Severe intestines ischemia throughout sufferers using significant coronavirus19 COVID19

288C>A];[962T>C] (p.[Ser96Arg];[Leu321Pro]) mutations. Due to the rarity in prevalence, early detection of the said disorder is critical; early treatment may result in improved outcomes, which may have potential significance for newborn screening.The objective of the current study was to analyze the expression of mir-29a-5p, osteosclerotin and fetuin-A in patients with chronic kidney disease and their correlation with vascular calcification. For this purpose, 162 patients with chronic kidney disease treated in our hospital from January 2020 to January 2022 were selected retrospectively, and then 162 healthy people who underwent physical examination with our hospital in the same period were selected. The expressions of serum mir-29a-5p, sclerostin and fetuin-A were analyzed after fasting venous blood was drawn from the two groups. According to the coronary artery calcification score (CACS), patients with chronic kidney disease were divided into the calcification group (69 cases) and the non-calcification group (93 cases). The expressions of mir-29a-5p, sclerostin and fetuin-A in the two groups were analyzed, and the correlation between the three in chronic kidney disease and vascular calcification was analyzed. Results showed that compared with the concorrelated with vascular calcification.Protein tyrosine phosphatase-1B (PTP-1B) is a well-known therapeutic target for diabetes and obesity as it suppresses insulin and leptin signaling. PTP-1B deletion or pharmacological suppression boosted glucose homeostasis and insulin signaling without altering hepatic fat storage. Inhibitors of PTP-1B may be useful in the treatment of type 2 diabetes, and shikonin, a naturally occurring naphthoquinone dye pigment, is reported to inhibit PTP-1B and possess antidiabetic properties. Since the cell contains a large number of phosphatases, PTP-1B inhibitors must be effective and selective. To explore more about the mechanism underlying the inhibitor's efficacy and selectivity, we investigated its top four pharmacophores and used site-directed mutagenesis to insert amino acid mutations into PTP-1B as an extension of our previous study where we identified 4 pharmacophores of shikonin. The study aimed to examine the site-directed mutations like R24Y, S215E, and S216C influence the binding of shikonin pharmacophores, which act as selective inhibitors of PTP-1B. To achieve this purpose, docking and molecular dynamics simulations of wild-type (WT) and mutant PTP-1B with antidiabetic compounds were undertaken. The simulation results revealed that site-directed mutations can change the hydrogen bond and hydrophobic interactions between shikonin pharmacophores and many residues in PTP-1B's active site, influencing the drug's binding affinity. These findings could aid researchers in better understanding PTP-1B inhibitors' selective binding mechanism and pave the path for the creation of effective PTP-1B inhibitors.Liver cancer poses a great threat to the life safety of patients, which is a common malignant tumor worldwide. This study aims to explore the effect of miR-144 negatively regulating CCNB1 on the biological behavior of liver cancer cells, including the proliferation, apoptosis and migration of liver cancer cells, so as to provide a sufficient biological basis for the treatment of liver cancer. A 3 armour hospital at the records of 100 patients with liver cancer in 2015-2019 as the research object, and resection of the liver cancer cells and tissue adjacent to carcinoma as the research samples, using polymerase chain reaction (PCR) for the organization of miR-144 gene and detect CCNB1 protein expression level, and by using a technique called RNA interference to silence the CCNB1 gene, and try to transfer by transfection CCNB1 protein, thus all kinds of biological behaviour of hepatocellular carcinoma cells. The liver tissue of miR-144 is low, the level of gene expression CCNB1 protein expression level is higher, the expression level in liver cancer cells directly influences the curative effect of hepatocellular carcinoma patients, the miR-144 gene can negative regulation CCNB1 protein, through this kind of negative adjustment to the biological behavior of liver cancer cells have a profound impact.An experiment was carried out to investigate the effect of hesperetin