Objective To explore the correlation between the components of immune cell subsets in tumor microenvironment of colorectal cancer and the progression of colorectal cancer disease, and to explore the differential regulatory effects of different CD4⁺ T cell subsets on the progression of colorectal cancer. Methods Using the single cell transcriptome sequencing data of colorectal cancer patients in GEO database, CIBERSORTx algorithm was used to assess the immune cell subsets score from the transcriptome sequencing data of colorectal cancer patients in The Cancer Genome Atlas (TCGA) database. The obtained immune cell subsets scores were combined with clinical data to analyze the correlation between metastasis and prognosis. Subsets related genes were calculated based on immune cell subsets scores, and functional enrichment scores performed by using DAVID analysis platform were used to compare the different regulatory function of immune cell subsets in colorectal cancer. Lasso algorithm/regression was used to screen immune cell subsets and Cox analysis was used to construct a risk prognosis model. Results The abundance of CD4-TCF7 was significantly increased in metastatic patients of colorectal cancer compared with non-metastatic patients (P<0.01), the abundance of CD4-CTLA4, CD8-LEF1, PLASMAB-IgG, and MACRO-IL1B decreased in metastatic patients(P<0.05). In the survival analysis, 15 of the 38 immune cell subsets were significantly associated with over survival based on the AUC curve (P<0.05). After analyzing the regulatory functions of CD4⁺ T cell subsets in colorectal cancer cells, we find the CD4-GNLY,CD4-ANXA1 and CD4-CXCR6 with more powerful regulation on the colorectal cancer angiogenesis related pathways compared to others, CD4-IL23R preferentially enriched in energy metabolism related pathways, CD4-GZMK compared to other subsets uniquely enriched in hypoxia stress related pathways, CD4-ANXA1, CD4-TCF7 and CD4-CTLA4 compared to other subsets preferentially enriched in the cell proliferation related pathways, CD4-ANXA1, CD4-TCF7, CD4-CTLA4, and CD4-CXCL13 preferentially enriched in the pathways of cell adhesion and cell migration compared to other subsets. Conclusions There are differences in the regulation of colorectal cancer cell function by immune cell subsets. The composition of immune cell subsets in colorectal cancer immune microenvironment affects the survival and prognosis of patients.

Breast cancer is the most common malignant tumor in the world. Endocrine therapy is an important treatment for HR positive breast cancer, and its drugs are mainly divided into premenopausal estrogen receptor antagonists and postmenopausal aromatase inhibitors, but drug resistance has become a major challenge in endocrine therapy for breast cancer. This article reviews the drug resistance mechanism and the latest research results of endocrine therapy in premenopausal and postmenopausal breast cancer from the aspects of gene regulation, estrogen and coregulatory cofactor, growth factor signal pathway, cell cycle regulation,autophagy and apoptosis, non-coding RNA regulation, immune surveillance, etc., in order to provide a new basis for clinical solution of endocrine therapy resistance in breast cancer.

The outbreak of coronavirus disease 2019 (COVID-19) has become a global pandemic. The pathogen responsible for this disease is a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It belongs to coronavirus family, a pathogen similar to SARS and Middle East respiratory syndrome (MERS), and manifests strong infectivity and pathogenicity to progress into severe pneumonia. Till now, there is no specific therapeutic drug targeting against this virus. With the rapid spread and deterioration of the epidemic situation, vaccination has become an urgent need. This review introduces the immune defense mechanism of human body against coronavirus briefly, set forth the key viral spike protein for coronavirus vaccine development, and then summarize the recent advances/progresses and potential challenges in safety and efficacy of vaccine development for SARS-CoV-2.

Patients with polycystic ovary syndrome (PCOS) have impaired follicular development and maturation. Ovarian granulosa cells play an important regulatory role in the initiation, growth and development of primordial follicles, in which the mitochondria of granulosa cells are involved in the regulation of cell cycle, metabolism, and signal transduction, and provide energy support for oocyte meiosis, fertilization, and up to early embryonic development through energy metabolic pathways. Studying the mitochondrial function of granulosa cells is one of the best non-invasive methods to study the pathological mechanisms in PCOS patients and to evaluate oocyte quality and embryonic developmental potential. A large number of evidences have shown that PCOS is associated with mitochondrial dysfunction in ovarian granulosa cells by mechanisms including altered mitochondrial DNA(mtDNA) copy number and mutations in the mtDNA gene. Some studies have explored the improvement of mitochondrial function in PCOS granulosa cells to improve the impaired follicular development and maturation in PCOS. Therefore, the relevant research progress in recent years have been reviewed in present paper about mitochondrial dysfunction in PCOS granulosa cells, for exploring the mechanism of mitochondrial dysfunction in PCOS granulosa cells, and the ways and methods of improvement.

