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We report a severe COVID-19 complicated with MIS-C in a girl treated by the author in China, and discuss the current research status and progress in the diagnosis and therapy of MIS-C in children. The patient was a 4-year-old child previously healthy who was referred to the hospital with a complaint of fever, finally, Multisystem inflammatory syndrome was diagnosed with COVID-19.

Abstract Background 99mTc-Rituximab is a new specific radiopharmaceutical that binds to the CD20 receptor which is highly expressed on the surface of B cells. We conducted a study in which 99mTc-Rituximab was compared with filtered 99mTc-sulfur colloid (fTcSC) for sentinel lymph node (SLN) detection in patients with breast cancer. Method The study is divided into three parts. 1. Initially, 25 patients were selected for an internal controlled trial to received both 99mTc-Rituximab and fTcSC, the interval time is separated by ≥2 days. 2. Then, 91 patients were selected for a randomized controlled trial (41 and 50 patients in the 99mTc-Rituximab and fTcSC groups, respectively). All patients were administered either agent at the 6- and 12-o’ clock positions by subareolar injection technique. SLN mapping was then performed 2 h after injection. 3. Serial dynamic images were further acquired for 2 h in 31 patients (22 and 9 patients from 99mTc-Rituximab and fTcSC cohorts, respectively). Results The identification rate of lymphoscintigraphy and SLNB in all and axilla regions for 99mTc-Rituximab and 99mTc-SC were 98.5% vs 98.7, 100% vs 98.4%, respectively. The mean number of SLNs identified by 99mTc-Rituximab and fTcSC was respectively 2.72 and 3.28, with a significant difference of P = 0.013 (paired sample t-test). The difference exists in the internal mammary and clavicular area, not in the axillary. The mean number of axillary sentinel lymph node biopsy (SLNB) for 99mTc-Rituximab and fTcSC was 2.95 vs 3.14, respectively, and no significant difference existed. 99mTc-Rituximab also exhibited a significantly faster injection site clearance rate when compared with fTcSC (0.193 ± 0.057 h− 1 vs 0.021 ± 0.007 h− 1, respectively). Conclusion No significant difference was observed in identification rate and number of axillary SLN imaging and SLNB, between the two tracers. Compared to fTcSC, 99mTc-Rituximab based imaging demonstrated a fewer number of secondary lymph nodes and had faster injection site clearance rate. Trial registration www.chictr.org.cn, ChiCTR1900024990 (retrospectively registered August 6, 2019).

Abstract. Objective:. This study was performed to elucidate the clinical and epidemiological characteristics of vitiligo patients of different ages in Northwest China. Methods:. We retrospectively reviewed the case records and questionnaires of all patients diagnosed with vitiligo, who visited People's Hospital of Xinjiang Uygur Autonomous Region from May 2016 to December 2017. The clinical and epidemiological characteristics of these patients were analyzed by Pearson's χ2 test and Fisher's exact test. Results:. In total, we collected data of 571 vitiligo patients with age of 32.9 ± 16.4 years. The prevalence of segmental vitiligo in children and adolescents ≤19 years old (24/175[13.7%]) was higher than that in adults aged from 20-59 years (23/370[6.2%]) and advanced patients aged ≥60 years (1/26[3.8%]) (P = 0.020). The prevalence of progressive vitiligo was higher in children and adolescents ≤19 years (72/175[41.1%]) and adults from 20–59 years (141/370[38.1%) than in patients ≥60 years (5/26[19.2%]) (P = 0.063). Children and adolescents ≤19 years with vitiligo had a higher rate of a family history of vitiligo (20/175[11.4%]) than adults (20/370[5.4%]) and advanced age (1/26[3.8%]) (P = 0.031). Conclusions:. This study provides clinical evidence that vitiligo at different ages has different characteristics, mainly regarding an increased incidence of segmental vitiligo, a higher prevalence of atopic dermatitis and halo nevus, and a more common positive family history among children and adolescent patients.