on isoproterenol-induced H9C2 cardiomyocyte hypertrophy and its possible mechanism. For this aim, H9C2 cardiomyocytes were coincubated with different concentrations of hesperetin (0.125, 0.25, 0.5, 1μmol/L) and isoproterenol to detect the changes in the area of H9C2 cells, the expression of cardiac hypertrophy marker β-MHC mRNA and autophagy marker LC3II; H9C2 cells were coincubated with hesperetin and isoproterenol at the optimal intervention concentration, and the intervention time was set to 6h, 12h, 24h, respectively, and the changes of H9C2 cell area, β-MHC mRNA and LC3II expression were detected. Results showed that hesperetin could reduce isoproterenol-induced H9C2 cardiomyocyte area enlargement; hesperetin can reduce β-MHC mRNA expression in isoproterenol-induced H9C2 cardiomyocyte; hesperetin can increase the expression level of LC3II in isoproterenol-induced H9C2 cardiomyocyte. Conclusion Hesperetin may improve the hypertrophy of H9C2 cardiomyocytes induced by isoproterenol by activating autophagy.The study aimed to investigate the influences of edaravone on necroptosis-related proteins and oxidative stress in rats with lower extremity ischemia/reperfusion (I/R) injury. The normal group (n=10), model group (lower extremity I/R injury model, n=10), treatment group (treatment with edaravone, n=10) and intervention group [lower extremity I/R injury model intervened with necrostatin-1 (Nec-1), n=10] were set. A conventional biochemical test was adopted to detect hepatic function indexes, and an enzyme-linked immunosorbent assay was performed to measure the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), malondialdehyde (MDA), superoxide dismutase (SOD) and myeloperoxidase (MPO). The apoptosis level in rat tissues was determined via terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL) assay. The expression levels of genes and proteins were measured via quantitative polymerase chain reaction (qPCR) and Western blotting assay. The content of serum alkaline phosphate stress in rats with lower extremity I/R injury by inhibiting the RIPK1-MLKL signaling pathway.Ulcerative colitis (UC) is a chronic inflammatory disease. Studies in China and foreign countries have shown that vitamins have anti-inflammation and immunoregulation functions in patients with UC, but the specific mechanism is not yet clear. In this study, the levels of inflammatory cytokines in the intestinal mucosa, serum inflammatory indexes, oxidative stress indexes and immune-related indexes were detected, and their correlations with vitamin deficiency and clinical significance were discussed. Enzyme-linked immunosorbent assay (ELISA) was adopted to detect the serum level of 25-hydroxyvitamin D3, immunohistochemistry was applied to examine the expression of inflammatory cytokines in the intestinal mucosa, serum inflammatory indexes, oxidative stress indexes and immune-related indexes were measured, and their correlations were analyzed. Inflammatory and oxidative stress indexes in the UC group were notably higher than in the control group. The Vitamin deficiency group had more inflammatory cytokines than the normal vitamin group. Oxidative stress indexes such as superoxide dismutase (SOD) and malondialdehyde (MDA) in the vitamin deficiency group were significantly different from those in the normal vitamin group, but no difference was found in myeloperoxidase (MPO). Immune-related indexes, complement 3 (C3) and interferon-gamma (IFN-γ), in the normal vitamin group were higher than those in the vitamin deficiency group. Besides, interleukin-4 (IL-4) (r=-0.37, p=0.04) and IL-1β (r=-0.31, p=0.04) had significant correlations with vitamins. Vitamins in patients with UC have significant correlations with inflammatory responses in vivo, which can be used to predict inflammatory responses in vivo and have strong clinical significance. Vitamins are also related to oxidative stresses to some extent but have little effect on immune-related indexes.Circular RNAs (circRNAs) are characterized as a class of new noncoding RNAs and function in tumorigenesis of colorectal cancer (CRC). In our study, the molecule mechanism of circ_0022340 in CRC was investigated. For this aim, quantitative real-time polymerase chain reaction (RT-qPCR) was used to test gene expression in CRC cells. Cell function assays including 5-ethynyl-20-deoxyuridine (EdU), colony formation and