Novel coronavirus has brought great threats to the people and challenges to the health systems around the world. Compared with general population, lymphoma patients are more vulnerable to novel coronavirus infection(COVID-19) and have poorer prognosis. So the clinical management of COVID-19 in lymphoma patients in more difficult and the great importance should be attached. This article reviews the clinical characteristics and current management strategies of lymphoma patients with COVID-19, to provide reference for the clinical treatment of lymphoma patients with COVID-19.

Sulforaphane (SFN), a natural anti-tumor compound from cruciferous vegetables, has been reported to induce protective autophagy to cancer cells, which might impair the anti-tumor efficiency of SFN. However, the accurate function and mechanism of SFN inducing autophagy in cancers are still obscure, especially in esophageal squamous cell carcinoma (ESCC), one of malignancies with high incidence in North China. Here, we mainly explored the potential function of autophagy upon SFN treatment in ESCC and molecular mechanism. We demonstrated that SFN could inhibit cell proliferation and induce apoptosis by activating caspase pathway. Moreover, we found activation of NRF2 pathway by SFN was responsible for the induction of autophagy and also a disadvantage element to the anti-tumor effects of SFN on ESCC, indicating that SFN might induce protective autophagy in ESCC. We, therefore, investigated effects of autophagy inhibition on sensitivity of ESCC cells to SFN and found that chloroquine (CQ) could neutralize the activation of SFN on NRF2 and enhance the activation of SFN on caspase pathway, thus improved the anti-tumor efficiency of SFN on ESCC

Dysregulation of mTORC1/mTORC2 pathway is observed in many cancers and mTORC1 inhibitors have been used clinically in many tumor types; however, the mechanism of mTORC2 in tumorigenesis is still obscure. Here, we mainly explored the potential role of mTORC2 in esophageal squamous cell carcinoma (ESCC) and its effects on the sensitivity of cells to mTOR inhibitors. We demonstrated that RICTOR, the key factor of mTORC2, and p-AKT (Ser473) were excessively activated in ESCC and their overexpression is related to lymph node metastasis and the tumor-node-metastasis (TNM) phase of ESCC patients. Furthermore, we found that mTORC1/ mTORC2 inhibitor PP242 exhibited more efficacious anti-proliferative effect on ESCC cells than mTORC1 inhibitor RAD001 due to RAD001-triggered feedback activation of AKT signal. Another, we demonstrated that down-regulating expression of RICTOR in ECa109 and EC9706 cells inhibited proliferation and migration as well as induced cell cycle arrest and apoptosis. Noteworthy, knocking-down stably RICTOR significantly suppresses RAD001-induced feedback activation of AKT/PRAS40 signaling, and enhances inhibition efficacy of PP242 on the phosphorylation of AKT and PRAS40, thus potentiates the antitumor effect of RAD001 and PP242 both and . Our findings highlight that selective targeting mTORC2 could be a promising therapeutic strategy for future treatment of ESCC.

Cas1-and-Cas2-mediated new spacer acquisition is an essential process for bacterial adaptive immunity. The process is critical for the ecology of the oral microflora and oral health. Although molecular mechanisms for spacer acquisition are known, it has never been established if this process is associated with the morphological changes of bacteria. In this study, we demonstrated a novel Cas2-induced filamentation phenotype in E. coli that was regulated by co-expression of the Cas1 protein. A 30 amino acid motif at the carboxyl terminus of Cas2 is necessary for this function. By imaging analysis, we provided evidence to argue that Cas-induced filamentation is a step coupled with new spacer acquisition during which filaments are characterised by polyploidy with asymmetric cell division. This work may open new opportunities to investigate the adaptive immune response and microbial balance for oral health.

OBJECTIVETo explore the differences in sensitivity to rapamycin of five esophageal squamous cell carcinoma cell lines with different differentiation and the changes of sensitivity of the cells after siRNA-interfered expression of p70S6K.

METHODSEffects of rapamycin on proliferation of ESCC cell lines with different differentiation, EC9706, TE-1, Eca109, KYSE790 and KYSE450 cells, were investigated using cell counting kit 8 (CCK-8) assay, and according to the above results, the EC9706 cells non-sensitive to rapamycin were chosen to be transfected with p70S6K-siRNA. The changes in sensitivity of cells to rapamycin were measured in vitro and in vivo using CCK-8 kit, flow cytometry and tumor formation in nude mice.

RESULTSCCK-8 results showed that all the five cell line cells were sensitive to low concentration of rapamycin (<100 nmol/L), but TE-1 and EC9706 cells, which were with poor differentiation, showed resistance to high concentration of rapamycin. After EC9706 cells were treated with 50, 100, 200, 500 and 1 000 nmol/L rapamycin and p70S6K-siRNA, the proliferation rates of EC9706 cells were (48.67 ± 1.68)%, (15.45 ± 1.54)%, (14.00 ± 0.91)%, (10.97 ± 0.72)% and (2.70 ± 0.32)%, respectively, and were significantly lower than that of cells treated with 50, 100, 200, 500 and 1 000 nmol/L rapamycin and control siRNA [(74.53 ± 1.71)%, (68.27 ± 1.35)%, (71.74 ± 2.44)%, (76.23 ± 1.02)% and (80.21 ± 2.77)%] (P<0.05 for all). The results of flow cytometry showed that the ratios of cells in G1 phase of the p70S6K-siRNA, rapamycin and p70S6K-siRNA+ rapamycin groups were (53.82 ± 1.78)%, (57.87 ± 4.01)% and (73.73 ± 3.68)%, respectively, significantly higher than that in the control group (46.09 ± 2.31)% (P<0.05 for all). The results of tumor formation test in vivo showed that the inhibitory effect of rapamycin on tumor growth was stronger after the cells were transfected with p70S6K-siRNA, and the inhibition rate was 96.5%.

