Objective:To investigate the clinical characteristics and outcome of novel coronavirus pneumonia (COVID-19)patients with different body mass index (BMI), and to provide the basis for disease assessment and prognosis.Methods:The clinical data of 541 patients with COVID-19 diagnosed in Xiaogan Hospital Affiliated to Wuhan University of Science and Technology from January 16 to March 28, 2020 were collected. The patients were divided into normal weight group, overweight group, and obesity group according to BMI. The clinical characteristics and outcomes of the three groups were compared. The correlation between BMI and clinical classification was analyzed by ordinal logistic regression.Results:There were 288 cases (53.23%) in normal weight group, 193 cases (35.67%) in overweight group, and 60 cases (11.09%) in obesity group. Compared with normal weight group, overweight and obesity groups displayed higher proportion of hypertension, with increased levels of white blood cells, neutrophils, C reactive protein, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and triglyceride in laboratory test results, and higher proportion of severe and critical illness ( P<0.05 or P<0.01). After adjusting for age, gender, and underlying diseases, regression analysis showed that higher BMI predicted more severe clinical classification ( OR=1.079, 95% CI 1.010-1.154). Conclusion:In COVID-19 patients, overweight and obese patients are more likely to develop into severe and critical illness, suggesting that obesity may be an important risk factor affecting the clinical outcome of COVID-19.

The monocot mannose-binding lectin can inhibit HIV from infecting the target cells. The total RNA of Zephyranthes grandiflora was extracted and reversely transcribed into cDNA. Degenerate primers were designed based on the conserved regions of other monocot mannose-binding agglutinins by homology alignment. The 694bp full-length cDNA of Zephyranthes grandiflora agglutinin (ZGA) was cloned by RT-PCR, 3' and 5' RACE (rapid amplification of cDNA ends). The start codon and stop codon of ZGA were at 37-39bp and 529-531bp respectively. The NCBI Blast analysis result showed that ZGA gene encoded a protein precursor with signal peptide, mature protein and C-terminal cleavage sequence. The mature ZGA protein contained 106 amino acids residues and its molecular weight was 11.6KD. The percentages of identity of the deduced mature ZGA protein with those of Galanthus nivalis agglutinin, Narcissus hybrid cultivar agglutinin, Lycoris radiate agglutinin and Clivia miniata agglutinin were 71.8%, 81%, 81.8% and 84.5%, respectively. Blocks analysis revealed that ZGA had three functional domains and three mannose-binding boxes (QDNY).
Agglutinins ; genetics ; Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; Liliaceae ; genetics ; Mannose-Binding Lectin ; genetics ; Molecular Sequence Data ; Sequence Analysis, DNA

Objective:To compare the efficacy of sakubatril valsartan and valsartan in the treatment of patients with chronic cardiac insufficiency and the influence on zinc finger protein A20 and nuclear factor-κB (NF-κB) in peripheral bloodmononuclear cells (PBMCs).Methods:Ninety-senven patients with chronic cardiac insufficiency admitted to the Affiliated Hospital of Jining Medical College from February 2019 to January 2020 were continuously selected and randomly divided into the control group (48 cases) and the observation group (49 cases). Both groups received routine anti-heart failure according to the guidelines. The control group added with valsartan and the observation group added with sakubatril valsartan treatment. Before the treatment and after 3 months of treatment, the changes of cardiac function indexes and the changes of inflammatory markers such as hypersensitive C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), matrix metalloproteinase 9 (MMP-9), and N-terminal pro B-type natriuretic peptide (NT-proBNP) were compared. PBMCs was extracted to detect zinc finger protein A20 and NF-κB levels. The incidence of adverse reactions in the two groups was recorded, and the relationship between zinc finger proteins A20, NF-κB and the myocardial injury marker NT-proBNP were analyzed.Results:After 3 months of treatment, the changes of cardiac function indexes in the observation group were better than those in the control group and the levels of hs-CRP, TNF-α, MMP-9, NT-proBNP in the observation group were lower than those in the control group: (1.96 ± 0.57) mg/L vs. (2.87 ± 0.79) mg/L, (7.11 ± 1.46) μg/L vs. (8.24 ± 1.57) μg/L, (110.14 ± 10.63) μg/L vs. (129.52 ± 17.96) μg/L, (716.91 ± 105.78) ng/L vs. (965.25 ± 97.41) ng/L, there were statistical differences ( P<0.05). After 3 months of treatment, the levels of finger protein A20, NF-κB in the observation group were lower than those in the control group: (3.57 ± 1.13) % vs. (4.41 ± 1.32) %, (29.87 ± 6.58) ng/L vs. (35.71 ± 10.02) ng/L, there were statistical differences ( P<0.05). Finger protein A20 and NF-κB in patients with chronic cardiac insufficiency were positively correlated with NT-proBNP ( r = 0.487, 0.738, P<0.01). Conclusions:On the basis of conventional treatment, compared with valsartan, the addition of sakubatril valsartan, can improve the cardiac function of patients with chronic cardiac insufficiency, reduce the body′s inflammatory response, reduce the expression of myocardial injury marker NT-proBNP, inhibit the activation of PBMCs NF-κB, and reduce the level offinger protein A20.