transwell investigated the proliferation and migration capacity in CRC cells. Luciferase reporter and RNA immunoprecipitation (RIP)assays determined the interaction between circRNA, miRNA and mRNA. Western blot was used to test protein expression. An immunohistochemistry assay was used to assess the tumor growth in vivo. Results showed that Circ_0022340 was highly expressed in CRC cells. Circ_0022340 was formed from exon 5 to 6 of the synaptotagmin 7 (SYT7). Silencing of circ_0022340 suppressed CRC cell proliferation and migration. Functionally, circ_0022340 recruited heterogeneous nuclear ribonucleoprotein C (HNRNPC) to stabilize EBF1 mRNA and thereby activated SYT7. Moreover, circ_0022340 targeted miR-382-5p to up-regulate ETS transcription factor ELK1 (ELK1). It is concluded that Circ_0022340 promoted colorectal cancer progression via recruiting HNRNPC to stabilize EBF1 mRNA and thereby activated SYT7 or miR-382-5p/ELK1 axis, which might provide a novel target for CRC treatment.With the development of chronic kidney disease (CKD), the patients showed a gradual decline in renal function, which eventually progressed to end-stage renal disease (ESRD), accompanied by various cardiovascular and cerebrovascular events. Maintenance hemodialysis (MHD) is one of the effective methods to treat ESRD, but some patients still die from cardiovascular and cerebrovascular complications. The purpose of this study was to investigate the relationship between troponin T (TnT), n-terminal brain natriuretic peptide (NT-proBNP), cardiac structure and function and cardiovascular disease in maintenance hemodialysis patients. In this experimental study, 100 patients with MHD were randomly selected as research objects. According to the level of NT-proBNP before dialysis, they were divided into two groups, namely the low NT-proBNP group and the high NT-proBNP group. The clinical and biological indicators and the average value of echocardiography were detected in the two groups. The degree of CKD disease was divided into six stages according to GFR, and the influence of different stages on the cardiac function of CKD patients was detected. The experimental results showed that the levels of TnT and NT-proBNP in MHD patients were significantly increased, and the levels of TnT and NT-proBNP and cardiac function were correlated with the patients with cardiovascular diseases. Cardiac ultrasound confirmed that the NT-proBNP level of patients with left ventricular hypertrophy was significantly higher than that of patients without left ventricular hypertrophy, and the difference between the two was statistically significant (P less then 0.005).Vascular calcification is one of the major complications of chronic kidney disease (CKD), which could be further accelerated by the osteogenic transition and apoptosis of smooth muscle cells, thereby advancing the progression of renal diseases and increasing the mortality rate of cardiovascular events. MicroRNA is a kind of key regulator in the phenotypic transition of vascular smooth muscle cells (VSMCs), but its role remains unclear in VSMCs. In this study, VSMCs were stimulated by platelet-derived growth factors - BB (PDGF-BB) in varying concentrations to establish the VSMC dysfunction models. The relative expression of miR-29a-5p was quantified via the quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation of VSMCs was determined via the BrdU method, analysis of cell cycle via flow cytometry, and the migration of VSMCs via Transwell assay. Expression of γ-secretase activating protein (GSAP) and markers of VSMC differentiation, including α-SMA, SM-22α, SMMHC and Calponin, was quantif5p/GSAP might be a potential target for the treatment of vascular calcification.The study aimed to explore the clinical efficacy of transjugular intrahepatic portosystemic shunt (TIPS) in treating cirrhotic portal hypertension and relevant influencing factors. 