Renal cancer, as a common urinary system tumor, its occurrence and development involve a series of genetic events including changes in the level of epigenetics. Its etiology is complex and highly heterogeneous. Renal cell carcinoma is the chief type of kidney cancer, while the clear cell renal cell carcinoma (CCRCC) is the most common subtype of renal cell carcinoma.Recently, exon sequencing revealed that the mutation rate of polybromo-1 (PBRM1) gene in CCRCC can be as high as 40%. BAF180 protein, which is encoded by PBRM1 gene, is one of the specific subunits of the chromatin remodeling complex PBAF (polybromo-associated BRG1-associated factor), a type of SWItch/sucrose nonfermentable (SWI/SNF) complexes. It not only participates in the formation of PBAF complex, but also mediates the binding of the complex to specific DNA regions, thus affecting the gene transcription and translation processes, so indicates that PBRM1 plays an important role in the occurrence and development of renal cell carcinoma. The research status, molecular mechanism and clinical transformation of the major cancer related genes in CCRCC,especially the tumor suppressor gene PBRM1, were reviewed in present paper, in order to provide reference for the basic and clinical transformation research of SWI/SNF in renal cell carcinoma and other related tumors.

Ferroptosis suppressor protein 1 (FSP1), confirmed as a ferroptosis-resistant factor recently, plays a key role in the oncogenesis and progress of human diseases, such as breast cancer, ovarian cancer, lung cancer, hepatocellular carcinoma,melanoma, lymphoma, leukemia, copper resistance, severe acute pancreatitis, and diabetes. FSP1 is regarded as a double-edged sword according to previous studies. Mechanically, FSP1 triggers caspase-independent apoptosis via its C-terminal fragments,nuclear translocation, or over-expression, and inhibits ferroptosis through FSP1-CoQ₁₀-NAD(P)H axis, being independent of the glutathione (GSH)-GPX4 axis. The research progress in action mechanism of FSP1 in human diseases is briefly described in this review for providing novel preventative and therapeutic target molecules for human diseases.

Male breast cancer (MBC) is a rare disease for which almost no prospective studies have focused on its diagnosis and treatment. MBC is more likely to be positive for hormone receptor while the ratio of triple negative and human epidermal growth factor receptor 2 (HER2) positive is very low. Most men have undergone radical mastectomy and modified radical mastectomy after diagnosis of breast cancer during past decades and sentinel lymph node biopsy has been gradually used in recent years. The indications of postoperative adjuvant radiotherapy refer to female breast cancer (FBC). Tamoxifen is the first choice of adjuvant endocrine therapy for MBC and chemotherapy can also improve MBC patients' prognosis. Anti-HER2 therapy is recommended for patients with high risks, though there is no definite evidence for its application. Data for the use of new drugs in MBC are lacking,whereas it may be a reasonable approach for metastatic MBC. In general, the overall prognosis of MBC is worse than FBC, but a few studies showed that MBC and FBC had similar survival rates after adjustment for demographic characteristics, disease stage, and treatment. Most of published articles are retrospective studies including small cohorts of MBC patients, which have been reviewed in this article. The review summarizes current data on the epidemiology of MBC, pathological and clinical characteristics, prognosis and treatment, and data published in our country during the past decade.

Trauma-induced hypercoagulopathy is a hypercoagulable phenotype of trauma-induced coagulopathy (TIC) characterized by vascular endothelial injury, excessive release of procoagulants, hyperfibrinogenemia, platelet hyperactivity, anticoagulant pathways impairment and fibrinolysis shutdown. Recent studies have found that the incidence, mortality and disability rate of trauma-induced hypercoagulopathy increased significantly with the severity of trauma. Therefore, the People's Liberation Army Professional Committee of Critical Care Medicine and China Medical Education Association Professional Committee of Thrombosis, Hemostasis and Critical Care Medicine jointly formulated Chinese expert consensus on diagnosis and treatment of trauma-induced hypercoagulopathy published in Military Medical Research in April, 2021. In present paper, the main contents of the consensus were interpreted from the definition, pathophysiological mechanism, assessment, prevention, and treatment of trauma-induced hypercoagulopathy.

