[Serum C-reactive protein, cholinesterase and prealbumin are correlated with prognosis of severe coronavirus disease 2019 patients].

Objective: To retrospectively analyze the relationship between serum C-reactive protein (CRP), serum cholinesterase (ChE), prealbumin (PA) and mortality in severe patients with coronavirus disease 2019 (COVID-19). Methods: During the period from January 29 to March 30, 2020, a total of 344 COVID-19 patients were admitted to west branch of Union Hospital, Tongji Medical College, Huazhong University of Science and Technology. One-hundred and ninety-two patients were diagnosed with common type and excluded, and 34 patients were transferred to LeiShenShan or other medical units. The remaining 118 patients were severe cases, and 18 cases were excluded due to incomplete data. A total of 100 severe COVID-19 patients were finally collected. According to the outcome, the patients were divided into death group (37 cases) and survival group(63 cases), and the levels of serum CRP, ChE and PA were compared. Statistical analysis were performed by SPSS25.0. Results: There were 53 male patients in this study. The level of CRP in death group was significantly more elevated compare to the survival group [(95.72±39.56) mg/L vs. (22.21±20.75) mg/L, P<0.01]. On the contrary, serum ChE in death group was remarkably decreased [(5 082±1 566) U/L vs. (7 075±1 680) U/L, P<0.01]. Also, serum PA in death group was significantly lower [(86.18±47.94) mg/L vs. (167.40±57.82) mg/L, P<0.01]. Univariate analysis showed that CRP and PA had an impact on the survival of critical patients, but multivariate Cox regression analysis suggested that CRP was the independent factor affecting the survival of critical patients. Conclusions: CRP is generally elevated in severe patients with COVID-19, and serum ChE and PA accordingly decrease. CRP and PA have influence on patients' survival, but only CRP demonstrates predictive value for prognosis in critical patients with COVID-19.

Characterization of dual leucine zipper-bearing kinase, a mixed lineage kinase present in synaptic terminals whose phosphorylation state is regulated by membrane depolarization via calcineurin.

The biochemistry and regulation of dual leucine zipper bearing kinase (DLK), a member of the mixed lineage kinase or MLK subfamily of protein kinases, was examined in the nervous system. DLK transcript expression in the nervous system was predominantly neuronal. DLK protein was present in synaptic terminals where it was associated with both plasma membrane and cytosol fractions. Within these two fractions, DLK had differing characteristics. Cytosolic DLK existed in both a phosphorylated and dephosphorylated state; DLK associated with plasma membrane existed in the dephosphorylated state only. On nonreducing SDS-polyacrylamide gel electrophoresis, cytosolic DLK migrated at 130 kDa, while membrane associated DLK migrated with an apparent Mr >/= 260,000. Similarly, DLK transiently expressed in COS 7 cells autophosphorylated in vivo and migrated at approximately 260 kDa when separated by nonreducing SDS-polyacrylamide gel electrophoresis. In cotransfection experiments, FLAG-tagged DLK or a FLAG-tagged truncated DLK mutant (F-Delta520) was coimmunoprecipitated with Myc-tagged DLK and formed complexes under nonreducing conditions consistent with the conclusion that DLK formed covalently associated homodimers in overexpressing COS 7 cells. In aggregating neuronal-glial cultures, depolarization of plasma membrane lead to dephosphorylation of DLK. Treatment of aggregates with 5 nM or 200 nM okadaic acid lead to a shift in electrophoretic mobility consistent with phosphorylation of DLK. Treatment with cyclosporin A, a specific inhibitor of the calcium/calmodulin-dependent protein phosphatase 2B (calcineurin), had no effect on DLK phosphorylation under basal conditions. However, cyclosporin A completely inhibited DLK dephosphorylation upon membrane depolarization.

Suppression of human nasopharyngeal carcinoma cell growth in nude mice by the wild-type p53 gene.

Wild-type and mutant human p53 genes were transfected into the nasopharyngeal carcinoma (NPC) cell line CNE-3. Tumorigenicity in nude mice showed that the tumor resulting from the cells transfected with the wild-type p53 gene grew more slowly and was smaller than that from the cells transfected with mutant p53 gene and that from control CNE-3 cells. In contrast, the tumor from the cells transfected with the mutant p53 gene grew faster than that produced by cells transfected with the wild-type p53 gene and that produced by control CNE-3 cells. The results demonstrate that the wild-type p53 gene could inhibit the NPC cell growth in nude mice and the mutant p53 gene could enhance the NPC cell growth in nude mice. The p53 gene may also play an important role in the pathogenesis of NPC.