100 patients with cirrhotic portal hypertension receiving TIPS in the 980 hospitals of PLA logistic force from January 2015 to January 2018 were enrolled. Blood was collected from patients to detect liver function indicators [aspartate aminotransferase (AST) and alanine aminotransferase (ALT)], renal function indicators [blood urea nitrogen (BUN) and creatinine (Cr)], glucose metabolism indicators [insulin and glucose (GLU)] and inflammatory factors [interleukin-6 (IL-6), IL-8 and CXCL9] before surgery and at1 and 6 month(s) after surgery. Surgical efficacy was evaluated. The physique of patients was examined. The portal venous pressure, diameter and hemorheological indicators of patients were measured. Additionally, postoperative complications and nursing satisfaction were observed. At 1 and 6 month(s) after an operation, the levels of AST, ALT, BUN, Cr, insulin, GLU and inflammatory factors IL-6, IL-8 and CXCL9 and the portal venous pressure were overtly reduced (p less then 0.05), the postoperative dry weight was increased (p less then 0.05), the postoperative nursing satisfaction was 97%, the patients with higher satisfaction had fewer complications (p less then 0.05), the diameter of the portal vein was notably lowered (p less then 0.05), while the blood flow rate was remarkably raised (p less then 0.05). After the application of TIPS in the treatment of cirrhotic portal hypertension, the liver function, renal function, glucose metabolism and portal venous pressure and flow rate of patients return to normal, and postoperative complications are clearly reduced after postoperative nursing, proving the overall efficacy. Hence, TIPS is worthy of popularization and application.Head and neck squamous cell carcinoma(HNSCC) is a malignant epidermal tumor that seriously threatens human life and health. The main factors affecting the death of patients are local recurrence and lymph node metastasis. Astrin antibody is the basic component of the mitotic spindle required for normal chromosome separation and later development. There are few domestic studies on the mechanism of Astrin in HNSCC. Based on this, this article is studying Astrin in HNSCC. The expression and function of Astrin, and analyze its correlation with clinical pathological parameters and prognosis of patients, and further explore the relevant mechanisms involved in the progression of Astrin in HNSCC. In this experiment, the real-time fluorescent quantitative polymerase chain reaction (PCR) method was used to detect the expression of the Astrin antibody in HNSCC cell lines A and B. Secondly, this article will focus on high metastatic HNSCC cells B. Divided into five groups (blank control group, overexpression positive group, overexpression negative control group, expression suppression positive group, expression suppression negative control group), using real-time fluorescent quantitative PCR technology to detect the expression of Astrin in each group, and then speculate the mechanism of Astrin in HNSCC. Experiments have shown that Astrin is expressed in A and B cells, but its expression in B is significantly higher than its expression in A, and the difference is statistically significant (P less then 0.001). This shows that the inhibition of Astrin expression has a significant anti-tumor effect and that Astrin plays an important role in the occurrence and development of tumors. It is expected to provide new ideas and reference basis for exploring new therapeutic strategies for targeted therapy of HNSCC.In recent years, it has been found that miRNA has a very close relationship with cardiovascular system diseases. Heart disease is accompanied by a change of the miRNA expression spectrum. Changing the expression of miRNA in or out of cells can cause heart diseases such as myocardial infarction, hypertrophy or arrhythmia. Mitogen-activated protein kinases (MAPKs) are important transmitters of cell surface signals to the nucleus. The family influences the biological responses of cells (e.g., proliferation, differentiation, transformation and apoptosis) by affecting the transcription and regulation of genes in animal cells. Based on the above background, the purpose of this study was to study the effect of the mir-1-mediated AMPK pathway on cardiomyocyte apoptosis in hypertensive rats. The expression level of miRNA-1 in cultured rat H9c2 cardiomyocytes was detected by real-time PCR to determine the success of the transfection. MTT method was used to detect the cell viability. Flow cytometry was used to detect the cell apoptosis, and real-time PCR and Western blot were used to detect the mRNA and protein expression of bcl-2. The results were compared with those of H9c2 cells (blank control group) and miRNA negative control fragments (negative control group). As an important kinase regulating energy homeostasis, AMPK is one of the central regulators of