANG-1, ANG-2, TGF-α, VEGF in K562 cells, promotes the antocrine ability of ANG-1 and TNF-α, moreover not stimulates the autocrine of TGF-α, the up-regulation of HIF-1α expression can inhibit the expression TGF-β1 in K562 cells and the autocrine of TGF-β1.HIF-1α对K562细胞血管生成相关因子的影响.通过在K562细胞过表达和干扰HIF-1α后检测K562细胞分泌血管生成相关因子的水平，探讨慢性白血病血管生成的机制.应用携带和干扰HIF-1α基因的慢病毒转染K562细胞，将转染携带和干扰HIF-1α基因的K562细胞分别纳入过表达组、干扰组，同时以空载病毒转染K562细胞纳入对照组。3组细胞在常氧状态下培养72 h后收集细胞，通过荧光显微镜观察3组转染效率，采用RT-PCR法检测HIF-1α和血管相关生成因子mRNA表达水平，ELISA法检测培养上清中血管相关细胞因子的浓度.慢病毒转染K562细胞最佳转染复数（MOI）为10，转染效率为50%左右；经过嘌呤霉筛选后转染阳性细胞达90%以上。干扰组ANG-I、ANG-II、TGF-α和VEGF mRNA表达均低于过表达组，而干扰组TGF-β1 mRNA表达高于过表达组。干扰组ANG-I、VEGF mRNA表达低于对照组；培养上清中未检测到TGF-α，干扰组ANG-I和TNF-α水平低于过表达组，而干扰组VEGF水平高于过表达组；过表达组和干扰组TGF-β1水平均低于对照组，过表达组VEGF水平低于对照组，干扰组VEGF水平高于过表达组和对照组，上述差异具有统计学意义（P＜0.05）.通过嘌呤霉素筛选获得慢病毒转染K562细胞阳性细胞，HIF-1α mRNA正向调控K562细胞ANG-1、ANG-2、TGF-α、VEGF mRNA的表达，促进ANG-I和TNF-α自身分泌的能力，而不刺激TGF-α的自分泌，HIF-1α上调可抑制K562细胞TGF-β1的表达并抑制TGF-β的自分泌.

To investigate the clinical significance of bone marrow microvessel density(MVD) and angiogenesis related factors in multipic myeloma(MM).Twenty cases of MM and 20 cases of simple fracture were selected and enrolled in MM group and control group respectively. The clinical data and results of laboratorial tests were collected; the bone marrow MVD of patients was detected by using the modified plastic-embedded pathologic sections of bone marrow tissue and histochemistry staining, the expression levels of amgiogenesis-related factors including VEGF, TNF-α, HGF, TGF-α, TGF-β1, bFGF, Ang-Ⅰ, Ang-Ⅱ in bone marrow supernatant were detected by ELISA; the mRNA expression levels of above-mentioned cytokines in bone marrow mononuclear cells were detected by real time-PCR; the pearson correlation analysis was used to analyze the correlation of MVD with VEGF, HGF and bFGF levels.The MVD in MM group was significantly higher than that in control group (P＜0.001); the mRNA expression of VEGF, TGF-α, TGF-β1 and HGF in bone marrow mononuclear cells of MM group was higher than that of control group(P＜0.001); the levels of VEGF, HGF, bFGF and THF-α in bone marrow supernatant of MM group were higher than those in control group(P＜0.05), moreover, the MVD positively correlated with levels of VEGF, HGF and bFGF in bone marrow(r=0.488, 0.472 and 0.457).The MVD and levels vessel-related factors in bone marrow supernatant of MM patients increase, among which the levels of VEGF and HGF in bone marrow supernatant are consistant with those mRNA expression level in bone marrow mononuclear cells, moreover, the MVD possitively cerrelates with levels of VEGF, HGF and bFGF in bone marrow supernatant, suggesting that the changes of bone marrow microenvironment vassel-related factors play an important role in angiogenesis and pathogenesis of multiple myeloma.骨髓微血管密度及血管相关生成因子在多发性骨髓瘤中的意义.探讨骨髓微血管密度及血管相关生成因子在多发性骨髓瘤中的临床意义.选取2014年1月到2017年12月就诊于本院就诊的多发性骨髓瘤（MM）患者和单纯骨折患者各20例并分别纳入MM组和对照组，收集患者入院基本临床资料，通过改良的塑料包埋骨髓活组织病理切片和免疫组织化学染色检测患者骨髓微血管密度（MVD）；ELISA法检测骨髓上清VEGF、TNF-α、HGF、TGF-α、TGF-β1、bFGF、ANG-Ⅰ、ANG-Ⅱ等血管生成相关因子的水平；real-time-PCR检测骨髓单个核细胞的上述因子mRNA表达水平，pearson相关分析MVD与骨髓上清VEGF、HGF、bFGF水平的相关性.MM组MVD明显高于对照组（P＜0.001），MM组骨髓单个核细胞VEGF、TGF-α、TGF-β1、HGF mRNA表达均明显高于对照组（P＜0.001），MM组骨髓上清VEGF、HGF、bFGF和TNF-α水平均高于对照组（P＜0.05），并且MVD与骨髓VEGF、HGF、bFGF水平呈正相关（r=0.488，0.472和0.457）.MM患者MVD和骨髓上清中血管相关因子水平升高，其中VEGF、HGF水平和骨髓单个核细胞mRNA表达水平一致，并且MVD和骨髓上清VEGF、HGF、bFGF水平呈正相关，提示骨髓微环境血管生成因子的变化在多发性骨髓瘤血管生成和疾病发生中起重要的作用.

