Malignant tumor metastasis is the key factor leading to poor prognosis of patients， and it is a difficult problem to be overcome in the field of tumor therapy. Metabolic reprogramming， as a key link in the regulation of tumor metastasis activity， affects the growth， invasion， and metastasis of tumor cells by changing the metabolic pathways of intracellular substances （such as glucose， amino acids， lipids， and nucleotides）. In particular， metabolic reprogramming plays a key role in the multistage linked steps related to tumor metastasis and can play a crucial role in several key stages of tumor tissue dissociation in situ， hematogenous metastasis， and remote colonization. Malignant tumor cells can selectively adjust their own metabolic state to adapt to the growth conditions of different metastatic microenvironments and colonization sites and then choose the most favorable growth and metabolism strategy. According to the holistic concept of traditional Chinese medicine （TCM）， the metastasis of malignant tumors is generally closely related to the metabolic state of the whole body. One of the advantages of TCM in the treatment of malignant tumors is systemic regulation. With its multi-pathway， multi-target， and multi-component therapeutic characteristics， TCM can effectively control the metastasis of malignant tumors by regulating the degradation of tumor epithelial mesenchymal transformation （EMT） and extracellular matrix （ECM）， anchoring the independent growth of tumor cells and the tumor microenvironment. In this paper， the potential regulatory effects of metabolic reprogramming on the metastasis of malignant tumors were discussed， and the latest research progress of the regulation of metabolic reprogramming by TCM on tumor metastasis was reviewed. At the same time， the key targets of TCM and its bioactive components in the process of tumor metastasis intervention were reviewed. This study aims to provide a more valuable basis and clearer idea for the treatment of malignant tumor metastasis by regulating metabolic reprogramming with TCM.

Platelet transfusion refractoriness (PTR) is one of the common problems in platelet transfusion, significantly impacting patient clinical outcomes and increasing the demand for allogeneic platelet transfusion. Both immune and non-immune factors contribute to PTR, among which the occurrence mechanism of immune platelet transfusion refractoriness (IPTR) involves humoral and cellular immune processes and is influenced by platelet storage, processing, and the patient's disease, therapy and immune status. This review comprehensively discusses the research related to the factors for alloimmune of IPTR, the mechanism of platelet clearance and its influencing factors. Furthermore, it explores feasible prevention and treatment measures such as platelet compatibility transfusion and clinical treatments. The aim is to provide a systematic cognition for a deeper understanding of the pathological process of platelet alloimmunization and clearance, and to provide a theoretical basis for the construction of precise clinical prevention and treatment strategies for IPTR, as well as to explore feasible research directions in this field in the future.

Objective:To compare the surgical outcomes of robotic natural orifice specimen extraction surgery (NOSES) and robotic-assisted radical resection for rectal cancer.Methods:A retrospective analysis using propensity score matching (PSM) was conducted on 547 patients who had undergone radical resection of rectal cancer at the First Affiliated Hospital of Nanchang University from June 2018 to March 2024. The study cohort comprised 157 patients in the robotic NOSES group and 390 in the robotic-assisted group. PSM was used in a 1:1 manner to match relevant general clinical preoperative data of the study patients (age, sex, body mass index, preoperative comorbidities, abnormal preoperative carcinoembryonic antigen (>6.5 μg/L) and carbohydrate antigen 19-9 levels (>27 kU/L), preoperative American Society of Anesthesiologists score, tumor diameter, tumor distance from the anal margin, and TNM stage), with a clamp value of 0.05. After performing PSM to match the general clinical data of the two groups of patients, 77 patients in each of the robotic NOSES and robotic-assisted groups were included in the analysis. We found no statistically significant difference in preoperative general clinical data between the robot NOSES and robot-assisted groups ( P>0.05). We compared the surgical outcomes, postoperative recovery, postoperative pathological data, and incidence of complications between the robotic NOSES and robot-assisted groups. Results:Compared with the robot-assisted groups. the robot NOSES group had a significantly shorter time to first postoperative passage of flatus (48 [38, 50] hours vs. 56 [50, 60] hours, Z=-7.513, P<0.001), time to taking a liquid diet (60 [54,63] hours vs. 66 [62, 72] hours, Z=-6.303, P<0.001), lower pain scores (3 [3, 4] vs. 4 [4, 5], Z=-5.237, P<0.001), and lower incision infection rates (0 vs. 5 [6.5%], χ 2=5.237, P=0.028) within 24 hours after surgery ( P<0.05). However, there were no significant differences in surgical time, intraoperative blood loss, postoperative hospital stay, postoperative anastomotic complications, or incidence of other complications between the two groups (all P>0.05). Conclusion:Robotic NOSES surgery is a safe and feasible procedure for resecting rectal cancer and postoperative recovery is faster after robotic NOSES than after standard robot-assisted surgery.

