Objective:To investigate the concern about pollen broadcasting in Chinese population from multiple dimensions and to understand the information about allergic rhinitis (AR) in China by analyzing related factors.Methods:From March 1 to September 30, 2022, a large-scale multi-center cross-sectional survey was conducted based on the Questionnaire Star platform in 21 Chinese hospitals. A total of 7 056 subjects from 7 regions in China: Northeast, North, East, Central, South, Southwest, and Northwest China were included. Basic characteristics (including social demographic characteristics and disease characteristics of AR patients), concern about pollen broadcasting, the willingness of pollen-induced AR (PiAR) patients to receive pollen broadcasting, and the treatment satisfaction rate of AR patients were collected. The chi-square test, multivariate linear regression model, and Logistic regression analysis were used to analyze the concern about pollen broadcasting in the Chinese population and related factors from multiple dimensions.Results:Among 7 056 subjects, 23.02% were concerned about pollen broadcasting. Among 3 176 self-reported AR and 1 019 PiAR patients, 25.60% and 39.16% were concerned about pollen broadcasting, respectively, which was higher than that of non-AR or non-PiAR subjects ( χ2 value was 21.74 and 175.11, respectively, both P<0.001). Among AR patients, the proportion of spring and autumn allergen-positive patients concerned about pollen broadcasting was higher than that in perennial allergen-positive patients ( χ2 value was 20.90 and 19.51, respectively, both P<0.001). The proportion of AR patients with asthma, sinusitis, allergic conjunctivitis, and cardiovascular and cerebrovascular diseases was higher than those without complications ( χ2 value was 50.83, 21.97, 56.78, 7.62, respectively, all P<0.05). The proportion of AR patients in North China who could find pollen broadcasting locally was 31.01%, significantly higher than those in other regions (all P<0.05). Multivariate linear regression model analysis showed that among PiAR patients, those with higher per capita household income and higher AR disease cognition levels had been concerned about pollen broadcasting in the past, and those complicated with allergic conjunctivitis had stronger intention to receive pollen broadcasting (B value was 0.24, 0.13, 0.66, 0.47, respectively, all P<0.05). The higher the disease cognition level of PiAR patients, the stronger their willingness to actively participate in treatment ( R2=0.72, P<0.001). Only 18.89% of AR patients felt satisfied with the treatment effect. Logistic regression analysis showed that in AR patients, the treatment satisfaction rate was significantly higher among those concerned about pollen broadcasting compared to those who were not ( OR=1.83, P<0.001). Conclusions:Currently, the dissemination of pollen broadcasting in China is hindered by various factors such as disease cognition level. The treatment satisfaction among AR patients remains unsatisfactory.

Ebola virus (EBOV) is an enveloped negative-sense RNA virus and a member of the filovirus family. Nucleoprotein (NP) expression alone leads to the formation of inclusion bodies (IBs), which are critical for viral RNA synthesis. The matrix protein, VP40, not only plays a critical role in virus assembly/budding, but also can regulate transcription and replication of the viral genome. However, the molecular mechanism by which VP40 regulates viral RNA synthesis and virion assembly/budding is unknown. Here, we show that within IBs the N-terminus of NP recruits VP40 and is required for VLP-containing NP release. Furthermore, we find four point mutations (L692A, P697A, P698A and W699A) within the C-terminal hydrophobic core of NP result in a stronger VP40-NP interaction within IBs, sequestering VP40 within IBs, reducing VP40-VLP egress, abolishing the incorporation of NC-like structures into VP40-VLP, and inhibiting viral RNA synthesis, suggesting that the interaction of N-terminus of NP with VP40 induces a conformational change in the C-terminus of NP. Consequently, the C-terminal hydrophobic core of NP is exposed and binds VP40, thereby inhibiting RNA synthesis and initiating virion assembly/budding.
Ebolavirus/physiology* ; HEK293 Cells ; HeLa Cells ; Humans ; Nucleocapsid Proteins/metabolism* ; RNA, Viral/metabolism* ; Viral Matrix Proteins/metabolism* ; Virion/metabolism* ; Virus Assembly