metabolism in eukaryotic cells and organisms, responsible for regulating cellular capacity input and output and maintaining the smooth functioning of cellular physiological activities. At the same time, AMPK is a key protein involved in a variety of signaling pathways. The results showed that the apoptosis rate of myocardial cells in the miRNA-1 group decreased (0.710 ± 0.009661)% vs (1.066667 ± 0.02603)% compared with that in the spontaneous hypertension control group (P less then 0.001). The transfected miRNA-1mimics can up-regulate the expression of miRNA-1 in cells, inhibit the proliferation of cardiomyocytes and promote apoptosis.To analyze the changes and correlation of Mir-129 and Mir-29A-5p in vascular calcification in end-stage renal disease. A total of 97 patients with end-stage renal disease admitted to our hospital from August 2021 to August 2020 were selected as the research objects, and another 97 healthy people who underwent physical examination in our hospital during the same period were selected as the control study. According to X-ray examination, 97 subjects were divided into the vascular calcification group (39 cases) and the non-vascular calcification group (58 cases). Blood samples were extracted from each group, and the expressions of serum Mir-129 and Mir-29A-5p were detected by RT-PCR after centrifugation. The expressions of Mir-129 and Mir-29A-5p in healthy people with end-stage renal disease and vascular calcification were analyzed. To analyze the correlation of Mir-129 and Mir-29A-5p in vascular calcification of end-stage renal disease and its correlation with vascular calcification of end-stage renal disease. Cositively correlated with vascular calcification in end-stage renal disease (R =5.426, P=0.001). Mir-129 was positively correlated with vascular calcification in end-stage renal disease (r=0.649, P=0.001). Mir-29a-5p was positively correlated with vascular calcification in end-stage renal disease (r=0.529, P=0.001). Mir-129 and Mir-29a-5p showed high expression in the patients with end-stage renal disease, and they also increased with the occurrence of vascular calcification, and they showed a positive correlation in the vascular calcification of end-stage renal disease.The purpose of this study was to establish a rat asthma model and extract MUC5AC to explore the mechanism of mucin 5AC (MUC5AC) signaling pathway regulating the function of asthmatic airway smooth muscle cells (ASMC) and participating in asthmatic airway remodeling. Western blot was used to detect β-catenin (β-catenin), glycogen synthase kinase-3β (GSK-3β), proto-oncogene MUC5AC and cyclin D1 (cyclin D1) in MUC5AC of asthmatic and normal groups. After inhibiting the interaction between β-catenin and transcription cofactor p300 / CBP in ASMC of the asthma group and control group, the cell viability and cycle changes of ASMC were detected by the CCK-8 method and flow cytometry. After inhibiting the activity of P38 mitogen-activated protein kinase (MAPK), the protein expression changes of c-Myc and cyclin D1 were detected by Western blot. Results showed that comprehensive HE staining results of lung tissue sections indicate that the experimental rat model of asthma airway remodeling was successfully established.t/β-catenin signaling pathway can regulate the proliferation and differentiation of ASMC by up-regulating the expression level of cMyc. Cyclin D1 interacts with the MAPK signaling pathway, thereby affecting the function of ASMC and participating in asthma airway remodeling.It has been noted that temozolomide resistance occurs in a number of malignancies, including glioma, although the underlying cause of this is unknown. The goal of the study in vivo investigation to show that increased CD147 expression in glioma cells is a factor in their resistance to the chemotherapy drug temozolomide. Proliferation assays, TUNEL assays, reactive oxygen species assays, protein degradation assays, immunohistochemistry, Western blotting, quantitative polymerase chain reactions, and tumorigenicity assays were all carried out. Using the human protein atlas databases, the expression levels of CD147 in different kinds of malignancies were examined. For immunohistochemistry, a total of 7, 12, 19, 15, and 16 glioma samples were taken from para-carcinoma tissue, representing stage I, stage II, stage III, and stage IV gliomas, respectively. The