Cell senescence deters the activation of various oncogenes. Induction of senescence is, therefore, a potentially effective strategy to interfere with vital processes in tumor cells. Sphingosine-1-phosphate receptor 1 (S1PR1) has been implicated in various cancer types, including ovarian cancer. The mechanism by which S1PR1 regulates ovarian cancer cell senescence is currently elusive. In this study, we demonstrate that S1PR1 was highly expressed in human ovarian cancer tissues and cell lines. S1PR1 deletion inhibited the proliferation and migration of ovarian cancer cells. S1PR1 deletion promoted ovarian cancer cell senescence and sensitized ovarian cancer cells to cisplatin chemotherapy. Exposure of ovarian cancer cells to sphingosine-1-phosphate (S1P) increased the expression of 3-phosphatidylinositol-dependent protein kinase 1 (PDK1), decreased the expression of large tumor suppressor 1/2 (LATS1/2), and induced phosphorylation of Yes-associated protein (p-YAP). Opposite results were obtained in S1PR1 knockout cells following pharmacological inhibition. After silencing LATS1/2 in S1PR1-deficient ovarian cancer cells, senescence was suppressed and S1PR1 expression was increased concomitantly with YAP expression. Transcriptional regulation of S1PR1 by YAP was confirmed by chromatin immunoprecipitation. Accordingly, the S1PR1-PDK1-LATS1/2-YAP pathway regulates ovarian cancer cell senescence and does so through a YAP-mediated feedback loop. S1PR1 constitutes a druggable target for the induction of senescence in ovarian cancer cells. Pharmacological intervention in the S1PR1-PDK1-LATS1/2-YAP signaling axis may augment the efficacy of standard chemotherapy.

AIM: To prevent neovascularization in diabetic retinopathy (DR) patients and partially control disease progression. METHODS: Hypoxia-related differentially expressed genes (DEGs) were identified from the GSE60436 and GSE102485 datasets, followed by gene ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Potential candidate drugs were screened using the CMap database. Subsequently, a protein-protein interaction (PPI) network was constructed to identify hypoxia-related hub genes. A nomogram was generated using the rms R package, and the correlation of hub genes was analyzed using the Hmisc R package. The clinical significance of hub genes was validated by comparing their expression levels between disease and normal groups and constructing receiver operating characteristic curve (ROC) curves. Finally, a hypoxia-related miRNA-transcription factor (TF)-Hub gene network was constructed using the NetworkAnalyst online tool. RESULTS: Totally 48 hypoxia-related DEGs and screened 10 potential candidate drugs with interaction relationships to upregulated hypoxia-related genes were identified, such as ruxolitinib, meprylcaine, and deferiprone. In addition, 8 hub genes were also identified: glycogen phosphorylase muscle associated (PYGM), glyceraldehyde-3-phosphate dehydrogenase spermatogenic (GAPDHS), enolase 3 (ENO3), aldolase fructose-bisphosphate C (ALDOC), phosphoglucomutase 2 (PGM2), enolase 2 (ENO2), phosphoglycerate mutase 2 (PGAM2), and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3). Based on hub gene predictions, the miRNA-TF-Hub gene network revealed complex interactions between 163 miRNAs, 77 TFs, and hub genes. The results of ROC showed that the except for GAPDHS, the area under curve (AUC) values of the other 7 hub genes were greater than 0.758, indicating their favorable diagnostic performance. CONCLUSION: PYGM, GAPDHS, ENO3, ALDOC, PGM2, ENO2, PGAM2, and PFKFB3 are hub genes in DR, and hypoxia-related hub genes exhibited favorable diagnostic performance.