Background Scrub typhus, caused by Orientia tsutsugamushi, an obligate intracellular gram-negative bacterium, along with hemorrhagic fever with renal syndrome (HFRS), caused by hantaviruses, are natural-focus infectious diseases prevalent in Shandong Province, China. Both diseases have similar clinical manifestations in certain disease stages and similar epidemic seasons, which has caused difficulties for physicians in distinguishing them. The aim of this study was to investigate whether misdiagnosis of scrub typhus as HFRS occurred in patients in Shandong Province. Methods Serum samples (N = 112) of clinically suspected HFRS patients from 2013 to 2014 in Shandong Province were analyzed with enzyme-linked immunosorbent assay (ELISA) for antibodies to both hantavirus and Orientia tsutsugamushi. Results ELISA showed that 56.3% (63/112) and 8.0% (9/112) of clinically suspected HFRS patients were IgM antibody positive to hantavirus and O. tsutsugamushi, respectively. Among the hantavirus IgM antibody positive patients, 7.9% (5/63) were also IgM antibody positive to O. tsutsugamushi. Among the hantavirus IgM antibody negative sera, 8.2% (4/49) of sera were positive to O. tsutsugamushi. Conclusions We concluded that some scrub typhus patients were misdiagnosed as HFRS and co-infection of scrub typhus and HFRS might exist in China. Due to the different treatments for scrub typhus and HFRS, physicians should carefully differentiate between scrub typhus and HFRS and consider administering anti-rickettsia antibiotics if treatment for HFRS alone does not work., Author summary Scrub typhus is caused by O. tsutsugamushi and hemorrhagic fever with renal syndrome (HFRS) is caused by hantavirus. Both diseases have similar manifestations and have their peak epidemic season in the fall, which makes their clinical differentiation difficult to be differentiated from each other clinically. In this study, we found that scrub typhus was indeed misdiagnosed as HFRS and co-infection of O. tsutsugamushi and hantaviruses might exist in China. Owing to different treatments of HFRS and scrub typhus, physicians need pay attention to differentiate them; identify co-infection of HFRS and scrub typhus; and consider administering antibiotics if antiviral treatment alone does not work.

OBJECTIVE: To investigate the age of diagnosis of autism spectrum disorder (ASD) and the factors influencing the age of diagnosis in children. METHODS: A retrospective analysis was performed for the clinical data of 1691 children who visited in the Children's Hospital of Chongqing Medical University for the first time and were definitely diagnosed with ASD between February 2011 and July 2017. A multiple linear regression model was used to identify the factors influencing the age of diagnosis of ASD. RESULTS: The ASD children had a mean age of 35±17 months (range 9-175 months) at diagnosis. Of all 1691 children, the children who received a diagnosis of ASD at the age of 24-35 months accounted for the highest proportion (46.13%, 780/1691), followed by those at the age of ≥ 36 months (33.41%, 565/1 691). The multiple linear regression analysis showed that the children who had language disorders or lived in the main urban area or whose parents had a high education level had a younger age at diagnosis than other children (P < 0.05). CONCLUSIONS: Most ASD children have an age of 24-35 months at diagnosis. The age of diagnosis of ASD is associated with children's symptoms, living area, and parents' education level.

