Intervertebral disc degeneration (IDD) is a common disease in orthopedics, and its pathogenesis is complicated. The main pathological changes are cell apoptosis and extracellular matrix degradation. Clinical therapies are mainly symptomatic and cannot cure diseases at the etiological level. IDD targeted therapy has become the focus of current research due to its small side effects and broad prospects. The apoptosis of nucleus pulposus cells caused by activation of the Fas signaling pathway is an important cause of IDD. It affects IDD's pathophysiological process through genetic factors and is closely related to the pathogenesis of IDD inflammation, immunity, and abnormal vascular growth. Targeting Fas signaling inhibition may be a new type of therapy to slow down the process of IDD effectively. This paper reviews Fas apoptotic pathway, etiology of IDD, the relationship between Fas pathway and IDD, and targeted inhibition of Fas pathway in the treatment of IDD.

Percutaneous coronary intervention (PCI) is one of the effective treatments for coronary heart disease (CHD), but it may cause stress events since its invasive might lead to various somatization symptoms, and then bring about anxiety, depression and other psychological disorders, thus affecting its curative effect and prognosis. In recent years, due to the extensive development of PCI treatment, such patients are not rare in clinic. It has been proved that anxiety and/or depression and CHD are reciprocal and influenced by multiple factors, but the pathophysiological mechanism is still not clear. With the continuous development of "double-heart medicine" model, clinical workers have paid more attention to the identification and diagnosis of cardiovascular disease complicated with psychological problems. The research progress of clinical diagnosis and treatment of patients with complicated anxiety and/or depression after PCI has been reviewed in present paper, thus provides a reference for the implementation of clinical work.

Objective To investigate whether Huaier can reverse the drug resistance of CEM-C1 cells to glucocorticoid(GC) in human acute T lymphocytic leukemia (T-ALL) and its possible mechanism. Methods CEM-C1 and CEM-C7 cells were set as control group (0 μg/ml) and experimental groups (200 and 600 μg/ml) after treated with different concentrations of Huaier; T-ALL CEM-C1 cells were set as Huaier (100 μg/ml) combined with dexamethasone (DEX)(12.5, 25, 50, 100, 200 μg/ml)groups; CCK-8 was used to detect the affect of Huaier on the inhibition rate to proliferation of each group of cells; Flow cytometry(FCM) was employed to detect the effect of different concentrations Huaier (200 and 600 μg/ml) on the apoptosis and cell cycle of CEM-C1 and CEM-C7 cells; Western blotting was performed to detect the MDR1 and Pim3 protein expression levels in CEM-C1, CEM-C7 cells and CEM-C1 cells treated with different concentrations of Huaier (200 and 600 μg/ml); qRT-PCR was used to detect the expression level of Pim3 mRNA in CEM-C1 and CEM-C7 cells and CEM-C1 cells treated with different concentrations of Huaier(200 and 600 μg/ml). Results Huaier inhibited the proliferation of CEM-C1 and CEM-C7 cells in a dose-dependent manner;For CEM-C1 cells, compared with DEX alone, the drug resistance was reversed by 1.34 times in Huaier+DEX group, and Huaier(100 μg/ml) combined with low concentration of DEX (12.5, 25, 50 μg/ml) increased the proliferation inhibition rate of CEM-C1 cells (P<0.05); the coeffcient of drug interaction (CDI) values of all groups were <1. Compared with control group, the apoptosis rate of CEM-C1 and CEM-C7 cells increased significantly with the increase of Huaier concentration (P<0.05). Compared with control group, the number of CEM-C1 and CEM-C7 cells decreased in G₀/G₁ stage and increased in S stage in 200 and 600 μg/ml Huaier groups. The expression levels of MDR1 and Pim3 protein and Pim3 mRNA in CEM-C1 cells were higher than those of CEM-C7 cells (2.41±0.32 vs. 1.34±0.43; 0.39±0.10 vs. 0.13±0.05; 1.00 vs. 0.37±0.02, respectively, P<0.05). Compared with control group, the expression levels of MDR1 and Pim3 proteins and Pim3 mRNA reduced obviously in CEM-C1 cells after treatment with 200 and 600 μg/ml Huaier (P<0.05). Conclusion Huaier can inhibit the proliferation and promote the apoptosis of CEM-C1 and CEM-C7 cells, and partially reverse the resistance of CEM-C1 cells to GC, the mechanism may be related to the down-regulation of Pim3.