expression of CD147 proteins is correlated with the tumor's aggressiveness. Cell development was slowed by suppressing the expression of the CD147 protein. The expression of the CD147 protein contributed to the emergence of temozolomide resistance. Expression of the CD147 protein reduced mRNA expression. The growth-inhibitory impact of temozolomide on glioma cells was enhanced by the suppression of CD147 protein. Nuclear factor E2-related factor 2 expression and CD147 protein expression showed a significant reciprocal connection with each other (p 0.0001, r2 = 0.3254). In glioma, resistance to temozolomide is due to overexpression of CD147 protein and induction of nuclear factor E2-related factor 2.Pelvic organ prolapse is seriously harmful to women's health and daily activities, and the incidence rate increases with age, which is more common among middle-aged and elderly women. Common treatment schemes are prone to relapse or complications. The purpose of this article was to study the clinical effect of laparoscopic pelvic floor reconstruction without mesh implantation in the treatment of pelvic organ prolapse and the influence of postoperative serum inflammatory factors, stress indicators, urination function and sexual function. The clinical curative effect of the operation plan was evaluated by the determination of POP-Q value and objective cure rate. The enzyme-linked immunosorbent assay determined the serum inflammatory factors and stress indexes before and after the operation. Urination function was detected by a urodynamics detector, and sexual function was investigated by a PISQ-12 questionnaire. The results show that laparoscopic pelvic floor reconstruction without mesh implantation has good clinical efficacy in the treatment of pelvic organ prolapse, with less stimulation to patients and less inflammation. After the operation, the patient's maximum urine flow rate exceeded 18mL/s, the sexual function score exceeded 45 points, and the urination function and sexual function were effectively improved.Glioma is a malignant tumor originating from the central nervous system. Glioma is the incidence rate of the central nervous system in adults. Nanotechnology has been widely used in drug delivery in vivo, achieving targeted drug delivery through surface modification. At the same time, the samples measured by NMR have no bias to all compounds, and there is no need for specific internal standards for quantification. Therefore, based on the use of nuclear magnetic resonance technology, this paper analyzed the inhibitory effect of nano-targeted micelles combined with in vitro radiotherapy on glioma. The results show that the coupling constants of β - CH3 of Ala and β - CH3 of Lac are close. It is difficult to distinguish the spectral lines of Ala and Lae by 1.5T NMR. DHA-PLys(s-s)P can efficiently deliver drugs across BBB and into brain parenchymal cells to release drugs. Due to its increased stability in the systemic circulation, DHA-PLys(s-s)P can help to improve drug delivery efficiency. The DNA damage of U87 and U251 cells was more serious than that of C6 cells. There was a positive correlation between DNA damage and Cho/Cr ratio, indicating that nano-targeted micelles combined with in vitro radiotherapy have an inhibitory effect on glioma.The highest mortality rate among cancer patients is lung cancer. A large proportion of cancer patients are lung cancer patients. The incidence rate of lung cancer is the highest in the world. In recent years, long-chain non-coding RNA, or LncRNA, has become more and more closely related to cancer and has gradually attracted the attention of many cancer researchers. LncRNA is the proto-oncogene of cancer. We can find out the cause of cancer and put forward effective methods to inhibit the occurrence of cancer by studying LncRNA. This study aimed to investigate the effect of noncoding long-chain RNA16 on the proliferation and molecular mechanism of lung cancer cells. During the operation, the distance between the excised lung cancer block and the adjacent tissue is 2cm from the corresponding lung cancer block. Then, the total RNA in lung cancer cells and tissues is extracted with a Trizole reagent. Then, the expression profile of LncRNA in three cases of lung cancer and the corresponding adjacent tissue is identified by RNA chip technology. The LncRNA related to proliferation and the expression