Association between the Missense Variant of PLCE1 and the Risk of Colorectal Cancer

Colorectal cancer(CRC) is a malignancy of the digestive system that poses a serious threat to human life and health. Approximately 1.93 million new CRC cases were identified in 2020, including0.94 million CRC-related deaths worldwide, which accounted for 10% of the global cancer incidence and 9.4% of all cancer-related fatalities[1].

Clinical Significance and Function of MALAT1 Gene Expression and the rs619586 Polymorphism in Colorectal Cancer

Colorectal cancer(CRC) is a malignant tumor of the digestive system that poses a serious threat to human health. In 2018, around 1.8 million people were newly diagnosed with CRC, and 881,000 people died from the disease. The identification of CRCrelated genes and genetic polymorphisms will aid in the prevention and treatment of this disease.

Role of cytokines in atherosclerotic inflammation response: A review

Cytokines play an important role in the pathological process of atherosclerosis(AS),affecting the progression and prognosis of cerebrovascular diseases concerned with AS.Cytokines mainly include C-reactive protein,interleukin,tumor necrosis factor,chemotactic cytokines,matrix metalloproteinases,etc.These These cytokines promote or inhibit the inflammatory response and plaque formation during AS process through different targets and mechanisms.A comprehensive understanding of the cytokines in the occurrence and development of AS is conducive to search for new therapeutic targets and drugs.

GTF2H4 regulates partial EndMT via NF-κB activation through NCOA3 phosphorylation in ischemic diseases

Partial endothelial-to-mesenchymal transition(EndMT)is an intermediate phenotype observed in endothelial cells(ECs)undergoing a transition toward a mesenchymal state to support neovascularization during(patho)physiological angiogenesis.Here,we investigated the occurrence of partial EndMT in ECs under hypoxic/ischemic conditions and identified general transcription factor IIH subunit 4(GTF2H4)as a positive regulator of this process.In addition,we discovered that GTF2H4 collaborates with its target protein excision repair cross-complementation group 3(ERCC3)to co-regulate partial EndMT.Furthermore,by using phosphorylation proteomics and site-directed mutagenesis,we demonstrated that GTF2H4 was involved in the phosphorylation of receptor coactivator 3(NCOA3)at serine 1330,which promoted the interaction between NCOA3 and p65,resulting in the transcriptional activation of NF-κB and the NF-kB/Snail signaling axis during partial EndMT.In vivo experiments confirmed that GTF2H4 significantly promoted partial EndMT and angiogenesis after ischemic injury.Collectively,our findings reveal that targeting GTF2H4 is promising for tissue repair and offers potential opportunities for treating hypoxic/ischemic diseases.

Efficacy Observation on Auricular Point Sticking Combined with Cupping in Treating Insomnia

Objective:To observe the clinical efficacy of auricular point sticking combined with cupping in treating insomnia.Methods:Sixty-four patients with chronic insomnia were randomly divided into two groups.Thirty-two patients in the treatment group were treated with auricular point sticking combined with cupping therapy;while thirty-two patients in the control group were treated by Diazepam.The Pittsburgh sleep quality index(PSQI)were observed before and after treatment,and the data were statistically analyzed to evaluate the clinical effect.Results:After treatment,PSQI scores in both groups after treatment significantly decreased(P<0.05),and there was a significant difference between the two groups(P<0.05).In the improvement of daytime function,the treatment group was more efficient than the control group(P<0.05).The total effective rate of the treatment group was higher than that of the control group(P<0.05).Conclusion:Auricular point sticking combined with cupping therapy for insomnia is more effective than oral Diazepam,and it has a better effect in improving the patient's daytime function.

miR-130b inhibits proliferation and promotes differentiation in myocytes via targeting Sp1

Muscle regeneration after damage or during myopathies requires a fine cooperation between myoblast proliferation and myogenic differentiation.A growing body of evidence suggests that microRNAs play critical roles in myocyte proliferation and differentiation transcriptionally.However,the molecular mechanisms underlying the orchestration are not fully understood.Here,we showed that miR-130b is able to repress myoblast proliferation and promote myogenic differentiation via targeting Sp1 transcription factor.Importantly,overexpression of miR-130b is capable of improving the recovery of damaged muscle in a freeze injury model.Moreover,miR-130b expression is declined in the muscle of muscular dystrophy patients.Thus,these results indicated that miR-130b may play a role in skeletal muscle regeneration and myopathy progression.Together,our findings suggest that the miR-130b/Sp1 axis may serve as a potential therapeutic target for the treatment of patients with muscle damage or severe myopathies.

Nanotechnology for cardiovascular diseases

Cardiovascular diseases have become the major killers in today’s world,among which coronary artery diseases(CADs)make the greatest contributions to morbidity and mortality.Although state-of-the-art technologies have increased our knowledge of the cardiovascular system,the current diagnosis and treatment modalities for CADs still have limitations.As an emerging cross-disciplinary approach.