Objective To report a case of atrial septal defect (ASD) with congenital fibrinogen deficiency (CFD), and review the literature. Methods A case of secondary ASD with CFD treatment in Xuanwu Hospital of Capital Medical University was reported, and the defect was repaired under CPB on beating heart. The management experience of cardiac surgery under CPB in patients with CFD was summarized by means of PubMed database and literature analysis. Results This patient was female,30 years old. She was admitted to the hospital with the complaint that ASD was found for 8 months after physical examination. On admission, echocardiography showed that the atrial septum was interrupted by about 34 mm. Color Doppler flow imaging(CDFI) detection indicated systolic left to right shunt, the pressure difference of tricuspid regurgitation was 66 mmHg, systolic pulmonary artery pressure (SPAP) was 76 mmHg, ejection fraction (EF) was 64%. Coagulation function: Prothrombin time was>120 s, thrombin time >240 s, activated partial thrombin time >180 s, and fibrinogen <0.6 g/L. Preoperative continuous intravenous infusion of fibrinogen 4 g per day was to maintain the plasma fibrinogen >1.5 g. Three days later ASD repair was performed under CPB on beating heart. Infusion of fibrinogen 2 g was performed by venous injection during operation, and another fibrinogen 2 g was given after heparin was neutralized by protamine. Operation time was 3.5 hours, and CPB time was 45min. Fibrinogen 4 g per day was supplemented postoperatively for 5 days. At the 3rd day chest drainage tube was removed. The patient was discharged at the 7th day. There were no hemorrhage and thrombosis complications. After 3 months, outpatient follow-up showed the surgical incision healed well, echocardiography showed no residual shunt in the atrial septum, and EF value was 67%. A total of 8 English literatures were obtained after searching PubMed database and manually screening, including 875 patients with hypofibrinogenemia after CPB cardiac surgery. Among them, 604 were males (69.0%) and 271 were females (31.0%). There were 6 case reports, including 1 infant(5 days old, weight 2.5 kg) and 5 adult cases, and they were all male. Patients with abnormal afibrinogenemia may have both bleeding and thromboembolic symptoms. Patients with fibrinogen deficiency who undergo CPB cardiac surgery need to be supplemented with fibrinogen, cryoprecipitation or fresh frozen plasma during the perioperative period to prevent severe postoperative bleeding complications. Conclusion Patients with fibrinogen deficiency should be given a individualized perioperative management plan according to the quantitative and other coagulation indexes of fibrinogen in plasma for cardiac surgery under CPB.

Diabetic nephropathy (DN) is a common complication of diabetes, and is one of the main causes of end stage renal disease (ESRD). At present, the practical therapeutic method for DN is still lacked due to unclear pathogenesis. However, as a traditional Chinese medicine, astragalus, especially Astragalus membranaceus, is commonly used in the treatment of DN. The main active ingredients of Astragalus membranaceus include astragaloside Ⅳ (AS-Ⅳ) and astragalus polysaccharide (APS), which can effectively reduce proteinuria and protect renal function. The mechanism of AS-Ⅳ and APS in treatment of DN was reviewed in present article including regulation of endoplasmic reticulum stress (ERS), anti-inflammatory, reducing cell apoptosis, inhibiting fibrosis, and regulating metabolism of sugar and lipid, in order to provide reference for the research and clinical application.