Objective:To analyze the application value of sakubatril valsartan in the treatment of chronic heart failure (CHF) based on cardiopulmonary test system.Methods:One hundred and thirty-five CHF patients admitted to the Affiliated Hospital of Jining Medical Collegefrom January 2019 to August 2020 were divided into the observation group (67 cases) and the control group (68cases) by random number table method. Both groups were treated with bisoprolol. The observation group was treated with the combination of sakubatril valsartan, and the control group was treated with the combination of benapril. The efficacy and cardiac function indicators of the two groups were compared. The cardiopulmonary exercise test system was used to measure the patient′s maximum exercise time (Tmax), maximum exercise Watt (Wmax), peak volume oxygen (Peak VO 2) and volume of anaerobic threshold oxygen (VO 2AT), and the incidence of adverse reactions were calculated. Results:The total effective rate in the observation group was higher than that in the control group: 92.54% (62/67) vs. 77.94%(53/68), the difference was statistically significant ( χ2 = 5.70, P<0.05). After the treatment, the levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and soluble ST2 (sST2) in the observation group were lower than those in the control group: (2 000.47 ± 517.85) ng/L vs. (2 777.39 ± 812.49) ng/L, (0.33 ± 0.10) μg/L vs. (0.37 ± 0.09) μg/L, and the left ventricular ejection fraction (LVEF) was higher than that in the control group: (8.12 ± 6.44)% vs. (41.93 ± 6.73)%, the differences were statistically significant ( P<0.05). After the treatment, the left ventricular end-diastolic diameter (LVEDd), left ventricular end-systolic diameter (LVEDs), left ventricular mass index (LVMI), left atrial volume index (LAVI) in the observation group were lower than those in the control group: (55.47 ± 6.93) mm vs. (62.00 ± 7.18) mm, (37.14 ± 6.36) mm vs. (41.35 ± 6.43) mm, (136.76 ± 7.13) mg/m 2 vs. (140.98 ± 7.47) mg/m 2, (28.23 ± 2.59) ml/m 2 vs. (31.98 ± 2.17) ml/m 2; the Tmax, Wmax, PeakVO 2 and VO 2AT in the observation group were higher than those in the control group: (619.08 ± 65.36) s vs. (58.70 ± 52.44) s, (142.96 ± 16.05) W vs. (124.19 ± 13.38) W, (20.00 ± 5.74) ml/(min·kg) vs. (18.13 ± 3.58) ml/(min·kg), (13.89 ± 3.69) ml/(min·kg) vs. (11.23 ± 2.36) ml/(min·kg), the differences were statistically significant ( P<0.05). However, there was no statistically significant in the incidence of adverse reactions between the two groups ( P>0.05). Conclusions:Sakubatril valsartan in the treatment of CHF can not only optimize the efficacy and improve cardiac function, but also benefit cardiac exercise rehabilitation of patients, and not increase the safety risk.