AIM: To study the protective effect and mechanism of swimming on kidney of diabetic mice. METHODS: The mice were randomly divided into normal control group, normal swimming group, type 2 diabetes mellitus (T2DM) mice model group, diabetic swimming group and metformin group. T2DM model was established by streptozotocin (STZ) method. The mice in normal swimming group and diabetic swimming group were given swimming exercise (1 h a day), and the metformin group were given metformin (200 mg/kg) by gavage once a day for 7 weeks. Fasting blood glucose and serum insulin were measured and insulin resistance index was calculated. The contents of uric acid, urea and creatinine in serum were determined. The ratio of renal mass to body mass was calculated, and the pathological changes of renal tissues were observed. The relative expressions of autophagy related proteins LC3 and P62 in renal tissues were detected by Western blot. RESULTS: Compared with normal control group, insulin resistance index and renal mass/body mass ratio in model group were significantly increased. Serum uric acid, urea and creatinine levels increased, and glomerular pathological changes were obvious. LC3II/LC3I ratio decreased significantly. The expression of P62 was significantly increased. Compared with model group, insulin resistance index and renal mass/body mass ratio in diabetic swimming group were significantly decreased. The contents of serum uric acid, urea and creatinine decreased, and the pathological changes of glomerular were alleviated. LC3II/LC3I ratio increased significantly. The expression of P62 decreased significantly (P even <0.05). CONCLUSION: Swimming protects the kidney injury of T2DM mice, and its mechanism may be related to promoting the autophagy process of renal tissue.

Aim To explore the effect of receptor component protein(RCP)in the signal transduction of vascular smooth muscle cell(VSMC)proliferation induced by static pressure.Methods The mouse-derived vascular smooth muscle cell line(A10VSMC)was employed in the experiment.Cells were exposed to static pressure,and MTT assay was used to detect the cell viability.Western blot was used to determine the expressions of PCNA,RCP and p-Akt,RCP mRNA was tested by RT-PCR,and co-immunoprecipitation was used to test the interaction between RCP and G proteins.Results The cell viability,expressions of PCNA and RCP increased with the elevation of static pressure and reached their peaks at 120 mmHg,and after 6 hours they got a plateau.The static pressure significantly increased the level of p-Akt,meanwhile,the binding of RCP and Gαs significantly decreased.However,the binding of RCP and Gβ increased in response to static pressure after stimuli of static pressure,but Gγ was obscure.Conclusion Static pressure can induce VSMC proliferation and expression of RCP,which may involve G protein signal transduction model.

This study is to investigate the impairment and possible mechanism of endothelium-dependent relaxation of mice mesenteric arteries induced by mmLDL. Wire myography was employed to examine endothelial function of mesenteric arteries. Ultramicrostructure of mesenteric vascular beds were detected by transmission electron microscope. The results showed that endothelium cell edema and peeling, vascular elastic membrane fracture traces in mmLDL group. Endothelium-dependent relaxation was decreased in a time-dependent and dose-dependent manner by using mmLDL, compared with normal arteries. In endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation, the Rmax and pIC50 were decreased from (63 +/- 5) % and 6.42 +/- 0.09 of normal saline control to (31 +/- 3) % and 5.67 +/- 0.07 in mmLDL group (P < 0.001, P < 0.001), respectively. In nitric oxide (NO)-mediated relaxation, the Rmax and pIC50 were decreased from (45 +/- 4) % and 5.93 +/- 0.08 in normal saline control to (32 +/- 4) % and 5.43 +/- 0.11 in mmLDL group (P < 0.05, P < 0.01), respectively. There is no significant alteration of prostacyclin I2 (PGI2) pathway between these two groups. In conclusion, mmLDL induced the impairment of the ultramicrostructure of mesenteric vascular endothelium cell as well as the endothelium-dependent relaxation. The latter includes the dysfunction of NO- and EDHF pathway mediated endothelium-dependent relaxation.