To explore the changes of CD64 on surface of neutrophils in patients with hematological malignancies combined with bacterial infections.Ninety-seven patients with hematological tumor admitted in our hospital from August 2014 to February 2016 were selected and divided into 2 groups: infection group(50 cases) and noninfection group(47 cases) according to their symptoms, physical sings and blood culture results for microbiologic detection. The CD46 index on surface of neutrophils, serum C- reactive protein (CRP), neutrophil count (NC) and procalcitonin (PCT) level were detected by flow cytometry. After treatment of infection patients, the CD46 index, CRP, PCT and NC were detected again.Before antibacterial treatment of patients, the CD64 index in infection group was significantly higher than that in noninfection group, the CRP, PCT and NC levels in infection group also were higher than those in noninfection group; after antibacterial treatment, the CD64 index, CRP, PCT and NC levels in infection group decresed.The CD64 index in hematologic malignancy patients complicated with bacterial infections significantly increased, after antibacterial treatment these indexes decreases, confirming the value of CD64 in the diagnosis of bacterial infections for patients with hematologic malignancies.

To investigate the effects of plasma HMGB1, IFN-γ, IL-4 and CD4Twenty-five patients diagnosed as ITP in our hospital from October 2014 to October 2015, and 20 healthy persons as controls were selected. The ELISA was used to detect the plasma levels of HMGB1, IFN-γ and IL-4 in 2 groups; the flow cytometry was used to detect the expression level of TLR4 on the surface of CD4Before treatment, the plasma HMGB1 level in ITP group was significantly higher than that in control group (t=4.259, P0.01), while after treatment it significantly decreased and close to level in control group (t=1.267, P0.05). The plasma IFN-γ level detected in ITP group before and after treatment was not significantly different from level in control group (P0.05), while the IL-4 level in ITP group before treatment was significantly lower than that in control grup (t=2.107, P0.05), but the IL-4 level in ITP group after treatment was significantly higher than that in control group (t=2.107, P0.05). The plasma IFN-γ/IL-4 ratio in ITP group before treatment was significantly higher than that in control group (t=5.436, P0.01), but it obviously decreased and was slightly lower than that in control group after treatment. The expression level of TLR4 in ITP group before and after treatment was all significantly lower than that in control group (P0.01). The HMGB1 level in ITP group was directly proportional to the CD3The HMGB1 and TLR4 expression levels in ITP patients are higher, and clinical therapy can relieve the disease by targetly control in HMGB1 and TLR4 expression.

Purpose The aim of the study was to investigate the signaling of growth hormone-releasing hormone receptor (GHRH-R) in the pathogenesis of pterygium and determine the apoptotic effect of GHRH-R antagonist on pterygium epithelial cells (PECs). Methods Fourteen samples of primary pterygium of grade T3 with size of corneal invasion ≥ 4 mm were obtained for investigation by histology, immunofluorescence, electron microscopy, explant culture, and flow cytometry. Results We found that PECs were localized in the basal layer of the epithelium in advancing regions of the head of pterygium. These cells harbored clusters of rough endoplasmic reticulum, ribosomes, and mitochondria, which were consistent with their aggressive proliferation. Immunofluorescence studies and Western blots showed that GHRH-R and the downstream growth hormone receptor (GH-R) were intensively expressed in PECs. Their respective ligands, GHRH and GH, were also elevated in the pterygium tissues as compared to conjunctival cells. Explanted PECs were strongly immunoreactive to GHRH-R and exhibited differentiation and proliferation that led to lump formation. Treatment with GHRH-R antagonist MIA-602 induced apoptosis of PECs in a dose-dependent manner, which was accompanied by a downregulation of ERK1 and upregulation of Caspase 3 expression. Conclusions Our results revealed that GHRH-R signaling is involved in survival and proliferation of PECs and suggest a potential therapeutic approach for GHRH-R antagonist in the treatment of pterygium.

Aplastic anemia(AA) is mostly considered as an immune-mediated bone marrow failure syndrome, characterized by pancytopenia and bone marrow hypoplasia. The pathogenesis of AA is complicated, until now it is not fully understood. Further study on the pathological mechanism will be helpful for the diagnosis and treatment of AA. CD8(+) T cells and their secreted cytokines play important roles in the abnormal immunity during the process of AA. Thus, this review focuses on the role of CD8(+) T cells and their secreted cytokines in the pathogenesis of AA.