Objective To evaluate the associations between serum level of trimethylamine oxide （TMAO） and vascular calcification and explore the risk factors of vascular calcification in patients with chronic kidney disease （CKD）. Methods A total of 118 CKD3-5 patients were assigned into two experimental groups of calcification and non-calcification according to whether or not there was calcification of abdominal aorta. And 60 healthy people with matching age and gender were selected as control group. Serum level of TMAO was determined by enzyme-linked immunosorbent assay （ELISA）. The clinical data of two groups were compared. Results TMAO（6.49 ± 0.76）μmol/L，serum phosphorus (1.73±0.62)μmol/L，calcium-phosphorus product(3.66±1.30)，parathyroid hormone （PTH）[232.90（96.90，521.60）ng/L]，alkaline phosphatase （ALP） [72.00（55.75，113.50）U/L]，serum creatinine （Scr）[684.50（511.25，921.00）μmol/L] and C-reactive protein （CRP）[5.00（1.28，21.88）mg/L] were higher in experimental group than those in control group （P＜0.05）. Serum calcium（Scr）(2.13±0.24)μmol/L，25-hydroxyvitamin D[23.67（16.84，30.06）μg/L]，albumin （Alb）(37.35±5.97)g/L and estimated glomerular filtration rate （eGFR）[6.02（4.70，8.50）mL·min-1·（1.73m2）-1] were lower in control group （P＜0.05）. TMAO(6.01±0.90)μmol/L，age(47.81±13.51)year，proportion of hemodialysis，serum calcium (2.07±0.21)μmol/L and CRP[4.70（0.80，19.44）mg/L] were higher in calcification group than that in non-calcification group （P＜0.05）. No statistically significant inter-group difference existed in gender，basic diseases （hypertension & diabetes mellitus），blood phosphorus，calcium-phosphorus product，PTH，ALP，Alb，total cholesterol （TC），triglyceride （TG），25 hydroxyvitamin D，Scr and eGFR （P＞0.05）. Vascular calcification was correlated positively with age （r = 0.446，P＜0.001），TMAO （r = 0.614，P＜0.001），serum calcium （r = 0.192，P = 0.038），CRP （r = 0.208，P = 0.024） and hemodialysis （r = 0.238，P = 0.009）. Logistic analysis revealed that age （OR = 1.069，95%CI: 1.025-1.115，P = 0.002） and TMAO （OR = 19.295，95%CI: 5.785-64.663，P＜0.001） were the independent risk factors for vascular calcification. ROC curve indicated that area under curve （AUC） of TMAO and serum calcium were 0.855 and 0.611 respectively for diagnosing vascular calcification. AUC of combination was 0.868 with a sensitivity of 85.2% and a specificity of 71.9%. Conclusion Serum level of TMAO is correlated with vascular calcification in CKD patients. And TMAO is expected to become an adjunct to diagnosing vascular calcification. Due to a low specificity，it should be combined with other risk factors for assessing vascular calcification. The common risk factors for vascular calcification include age，TMAO，serum calcium，CRP and hemodialysis. And age and serum level of TMAO are independent risk factors for vascular calcification in CKD patients.

To further explore the metabolism of Lycium barbarum polysaccharides, the cell wall microstructure of Lycium barbarum fruits in different growth periods was observed by transmission electron microscopy, and the cell wall polysaccharide content and its degrading enzyme activity were extracted by chemical method. The changes of polysaccharide components in cell wall of Lycium barbarum fruits in different growth periods were analyzed by microcopolymer Raman spectroscopy. The correlation between the content of polysaccharide in cell wall and the activity of degrading enzyme was analyzed. The results showed that the changes of cell wall structure mainly occurred during 28~35 d, with the cell wall becoming significantly thinner, pectin degrading, and the cell wall structure gradually collapsing. Cell wall material (CWM) content increased first and then decreased, and water-soluble pectin (WSP) content increased significantly (P

Abstract Background According to traditional Chinese medicine (TCM), drugs supplementing the vital energy, Qi, can eliminate tumors by restoring host immunity. The objective of this study is to investigate the underlying immune mechanisms of anti‐tumor activity associated with Qi‐supplementing herbs, specifically the paired use of Huangqi and Danggui. Methods Analysis of compatibility regularity was conducted to screen the combination of Qi‐supplementing TCMs. Using the MTT assay and a transplanted tumor mice model, the anti‐tumor effects of combination TCMs were investigated in vitro and in vivo. High content analysis and flow cytometry were then used to evaluate cellular immunity, followed by network pharmacology and molecular docking to dissect the significant active compounds and potential mechanisms. Finally, the anti‐tumor activity and the mechanism of the active ingredients were verified by molecular experiments. Results There is an optimal combination of Huangqi and Danggui that, administered as an aqueous extract, can activate immunity to suppress tumor and is more effective than each drug on its own in vitro and in vivo. Based on network pharmacology analysis, PIK3R1 is the core target for the anti‐tumor immunity activity of combined Huangqi and Danggui. Molecular docking analysis shows 6 components of the combined Danggui and Huangqi extract (quercetin, jaranol, isorhamnetin, kaempferol, calycosin, and suchilactone) that bind to PIK3R1. Jaranol is the most important component against breast cancer. The suchilactone/jaranol combination and, especially, the suchilactone/kaempferol combination are key for immunity enhancement and the anti‐tumor effects of the extract. Conclusions The combination of Huangqi and Danggui can activate immunity to suppress breast cancer and is more effective than the individual drugs alone.