To investigate the effect of losartan on the axis of prolylcarboxypeptidase (PRCP)--kallikrein of the two-kidney, one-clipped (2K1C) hypertensives rats, and explore the novel protection mechanism of losartan on the kidney. Sprague-Dawley (SD) rats were used to develop the 2K1C hypertensive rats. Then, the rats were treated with prazosin (5 mg x kg(-1) x d(-1)) or losartan (5, 15 and 45 mg x kg(-1) x d(-1)) or vehicle, separately. At the same time, the blood pressures were observed. After treated for four weeks, the ratio of right kidney weight and body weight, the change of glomerular morphology, and K+, Na+, creatinine and blood urea nitrogen (BUN) of the serum were used for evaluation of kidney. The expressions of PRCP mRNA in the kidneys were determined by RT-PCR. The protein levels of PRCP, tissue kallikrein, plasma kallikrein, TGF-beta1 in kidney or plasma were measured by Western blotting. Results showed that the changes of body weight and kidney weight ratio, glomerular fibrosis degree and the biochemistrical index of serum induced by hypertension were relieved when the hypertensive rats treated with losartan for four weeks. Meanwhile, treatment of losartan also significantly decreased expression of TGF-beta1 and increased expressions of PRCP, plasma kallikrein and tissue kallikrein. The protective effects of losartan on the kidney of 2K1C hypertensive rats are activation of the axis of PRCP-kallikrein and reducing the expression of TGF-beta1.

Objective To observe the occurrence and risk factors of arrhythmia in chronic kidney disease (CKD) patients in different stages of renal function. Methods A total of 405 CKD patients were enrolled in this study and none of them received renal replacement therapy.The 24 h dynamic electrocardiogram (DCG) was performed,and baseline characteristics were compared.Multivariable Logistic regression analysis was used to examine the relationship between the severe arrhythmia and the potential risk factors,such as age,gender,CKD stage,diabetes,hypertension,hyperpotassaemia,left ventricular hypertrophy (LVH),etc. Results There were 69 patients (17.04％),79 patients (19.51％),82 patients (20.25％),88 patients (21.73 ％) and 87 patients (21.48％) in CKD stage 1,2,3,4 and 5,respectively.As high as 45.68％ of all the patients had severe arrhythmia,represented by 27.54％,29.11％,42.68％,57.95％ and 65.52％ in CKD stages 1-5 respectively.The occurrence of severe arrhythmia increased as the eGFR decreased in CKD stages 2,3,4 (p＜0.05).On multivariable Logistic regression analysis,the occurrence of severe arrhythmia was related to LVH,CKD stage,diaberes hyertension and hyperpotassaemia are signidicantly assoxiated with severe arrhythmia.

BACKGROUND: Research has been reported that serum soluble CD146 (sCD146) expression was improved on the surface of endothelial cells and activated T cells by the stimulation of inflammatory factor. Therefore, it predicts that CD146 may participate in inflammatory reaction of tissue.OBJECTIVE: To investigate the expression and clinical significance of serum sCD146 in peripheral blood from patients with ankylosing spondylitis.METHODS: A total of 62 patients with ankylosing spondylitis were selected from the Sixth People's Hospital AffiUated to Shanghai Jiao Tong University. All patients were divided into two groups: active group (n=46) and inactive group (n=16); while, 20 healthy subjects were selected as the control group. Indicators including Bath Ankylosing SpondyUtis Disease ActivityIndex (BASDAI),Bath Ankylosing Spondylitis Functional Index (BASFI), patient's global assessment (PGA), night pain, visual analogue scale (VAS),morning stiffness time, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were measured in all patients. The serum concentration of sCD146 from 62 patients with ankylosing spondlitis and 20 healthy controls was measured by enzyme-linked immunosorbent assay. Westergren method was used to measure ESR and immunoturbidimetry for CRP. Clinical data of the patients were collected as well.RESULTS AND CONCLUSION: sCD146 levels of patients with ankylosing spondlitis were significantly higher than normal control group (P ＜ 0.05). The sCD146 expression in the active group was significantly higher than inactive and normal control groups (P ＜0.05). Positive correlations were observed between sCD146 and BASDAI index of patients with ankylosing spondlitis (P ＜ 0.05).The sCD146 levels of ankylosing spondUtis patients with peripheral joint involvement were significantly higher than the patients with axial involvement alone or the normal controls (P ＜ 0.05).The expression level of sCD146 in peripheral blood was positively correlated with disease activities of patients with ankylosing spondlitis. It may play important roles in the pathogenesis in ankylosing spondlitis.