To study the expression and significance of IL-27 in patients with multiple myeloma (MM) and in the supernatant of MM cell lines U266 and RPMI8226 cells culture medium.A total of 20 MM patients and 20 controls were enrolled in this study. The expressions of IL-27 and IL-6 in MM patient's blood plasma, and the expression of IL-27 in U266 and RPMI8226 culture supernatant were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA expression of IL-27 in mononuclear cells of MM patients' peripheral blood was measured by real-time quantitative polymerase chain reaction (RT-PCR).The levels of IL-27 in plasma of MM patients and normal controls were (61.82 ± 8.01) ng/L and (8.29 ± 4.41) ng/L (P0.05), and those of IL-6 were (45.62 ± 1.24) ng/L and (2.27 ± 0.18) ng/L (P0.05), respectively. The levels of IL-27 in U266 and RPMI8226 culture supernatant were (50.06 ± 5.72) ng/L and (335.47 ± 41.88) ng/L. RT-PCR revealed that the levels of IL-27 mRNA were up-regulated in MM patients compared to controls.High expression of IL-27 is observed in MM patients and MM cell lines U266 and RPMI8226 cells. IL-27 may play a important role in pathogenesis of MM.

To investigate the roles of the chemokine receptor CXCR3 and its ligand I-TAC in the pathogenesis of immune thrombocytopenic purpura (ITP).A total of 48 ITP patients were enrolled in this study: 30 with newly diagnosed or relapse ITP and 18 in remission after treatment, and 24 healthy volunteers were as controls. IFNγ and I-TAC in plasma were detected by ELISA. The mRNA expression of CXCR3 in the peripheral blood mononuclear cells (PBMNCs) was determined by quantitative RT-PCR.The IFNγ level in the plasma of ITP patients before the treatment was obviously increased than those in the remission group and controls [(71.45 ± 17.62) ng/L vs (36.94 ± 14.86) ng/L and (25.28 ± 12.85) ng/L, all P0.05] and those in the remission group was higher than in the controls (P0.05). In contrast, there were no statistic differences of the levels of I-TAC among the three groups [(455.56 ± 144.70) ng/L, (488.24 ± 164.70) ng/L and (382.97 ± 167.43) ng/L, P0.05]. Both ITP patients before the treatment and remission groups expressed more CXCR3 mRNA [6.76 (3.03, 37.00), 1.76 (0.45, 14.18) vs 0.12 (0.04, 0.28), P0.05]. After effective therapy, CXCR3 mRNA expression decreased, while it was still higher than that in the controls.Our data demonstrate that Th1 cytokine (IFNγ) dominance is reflected in ITP. Simultaneously, the CXCR3(+) cell may play a role in cell-mediated immunity through chemotaxis in ITP.

To explore the clinical significance of immunocyte subsets before and after immunosuppressive therapy in the peripheral blood of patients with immune thrombocytopenic purpura (ITP).The percentages of immunocyte subsets in the peripheral blood of 35 patients with ITP and 20 healthy controls were detected by flow cytometry, including CD(3)(+), CD(4)(+), CD(8)(+), CD(+)(56), CD(19)(+) lymphocytes and CD(4)(+)/CD(8)(+).The percentages of CD(3)(+) T lymphocyte (61.58 ± 6.45)%, CD(4)(+) T lymphocyte (28.38 ± 4.89)% and the ratio of CD(4)(+)/CD(8)(+) 0.99 ± 0.22 in patients with ITP were lower than those in healthy controls [(67.85 ± 4.68)%, (38.00 ± 3.37)%, 1.54 ± 0.13, all P0.05]. After immunosuppressive therapy, the percentages of CD(3)(+)T lymphocyte (69.41 ± 5.03)%, CD(4)(+)T lymphocyte (38.17 ± 3.18)% and the ratio of CD(4)(+)/CD(8)(+) 1.60 ± 0.15 recovered to control levels. The percentages of CD(8)(+)T lymphocyte (29.20 ± 4.50)% and CD(19)(+)B lymphocyte (17.74 ± 4.14)% were higher than those in healthy controls [(24.82 ± 2.93)% and (12.09 ± 3.51)%, all P0.05]. After the immunosuppressive therapy, the percentages of CD(8)(+)T lymphocyte (24.06 ± 3.02)% and CD(19)(+)B lymphocyte (10.90 ± 3.55)% recovered to control levels. There were no significant difference of the percentage of CD(56)(+) lymphocyte among ITP patients (15.80 ± 2.85)%, ITP patients after immunosuppressive therapy (15.16 ± 2.77)% and healthy controls (16.36 ± 2.75)%.The aberrant immunocyte subsets are involved in the pathogenesis of ITP, and detection of immunocyte subsets might be helpful for the diagnosis and determination of therapeutic outcome of ITP.