In order to establish an infectious clone for CDV-3, a commercial vaccine strain of canine distemper virus for mink, to provide reference for the studies of pathogenesis and novel vaccine development of CDV. Thirteen pairs of primers were used to amplify the full-length genome of CDV-3 strain. Five long fragments were obtained based on single restriction site analysis of the whole genome of CDV-3 by RT-PCR. Five fragments were successively inserted into the multiple clone sites in the modified eukaryotic vector of pcDNA3.2 by restriction enzymes and splicing. Meanwhile, the hammerhead ribozyme and hepatitis delta virus ribozyme sequences were added to the beginning of F1 fragment and the ending of F5 fragment, respectively. Then, the full-length cDNA recombinant plasmid of CDV-3 was obtained and named as pcDNA3.2-CDV-3. In addition, three helper plasmids, expressing the N protein, P protein and L protein of the CDV-3 strain respectively, were constructed. The 293T cells were transfected with the full-length cDNA recombinant plasmid and three helper plasmids by Lipofectamine™ 2000. At 3 days post transfection, the supernatant was added to the monolayer of Vero cells to observe the typical syncytium of CDV. Indirect immunofluorescence and artificial label identification of recombinant virus rCDV-3 were conducted after the occurrence of lesions. Finally, the growth characteristics of wtCDV-3 and rCDV-3 were compared after passaging of rCDV-3. The identification of the full-length cDNA recombinant plasmid and three helper plasmids by restriction enzyme digestion and sequencing were consistent with expected. The Vero cells infected with the recombinant rCDV-3 showed typical syncytic. The identification of indirect immunofluorescence and labeled marker, and observation under electron microscope proved that the rCDV-3 was indeed rescued from the recombinant plasmid of pcDNA3.2-CDV-3. In comparison of the virus titers of wtCDV-3, rCDV-3 replicated massively and rapidly and reached the maximize virus titer of 10⁷·⁶⁶⁷ TCID₅₀/mL within 36 h post infection (p.i.) in Vero cells, while wtCDV-3 grew gradually to 10⁶·⁶⁶⁷ TCID₅₀/mL at 72 h p.i. in Vero cells. This reverse genetic system of CDV-3 strain has been established successfully, to provide reference for the studies of pathogenesis and novel vaccine development of CDV.
Animals ; Chlorocebus aethiops ; Clone Cells ; DNA, Complementary ; Distemper Virus, Canine/genetics* ; Plasmids/genetics* ; Vero Cells

Detailed characterizations of genomic alterations have not identified subtype-specific vulnerabilities in adult gliomas. Mapping gliomas into developmental programs may uncover new vulnerabilities that are not strictly related to genomic alterations. After identifying conserved gene modules co-expressed with EGFR or PDGFRA (EM or PM), we recently proposed an EM/PM classification scheme for adult gliomas in a histological subtype- and grade-independent manner. By using cohorts of bulk samples, paired primary and recurrent samples, multi-region samples from the same glioma, single-cell RNA-seq samples, and clinical samples, we here demonstrate the temporal and spatial stability of the EM and PM subtypes. The EM and PM subtypes, which progress in a subtype-specific mode, are robustly maintained in paired longitudinal samples. Elevated activities of cell proliferation, genomic instability and microenvironment, rather than subtype switching, mark recurrent gliomas. Within individual gliomas, the EM/PM subtype was preserved across regions and single cells. Malignant cells in the EM and PM gliomas were correlated to neural stem cell and oligodendrocyte progenitor cell compartment, respectively. Thus, while genetic makeup may change during progression and/or within different tumor areas, adult gliomas evolve within a neurodevelopmental framework of the EM and PM molecular subtypes. The dysregulated developmental pathways embedded in these molecular subtypes may contain subtype-specific vulnerabilities.
Humans ; Brain Neoplasms/pathology* ; Neoplasm Recurrence, Local/metabolism* ; Glioma/pathology* ; Neural Stem Cells/pathology* ; Oligodendrocyte Precursor Cells/pathology* ; Tumor Microenvironment