Objective To evaluate the clinical application of May-Grunwald-Giemsa staining followed by fluorescence in situ hybridization (MGG-FISH) technique in the differentiation diagnosis of Ph-chromosome positive acute lymphoid leukemia (Ph + ALL) from chronic myeloid leukemia in lymphoid blast crisis(CML-LBC). Methods The bone marrow smears of 4 patients with Ph+ ALL, 4 patients with CML-LBC, 1 patient with CML in myelocytic blast crisis complicated with lymphoma and 1 patient with CML in mixed blast crisis were assayed with the MGG-FISH technique in which the spectrum green labeled BCR and spectrum orange labeled ABL dual color dual fusion probes were used. Based on the morphological classification, the percentages of BCR-ABL positive cells were subsequently determined respectively in the erythroid, myeloid and lymphoid hneages for the 10 specimens. Results According to the MGG-FISH analysis, the erythroid lineage was not involved in the 4 Ph+ ALL specimens without BCR/ABL positive cells. While the BCR/ABL positive percentage of myeloid cells was 11% (1/9), 8% (1/12), 0% (0/8) and 10% (1/10) respectively and that of lymphoid cells was 97% (76/78), 98% (87/89), 98% (97/99) and 97% (75/77) respectively. On the other hand, the BCR/ABL positive percentage was 100% (8/8), 91% (10/11), 82% (9/11), 88% (7/8) in the erythroid lineage, 89% (8/9), 96% (94/98), 100% (47/47), 98% (40/41)in the myeloid lineage and 96% (78/81), 93% (52/56), 96% (68/71), 95% (58/61) in the lymphoid lineage respectively for the 4 CML-LBC specimens. The BCR/ABL positive percentages of the other 2 specimens were all above 80% and through MGG-FISH analysis we also identified the source of the malignant clones and ascertained the diagnosis of the 2 patients. Conclusions The MGG-FISH technique has proved useful in providing rapid and precise differentiation between Ph + ALL and CML-LBC. The source of the malignant clones can also be analyzed by this technique.

AIM: To elucidate the effects of losartan on the expression ofmatrix metalloproteinases-2, JNK1/2 and proliferation in cardiac fibroblast. METHODS: Neonatal rat cardiac fibroblasts were cultured. The cells proliferation was determined by MTT. To determine effects of AngⅡ on JNK1/2 activity, cells were incubated (for 0, 2, 5, 10, 30, 60, 120 min) in serum-freemedia with AngⅡ, and the other group fibroblasts were exposed to serum-free media with or without AngⅡ and losartan (AngⅡ 100 nmol/L, AngⅡ 100 nmol/L+losartan 100 nmol/L, losartan100 nmol/L, losartan for 45 min before). Cells protein was collected with MBST buffer. The relative abundance of MMP-2, JNK1/2 and p-JNK1/2 in cells was determined by immunoblotting. The secretion of MMP-2 in media of cell culture was determined by ELISA. RESULTS: AngⅡ increased the proliferation of CFB in a dose-dependent manner, whereas losartan decreased the proliferation of CFB stimulated by AngⅡ in a dose-dependant manner, too (P＜0.05). The relative abundance of JNK1/2 was highest in AngⅡ of the 2-min-stimulated group. AngⅡincreased expression of JNK1/2 and MMP-2 protein (P＜0.05), on the contrary, losartan inhibited JNK1/2 and MMP-2 protein expression.CONCLUSION: AngⅡ induce the increase of proliferation of CFB, expression of JNK1/2 and MMP-2 in CFB, and losartan inhibits these effects of AngⅡ.