difference is significant through bioinformatics. The conclusion was that the A549 and H1299 groups of shLncRNA16 could significantly reduce the incidence by 64% and 40% percentage points compared with the experimental group, which indicates that LncRNA16 can be used as a potential treatment target for patients.Fibromyalgia syndrome (FMS) is a multifactorial disease characterized by chronic diffuse pain. Genetic factors are also involved in the etiology. However, there is not enough information on the genetic factors that play a role in the pathogenesis of FMS. The aim of this study is to investigate the relationship between estrogen receptor 1 gene (ESR1) 594G>A (rs2228480) and 325C>G (rs2295190) polymorphisms and fibromyalgia syndrome (FMS). A total of 294 women, 146 of who were FMS patients and 148 of whom were healthy controls, were enrolled in the study. The instruments used to collect data from patients included patient follow-up form, Visual Analogue Scale (VAS), and Fibromyalgia Impact Questionnaire (FIQ). Genotyping of ESR1 594G>A and 325C>G polymorphisms in the extracted DNA samples was performed using an RT-PCR device and TaqMan hydrolysis probes. It was found that, for rs2295190 polymorphism, patients with CG and GG genotypes versus CC genotypes showed a decreased risk for FMS (OR 0.442; 95% CI 0.234-0.833). But there were no significant differences were found in the genotype distribution of rs2228480 polymorphism between the FMS patients and controls. The intragroup evaluation of FMS patients revealed no significant association between symptoms, pain score, FIQ score, and polymorphisms (p>0.05). We are of the opinion that there is a significant association between ESR1 rs2295190 polymorphism and FMS and that this polymorphism may be protective against FMS. However, there is a need for comprehensive studies on different populations to obtain clearer data as well as further studies to elucidate the possible mechanism of association.Non-coding RNAs (ncRNAs) are important molecular modulators in diverse pathological processes, influencing the occurrence and progression of carcinomas. Thoracic aortic aneurysm (TAA) is an infrequent disease among aneurysmal diseases and accounts for nearly 3% of diagnosed aneurysms. The functional roles of long ncRNA (lncRNA) XIST and miR-193a-5p and the associated molecular mechanisms are yet to be investigated. In the current study, we discovered that miR-193a-5p was expressed at low levels in the blood of TAA patients. Further, loss-of-function and gain-of-function assays disclosed that miR-195-3p impacted the proliferation ability of TAA cells. XIST was found to be the most overexpressed lncRNA among predicted lncRNAs binding to miR-193a-5p. The promotive function of XIST in TAA was also explored. Subsequently, KLF7 was proved to be the downstream factor of the XIST/miR-193a-5p axis. Rescue assays testified the whole regulation mechanism of the XIST/miR-193a-5p/KLF7 axis in TAA. MiR-193a-5p was absorbed by XIST for the improvement of KLF7 in TAA. These results concluded that XIST might be engaged in TAA pathogenesis via regulation of the miR-193a-5p/KLF7 axis, supplementing more therapeutic options for TAA treatment.This study aimed to evaluate the effect of various heating temperatures on the antioxidant activities of camel milk caseins. The samples were processed with three different heat treatments Pasteurization at low and high temperatures and boiling. Fresh camel milk (unheated) was used as a control. Camel milk caseins were separated by fast ion exchange liquid chromatography (FPLC) and identified by the sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS page). The antioxidant activities of caseins were measu- red by three different in vitro methods 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity, 2, 2'-azino-bis (3-ethylbenzthiazoline-6-sulfonate) (ABTS) radical scavenging activity and ferric reducing power assay (FRAP). The antioxidant activity evaluated by the DPPH assay decreased significantly (p less then 0.05) with the increase in heat treatment of caseins. However, there was no significant difference in ABTS radical scavenging activity and Ferric Reducing Antioxidant Power assay (FRAP) of heat-treated camel caseins compared to unheated onesStill, a decrease was observed in those activities by the increase of temperature in the different casein concentrations.