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is an etiology-unknown, non-specific, chronic inflammatory disorder of the intestinal tract with complex pathogenesis. Generally, patients with IBD present with repeated abdominal pain, diarrhea, mucus and blood in the stool, and even various systemic complications. More and more studies believe that it is a chronic inflammatory disease that occurs through the interaction of environment, genetics, intestinal flora, visceral sensitivity, and mental factors. In recent years, the incidence of IBD has been increasing year by year. Early-life exposure refers to the exposure from fetal period to childhood. Early-life adverse exposure (drug exposure, stress exposure, delivery methods, etc.) can have short-term or long-term effects on the intestines of infants, further affecting the physical and mental health of adolescents, adults, and even the elderly, this leads to long-term health effects. A number of studies have found that early-life adverse exposures are involved in the occurrence and progression of IBD. The occurrence of adverse exposure in early life can promote the occurrence and progression of IBD by changing the intestinal flora, immune function, epigenetic inheritance and visceral sensitivity. However, the mechanism by which early-life adverse exposure changes susceptibility to IBD remains unclear. In-depth study of the relationship between early-life adverse exposure and the occurrence of IBD can help prevent the occurrence of diseases at an early stage and reduce the burden of adulthood. This will greatly benefit the improvement of life and health and the rational use of medical resources. This article reviews the relationship between common early-life adverse exposure and the risk of IBD.

Gastric cancer is the fifth leading incidence and the third leading cause of death in the world. Gastric cancer patients in China are often in advanced stages and have a poor prognosis. Cancer progression depends not only on the cancer cells themselves, but also on the physiological state and composition of the tumor microenvironment in which they are located. Cancer-associated fibroblasts as the major cell type in the tumor microenvironment played an important role in cancer progression. This paper mainly expounds the origin and classification of cancer-associated fibroblasts, and its research progress on gastric cancer invasion and metastasis, growth, angiogenesis, matrix remodeling, immunomodulation and cancer suppression, and summarizes the relevant anti-tumor strategies by targeting cancer-associated fibroblasts in gastric cancer, to provide more information for use of cancer-associated fibroblasts in targeted therapy of gastric cancer.

Objective To investigate the changes of cognitive function in early stage of severe heatstroke (HS) in a rat model, and analyze the metabolic changes of central nervous system by ¹H NMR-based metabonomics. Methods Twenty-five male Sprague-Dawley rats were randomly divided into control group (n=11) and HS group (n=14). The rats in HS group were exposed to 40 ℃ heat chamber. When the core temperature reached 42 ℃, they were taken out and rewarmed for 3 h. The rats in control group were placed at (25.0±0.5) ℃. The rats in HS group were evaluated for neurological deficits before modeling and 0 and 3 h after the rewarm by the modified neurological severity score (mNSS); the tissues of the control group (n=3) and HS group (n=3) were taken and HE staining was used to detect the pathological changes; the brain tissues of the rats in control group (n=8) and HS group (n=11)were taken and the MestReNova software (v9.0.1) was used to perform ¹H NMR detection in the NMR spectrometer. The related mechanism of early HS brain injury in rats was expounded from the perspective of metabolomics. Results In the early stage of HS, nerve cell necrosis and apoptosis can be seen in pathological observation. The escape latency time and distance was significantly increased in the HS group compared with control group [(33.14±1.51) s vs. (53.14±2.14) s, P<0.05; (360.79±13.50) cm vs.(693.29±28.63) cm, P<0.05]; the number of platform-crossing and the activity time of target quadrant was significantly reduced in the HS group compared with control [(6.36±0.84) times vs. (2.64±0.75) times, P<0.05; (65.78%±1.06%) vs. (35.81%±1.14%), P<0.05]. The metabolic patterns of central nervous system were significantly changed in early stage of severe heatstroke. Compared to the control group, glutamine, glutamate, lactate and succinate were distinctly increased, while the levels of aspartate, glycine, glutathione and pyruvate were markedly decreased. Conclusions The neurological impairment and cognitive dysfunction can occur in the early stage of severe heat stroke, and the metabolic pattern of central nerve system is changed, resulting disorders of neurotransmitters as amino acids and energy metabolism and oxidative stress.

