Objective:To explore the acupoint selection law of acupuncture and moxibustion in treating diabetic gastroparesis (DGP) using data mining technology.Methods:The clinical literature on acupuncture and moxibustion treatment for DGP was retrieved from CNKI, Wanfang Data, VIP, SinoMed, PubMed, the Cochrane Library from the establishment of the databases to July 31, 2023. The acupoint prescriptions were extracted to Excel 2016 to establish a database, and the statistics of acupoint frequency, meridian, distribution site and specific acupoint use were collected. SPSS Modeler 18.0 was used to analyze the association rules among acupoints, and SPSS Statistics 25.0 was used for clustering analysis and factor analysis to summarize the acupoint selection law for acupuncture treatment of DGP.Results:Totally 153 articles were included, involving 59 acupoints, with a total frequency of 802 times. The 5 most frequently used acupoints were "Zusanli" (ST 36), "Zhongwan" (CV 12), "Neiguan" (PC 6), "Sanyinjiao" (SP 6), "Pishu" (BL 20). The commonly used meridians were stomach meridian, Conception Vessel and bladder meridian. The involved acupoints were mostly located in the chest-abdomen and lower limbs, and most of them were Wushu acupoints, Mu acupoints, and Xiahe acupoints. The core acupoints group was "Zusanli (ST 36)-Zhongwan (CV 12)-Neiguan (PC 6)-Pishu (BL 20)-Weishu (BL 21)-Sanyinjiao (SP 6)-Tianshu (ST 25)", 24 groups of association rules, 5 effective clusters and 6 factors were obtained.Conclusion:Acupuncture and moxibustion treatment of DGP focuses on both spleen and stomach, treating both symptoms and root causes, and uses methods of combining acupoints such as distant and near matching, combining Mu acupoints, and Xiahe acupoints, and combining of Wushu acupoints and Mu acupoints, to achieve the therapeutic effect of nourishing yin and tonifying qi, dispelling upper abdominal fullness and resolving turbidity, and harmonizing stomach and strengthening spleen.

Gastroparesis is a gastric disease characterized by delayed gastric emptying."Vomiting"is the main clinical manifestation of this disease,while"atrophy"indicates dysfunction of the stomach.Based on the theory of"atrophy,dyspnea and vomiting are ascribed to the upper part",originating from the Chapter of"Zhi Zhen Yao Da Lun"from the Suwen(Basic Questions)section this paper explored the pathogenesis and treatment idea of gastroparesis from the function of the lung.It is put forward that failure of lung qi in dispersion,so the lung qi cannot maintain the circulation of harmonizing qi and blood,leading to malnutrition of stomach and loss of stomach receiving food and drink function.Melancholy impairing lung,so lung cannot govern diffusion,leading to stomach governing the disfunction of dredging and descending.Impaired depurative descending of lung qi,so the large intestine and stomach are lost in the alternating operation of deficiency and excess,leading to stomach governing the disfunction of transportation and transformation.Therefore,the treatment approach is proposed to improve the stomach's function to receive food and drink,transport and transform and promote the recovery of gastric motility by replenishing and restoring lung qi,regulating emotions and catharsis and smoothing lung.Analyzing the effect of function of the lung on gastric motility is of great value for expanding the application of traditional Chinese medicine in gastrointestinal motility disorders,and digging new connotations of classic theories in modern clinical practice.

Objective:To explore the genetic etiology and clinical phenotype of Feingold syndrome due to chromosome 2p24.3p24.2 microdeletion.Methods:The clinical data of a child admitted to Henan Provincial People′s Hospital in November 2021 and diagnosed as Feingold syndrome type 1 (FGLDS1) associated with chromosome 2p24.3p24.2 microdeletion were collected. The clinical and genetic variation characteristics of the patient were summarized, and 10 patients with chromosome 2p microdeletion reported until November 2022 were reviewed.Results:The boy was 12 years and 5 months old. He presented with backward physical development, motor development retardation, low intelligence, special body and facial appearance, finger developmental deformity and other manifestations, accompanied by hyperactivity and aggressive behavior, impulsive irritability, self-injury and other behavior problems. The proband showed normal chromosome karyotype; the genome-wide copy number variant sequencing and trio-whole exome sequencing revealed a 2.61 Mb deletion at chromosome 2p24.3p24.2 region, and 10 genes including MYCN gene (exons 1 to 3) in the deleted region.The same deletion was not found in either of his parents. The genetic features of 11 cases (including this case) with chromosome 2p microdeletion were summarized, all of whom had insufficient haploid dosage of the MYCN gene due to chromosome 2p microdeletion, and the clinical manifestations of these 11 patients matched the clinical diagnosis of FGLDS1. Conclusion:The proband is consistent with the clinical presentation of the typical Feingold syndrome, and the haploinsufficiency of the MYCN gene due to the microdeletion of chromosome 2 is the genetic etiology of the proband.

Ferroptosis is a form of programmed cell death driven by iron-dependent lipid peroxidation and is closely associated with a wide range of biological processes, such as aging, immunity, and cancer. Tumor multidrug resistance, especially resistance to apoptosis, has prompted the urgent search for a new antitumor treatment option. Remarkable progress has been made in the study of the role of ferroptosis in antitumor, especially the interaction with immune cells. Studying immunotherapy based on ferroptosis pathways has become a new direction in antitumor research. In this work, we review the role of ferroptosis in immune cells and antitumor immunotherapy to provide new ideas for ferroptosis-mediated antitumor immunotherapy.