CONCLUSIONESCC cells with different differentiation have different sensitivity to rapamycin, and p70S6K-siRNA can improve the sensitivity of cells to rapamycin in vitro and in vivo.

Animals ; Antibiotics, Antineoplastic ; pharmacology ; Carcinoma, Squamous Cell ; drug therapy ; metabolism ; pathology ; Cell Differentiation ; Cell Line, Tumor ; Cell Proliferation ; Esophageal Neoplasms ; drug therapy ; metabolism ; pathology ; Humans ; Mice ; Mice, Nude ; RNA, Small Interfering ; Ribosomal Protein S6 Kinases, 70-kDa ; genetics ; metabolism ; Signal Transduction ; Sirolimus ; pharmacology ; Transfection

Objective To investigate the effects of rapamycin on tumor growth and mTOR/4E-BP1 signaling pathway in xenograft of esophageal squamous cell carcinoma ( ESCC ) EC9706 cells. Methods The expression of factors in mTOR/4E-BP1 signaling pathway of the tumor tissues was analyzed by RT-PCR and Western blot. Results Both rapamycin and cisplatin significantly inhibited the growth of transplantable tumors as compared to control group ( P < 0. 05 ) and their combination had a synergestic effect. The results of RT-PCR and Western blot show that rapamycin significantly decreased the expression of Mtor and p-4E-BP1 but increased the expression of 4E-BP1. Conclusion Rapamycin inhibits the mTOR/4E-BP1 signalling pathway, resulting in the growth inhibition of xenograft of EC9706 cells.

AIM: To clone and express mouse canstatin (m canstatin)cDNA and provide a basis for the further research on its anti-angiogenic activity and potential application for cancer therapy. METHODS: Total RNA was extracted from mouse liver tissue by Trizol Reagent, and mouse canstatin cDNA was amplified by RT- PCR, then cloned into vector pMD18-T for sequencing. pET30a(+)-m canstatin recombinant plasmid was constructed and expressed in E.coli BL21 with induction of IPTG. RESULTS: Mouse canstatin cDNA is 684 bp coding 227 amino acids. The sequences of both cDNA and amino acid share high homology with human canstatin, with cDNA identity at 89% and amino acids identity at 96% to human canstatin. In the present study, pET30a(+)-m canstatin recombinant plasmid was expressed in E.coli BL21. CONCLUSION: Mouse canstatin cDNA has been cloned for the first time. Constructed pET30a(+)-m canstatin recombinant plasmid is highly expressed in E.coli BL21.

The coronary arteries of 80 rabbit hearts were studied.Suspension of red lead oxide (Pb_3O_4)in turpentine was injected into the coronary artery.With clearing method and angiographic technique,we studied the branches of the left and right coronary artery, the angle between the anterior descending branch and the left circumflex branch of the left coronary artery,the relationship between the anterior descending artery and the great cardiac vein,the origin of the sinoatrial nodal artery and the atrioventricular nodal artery as well as the type of branch in coronary artery.The results were outlined as follows: 1.The angle between the anterior descending branch and the left circumflex branch is 35～45?in more than one half of the cases(54.5%). 2.The anterior descending branch is often small and short and accompanies the great cardiac vein.It may exist in four forms:1)Both branches run closely to each other. 2)Both run along with each other but leaving a distance in between.3)Both are over- lapping each other.4)Both are crossing each other between the inferior margin of the left auricle and pulmonary artery cone.Ligation of the anterior descending branch in animal experiments should be appropriately made between the right inferior margin of the auricle and the pulmonary artery cone. 3.The left ventricular branch is a direct continuation of the circumflex branch and gives off branches to anterior and posterior wall of the left ventricle. 4.There is an independent ventricular septal artery in the rabbit heart. 5.The sinoatrial nodal artery of the rabbit heart arises frequently from the right coronary artery(86.6%)and the atrioventricular nodal artery from the left coronary artery(72.5%). 6.Commonly the distribution of the coronary blood supply from the left and right coronary arteries to rabbit heart is nearly a balanced circultion(67.5%).Next frequent is the preponderance of the left coronary artery(28.8%),and the preponderance of the right coronary artery occurs only in 3.7%.

The architecture of the alveolus and its capillaries of human lung injected withsolution of ABS in methyl ethyl ketone was studied under the SEM.The results wereoutlined as follows:1.The alveolar casts were observed from the subpleural and intralobular septu-lar surfaces.The human alveolus is irregular polygon in appearance.The size ofthe alveolus is variable,its surface is smooth,there are many depressions of the topof type Ⅱ cells.The bridge-like structure between two adjacent alveoli are thecasts of the alveolar pores.They are variable both in size and number,and ofround or oval shapes with smooth surface.2.Capillaries of the subpleural space and interlobular septulum are transitional,and identical in appearance.Meshes of the capillary network are larger than thoseof other parts,but more closer in density compared with those in dog.Each capil-lary is branched from the metaarteriole.3.Capillaries in the alveolar septum is a single layer of dense network,theirdiameter are larger than those of the mesh hole.They originate mainly from thecapillaries of subpleural space and interlobular septulum.