Objective To investigate the curative effect of low molecular weight heparin (LMWH) on preventing the formation of deep vein thrombosis (DVT) of high-risk pregnant women during pregnancy and puerperium. Methods A total of 1099 high-risk pregnancy patients were collected as LMWH group who received LMWH for preventing the formation of DVT in Zhujiang Hospital of Southern Medical University from January 2019 to July 2020; and 2107 high-risk pregnancy cases without LMWH were selected as control group from January 2016 to December 2018. SPSS 20.0 was employed for statistical analysis, and the number of thrombosis cases, the incidence of prepartal and puerperal hemorrhage, the cesarean section rate and other indicators were compared and analyzed between the two groups. Results After LMWH treatment, no new case of DVT occurred in LMWH group during pregnancy and puerperium, while there were 24 cases of new thrombosis in control group, the difference was statistically significant between the two groups (P=0.000). There were 2 cases of placental abruption before delivery occurred in the LMWH group, and only 1 case in control group. The 2 h postpartum hemorrhage was (182.25±120.62) ml in LMWH group, and (165.00±68.58) ml in control group. The cesarean section rate was 37.5% in LMWH group and 38.9% in control group. No significant differences existed in the incidence of placental abruption, postpartum hemorrhage and cesarean section between the two groups (P>0.05). Conclusion For pregnant women with high risk factors for thrombosis, LMWH can be used according to the score to prevent thrombosis, and it is safe and effective.

Objective To document the dynamics of secondary liver injury in pigs with traumatic hemorrhagic shock(THS) induced by simulated desert dry heat environment and to explore its possible mechanism. Methods Sixty male Landrace piglets were randomly divided into three groups: Dry heat trauma hemorrhagic shock group (DHS group, n=20), dry heat trauma hemorrhagic shock sham operation group (DHC group, n=20), normal temperature trauma hemorrhagic shock group (NTS group,n=20). DHS group and DHC group were exposed to a dry and hot environment [temperature (40.5±0.5) ℃, humidity 10%±2%];while NTS group were exposed to normal temperature environment [temperature (25.0±0.5) ℃, humidity 35%±5%] for 3 h. Then the model of blood pressure controlled hemorrhagic shock was established. Animals were euthanized at 0 min (T₀), 50 min(T₁), 100 min (T₂) or 150 min (T₃) after the successful establishment of the hemorrhagic shock model, blood and live tissue were collected. The pathological changes of liver tissue were observed by HE staining; the levels of TNF-α and IL-1β in liver tissue were detected by ELISA; the expressions of HMGB-1 and ICAM-1 in liver tissue were detected by Western blotting; the contents of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum were determined. Results HE staining results showed that the DHS group had different degrees of injury at each time point, and gradually aggravated with time, and gradually appeared different degrees of hepatic sinusoidal expansion, congestion, hepatic lobule, portal area structure disorder, inflammatory cell infiltration, liver cell degeneration, necrosis and so on. In the NTS group, the injury began to appear at T₂ and gradually worsened. In the DHC group, there was no obvious pathological change at each time point (P>0.05). In the DHS group, ALT and AST showed dynamic changes, and the changing trend was the same, compared with the DHC group, it began to rise at T₀, the difference was statistically significant (P<0.01), and reached the peak at T₁ and T₃, respectively, and the differences were statistically significant compared with DHC group and NTS group at the same time point (P<0.01); however, there was no significant change in DHC group at each time point. TNF-α and IL-1β began to increase at T₀ in the DHS group, and the differences were statistically significant compared with the DHC group and NTS group at the same time point (P<0.01). Both the DHS group and NTS group showed a continuous growth trend in a time-dependent manner with a significantly faster growth rate in the DHS group than that of the NTS group (P<0.01). There were no statistical significances on ALT or AST levels in the DHC group (P>0.05). As time went on, the expression of ICAM-1 and HMGB-1 in the DHS group was higher than that in the previous time point (P<0.05 or P<0.01). Conclusion In desert dry and hot environment, the secondary liver injury of THS occurs early and progresses seriously. This can activate more Kupffer cells in the liver to promote the release of TNF-α and IL-1β leading to elevated expression of HMGB-1 and ICAM-1 resulting in further liver injury.