Objective To understand the effect of resveratrol (RSV) on vascular repair after the common carotid balloon injury in rats. Methods Forty SD rats were randomized into four groups (n=10): sham group, model group, solvent control group(DSMO group) and RSV group. After establishing the carotid artery balloon injury model, the rats in model group had no special treatment, while the rats in DMSO group and RSV group were given the same dose of DMSO or RSV respectively at the outside of the adventitia of carotid balloon injury segments. The rats in sham group received external carotid artery ligation. Fourteen days after the surgery, excessive anesthesia was applied to rats. The injured segments of the carotid arteries were collected, followed by HE staining to observe the degree of vascular intimal hyperplasia and stenosis. The expression of CD31 using immunohistochemical staining was detected to evaluate the degree of the re-endothelialization, and Western blotting was used to detect the expression levels of vascular endothelial growth factor (VEGF) in the arterial tissues. Results HE staining results showed that there was no significant difference in EEL circumference, EEL area and IEL area between groups (P>0.05); compared with sham group and DMSO group, the lumen area of RSV group decreased significantly (P<0.05). Compared with sham group, the degree of intimal hyperplasia increased in model group and RSV group (P<0.05); compared with model group, the degree of intimal hyperplasia decreased in DMSO group (P<0.05); compared with DMSO group, the degree of intimal hyperplasia increased in RSV group(P<0.05). Compared with sham group, the degree of stenosis in model group and RSV group were significantly higher (P<0.05); compared with model group, the degree of stenosis in DMSO group decreased significantly (P<0.05); compared with DMSO group, the degree of stenosis in RSV group was significantly higher (P<0.05). CD31 immunohistochemical staining results showed that the expression of CD31 in model group was significantly lower than that in sham group (P<0.05), and the expression of CD31 in RSV group was significantly higher than that in model group (P<0.05). Western blotting results showed that the expression of VEGF in model group significantly decreased than that in sham group (P<0.05); compared with model group and DMSO group, the expression of VEGF in RSV group significantly enhanced (P<0.05). Conclusion RSV can promote vascular repair and intimal hyperplasia, and enhance re-endothelialization after the common carotid balloon injury in rats, and the mechanism may be related to the proliferation and migration of adjacent resident endothelial cells and the recruitment of bone marrow endothelial cells or circulating endothelial cells.

Objective To explore the effect of propofol on human gastric cancer transplant BALB/c mice model treated with oxaliplatin. Methods We established a human gastric cancer model in the BALB/c mice using MGC 803 cells subcutaneous transplantation. Then the mice were randomly divided into control group (n=6), propofol group (n=6, 5 mg/kg propofol), oxaliplatin group (n=6, 6 mg/kg oxaliplatin), and propofol with oxaliplatin group (n=6, 5 mg/kg propofol+6 mg/kg oxaliplatin). The mice in each group received a total of 3 consecutive drug administrations through intraperitoneal injection once every 3 days. Mice were sacrificed two days after the last injection. Blood samples were then collected. The tumor volume and mass tumor inhibition rates were analyzed, respectively. The histological features of the tumor were evaluated with HE staining. The expression levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the serum were quantified using ELISA. In addition, the expression levels of epidermal growth factor (EGF), matrix metal protease-2 (MMP-2) and MMP-9 proteins in transplanted tumor tissue were quantified using ELISA. Results Compared with control group, the volume tumor inhibition rates (F=248.717, P<0.05) and mass tumor inhibition rates (F=376.205, P<0.05) of propofol group, oxaliplatin group, and propofol+oxaliplatin group were significantly reduced. The tumor volume inhibition rate and mass tumor inhibition rate of propofol+oxaliplatin group were significantly lower than those of oxaliplatin group, and the differences were statistically significant (tumor volume inhibition rate: 82.44%±4.69% vs.47.18%±5.71%, P<0.05; mass tumor inhibition rate: 77.95%±3.64% vs. 46.43%±3.99%, P<0.05). Compared with control group, cancer cell volume was reduced to varying degrees as well as the number of cancer cells was decreased in the remaining drug-treated groups using HE staining. In addition, the most significant decrease in cancer cell number happened in propofol+oxaliplatin group.The cell nucleus shrinks into a uniform blue-black dense body with an increased cytoplasmic density, increased cancer cell nuclear fragments, and large areas of necrosis. ELISA results showed that the levels of TNF-α and IL-6 in serum and EGF, MMP-2 and MMP-9 in transplanted tumor tissues of propofol group, oxaliplatin group and propofol+oxaliplatin group were significantly lower than those in control group, and those in propofol+oxaliplatin group were significantly lower than those in oxaliplatin group, and the differences were statistically significant (P<0.05). Conclusion Propofol can increase the sensitivity of gastric cancer cells to oxaliplatin, inhibit the proliferation, invasion and metastasis of gastric cancer cells, and enhance the anti-tumor effect of oxaliplatin.The mechanism may be related to the inhibition of inflammatory response by propofol and the regulation of EGF expression.