Oxcarbazepine(OXC)is a new antiepileptic drug developed through structural variation of carbamazepine and widely used for the patient who cannot tolerate carbamazepine. Although OXC has a lower risk of cutaneous adverse drug reactions(cADRs)than carbamazepine,it has been reported that OXC-induced cutaneous adverse drug reactions(OXC-cADRs)are prevalent and may lead to drug discontinua-tion. HLA-B﹡15:02 is associated with oxcarbazepine-induced SJS/TEN,but not maculopapule,which is similar to carbamazepine. In addition,HLA-A﹡13:02,HLA-B﹡38:02 and HLA-B﹡40:02 are HLAⅠtype genes which is related to oxcarbazepine-induced maculopapule(OXC-MPE),and HLA-DRB1﹡04:03 was first HLA class Ⅱ gene found associated with OXC-MPE. The risk factor of OXC-cADRs is still not completely clear. Age,gender,weight and total dose of medication were not correlated with OXC-MPE. Allergy induced by antiepileptic drugs and non-antiepileptic drug induced allergy may be risk factors of OXC-cADRs. Attention should be paid to cross-allergic reactions before using oxcarbazepine for patients with a history of carbamazepine-induced allergy. Genetic test is not currently recommended in patients with maculopapule. Aromatic antiepileptic drugs should be avoided in patients with positive expression of HLA-B﹡15:02 gene.

Oxcarbazepine(OXC)is a new antiepileptic drug developed through structural variation of carbamazepine and widely used for the patient who cannot tolerate carbamazepine. Although OXC has a lower risk of cutaneous adverse drug reactions(cADRs)than carbamazepine,it has been reported that OXC-induced cutaneous adverse drug reactions(OXC-cADRs)are prevalent and may lead to drug discontinua-tion. HLA-B﹡15:02 is associated with oxcarbazepine-induced SJS/TEN,but not maculopapule,which is similar to carbamazepine. In addition,HLA-A﹡13:02,HLA-B﹡38:02 and HLA-B﹡40:02 are HLAⅠtype genes which is related to oxcarbazepine-induced maculopapule(OXC-MPE),and HLA-DRB1﹡04:03 was first HLA class Ⅱ gene found associated with OXC-MPE. The risk factor of OXC-cADRs is still not completely clear. Age,gender,weight and total dose of medication were not correlated with OXC-MPE. Allergy induced by antiepileptic drugs and non-antiepileptic drug induced allergy may be risk factors of OXC-cADRs. Attention should be paid to cross-allergic reactions before using oxcarbazepine for patients with a history of carbamazepine-induced allergy. Genetic test is not currently recommended in patients with maculopapule. Aromatic antiepileptic drugs should be avoided in patients with positive expression of HLA-B﹡15:02 gene.

The chemical constituents of Rosa chinensis Jacq were diverse ,mainly including flavonoids ,flavonoid glyco-sides ,phenolic acids ,aromatic oils ,tannins and pigments .Its extract and some chemical constituents had shown multiple phar-macological activities ,such as antitumor ,antifungal ,anti-viral ,anti-oxidation etc ..The advances in the study on chemical com-ponents and pharmacological actions of Rosa chinensis Jacq were reviewed and its application prospect was prospected .

Endoplasmic reticulum plays a key role in both basic structure formation and function performance of microenviron-ment. Endoplasmic reticulum homeostasis unbalance caused by endoplasmic reticulum stress has become a hot research topic in recent years. This paper focuses on the role of endoplasmic retic-ulum stress in ischemic stroke. Research progress of related sig-naling pathways were reviewed, especially mechanisms through which endoplasmic reticulum stress trigger the inflammatory reac-tion, so as to provide a new research method for prevention of is-chemic stroke.

The target of rapamycin ( TOR) , a Ser/Thr protein kinase of PIKKs ( phosphatidylinositol kinase-related kinases ) , is the central factor of a highly conserved signaling pathway in eukaryotes , and regulates cell growth in response to nutrients , hor-mones, and stresses.It controls temporal growth by activating anabolic processes such as translation , ribosome biogenesis , protein syn-thesis, transportation of amino acid and metabolic enzymes .The advances in TOR pathway in the most pervasive human fungal patho-gen Candida albicans.

Objective To investigate the protective effects and mechanism of TG 6 on myocardial ischemia/reperfusion injury . Methods the protective effects of TG 6 on myocardial ischemia/reperfusion was investigated by setting up models of ischemia and reperfusion of rats induced by ligating the left coronary anterior descending artery in vivo,isolated rat hearts through an improved Lange-ndorff device, and hypoxia /reoxygenation injury of neonatal rat cardiomyocytes , and the serum CK,LDH,T-SOD, MDA were taken as research markers .Results TG6 significantly reduced the myocardial infarct size , decreased the activity of CK and the content of MDA in serum, reduced the activity of LDH, and increased the activity of T-SOD in vivo;TG6 obviously increased the coronary blood flow after low rate perfusion and reperfusion , decreased the content of MDA and the leakage of CK , LDH in myocardial tissue , elevated the activity of T-SOD in vitro of isolated rat hearts;TG6 had no effects on cells in normal growth condition , raised the viability of cardio-myocytes significantly, and reduced the rate of CK leakage and the content of [Ca2+]i obviously in Na2S2O4 treated cells in vitro of neonatal rat cardiomyocytes .Conclusion TG6 could effectively protect myocardial ischemia/reperfusion injury .