Vector flow imaging(VFI)is an innovative ultrasound flow measurement technology.Compared with the traditional color Doppler and spectral Doppler,VFI has the advantages of independence of angle correction and direct acquisition of real-time amplitude and direction of flow.Transverse oscillation(TO)method is one of the effective methods for vector flow imaging.However,a complete and detailed algorithm validation process based on commercial ultrasound machines is still lacking due to more complex convex probes.This study starts with introducing the imaging process and principle of transverse oscillation vector flow technique,and calculates the error between the set velocity value and the measured velocity value through the simulation experiment,and verifies the error between the set velocity value and the measured velocity value through the Doppler flow phantom experiment.Among them,the velocity value measured by the TO vector flow technique in the simulation experiment is 0.48 m/s and the preset value is 0.50 m/s,the error between them is-4％.The velocity values are 8.33,11.14,14.44 and 16.67 cm/s measured by the Doppler flow phantom experiment,the actual velocity values are 7.97,10.78,14.06 and 17.34 cm/s,the errors between them are all within±5％.Both experiments verify the feasibility of using vector flow technique on abdominal convex probe.

Objective To investigate the role and possible mechanisms of transactive response DNA binding protein 43 (TDP-43)in mediating neuronal injury induced by oxidative stress in mouse neuro-2a (N2a)cells and mouse pain sensitization.Methods ①To evaluate the optimal induction concentration,N2a cells were treated with different concentrations of H2O2,and the cells were divided into control group,200,400 and 800 μmol/L H2O2 groups.②To assess the optimal induction duration,N2a cells were treated with 400 μmol/L H2O2,and the cells were divided into control group,and the cell groups treated for 6,12 and 24 h,respectively.③To validate the mitochondrial DNA (mtDNA)release pathway,cyclosporin A (CsA) was used to inhibit the mitochondrial permeability transition pore (mPTP),and the cells were divided into control group,24 h H2O2 group and 24 h H2O2+CsA group.④To validate TDP-43-mediated cellular damage,the cells were divided into control group,24 h H2O2 group and 24 h H2O2+siTDP-43 group.⑤Cell viability was assessed using CCK-8 assay,while cell proliferation was determined using EdU assay.Western blot analysis was employed to examine the expression levels of TDP-43,neuronal nuclei (NeuN),cyclic GMP-AMP synthase (cGAS),and stimulator of interferon genes (STING).qPCR was utilized to measure the release of mtDNA.Immunostaining was conducted to observe intracellular expression of TDP-43,and Calcein AM staining was employed to evaluate mPTP opening status.⑥To elucidate the role of TDP-43 in neuropathic pain (NP),24 healthy SPF male C57BL/6J mice (6～8 weeks old,25～30 g)were randomly divided into control group,chronic constriction injury (CCI)group,and CCI+siTDP-43 group.In 1 d before and 7,14 and 21 d after surgery,intrathecal injections of siTDP-43 were administered.Mechanical and thermal pain thresholds of the mice were assessed using von Frey filaments and radiant heat,respectively,on 1 preoperatively and 1,3,5,7,14 and 21 d postoperatively.Immunofluorescence assay was conducted on 21 d postoperatively to examine the changes in TDP-43 and NeuN in the lumbar spinal dorsal horn (L5-L6).Results Oxidative stress induced a significant increase in TDP-43 protein level in N2a cells,prompted mtDNA release through mPTP,markedly up-regulated the expression of cGAS and STING,and consequently impacted the viability of N2a cells (P<0.05).CsA treatment inhibited mPTP channel opening and thus effectively blocked mtDNA release (P<0.05),down-regulated TDP-43 and thus significantly reduced mtDNA release,suppressed the expression of cGAS and STING,and finally restored the proliferation ability of N2a cells (P<0.05).The mechanical and thermal pain thresholds exhibited a significant decrease since 5 d after CCI,which then persisted until 21 d (P<0.05).The expression of TDP-43 in spinal cord dorsal horn neurons was increased in the mice in 21 d after CCI (P<0.05),and intrathecal injection of siRNA inhibited TDP-43 expression and effectively increased the mechanical and thermal pain thresholds in the CCI mice (P<0.05).Conclusion Oxidative stress induces an up-regulation in TDP-43 protein in neurons,which stimulates the release of mtDNA into the cytoplasm through mPTP,and subsequently activates the cGAS/STING pathway,and finally,results in neuronal injury and pain sensitization in CCI mice.

Objective To investigate the effects of damaged nerve-derived mitochondrial DNA (mtDNA)on GRP75 protein expression,mitochondrial Ca2+level and apoptosis in human glioblastoma cell line U-87MG (U87)cells,and its mechanism of inducing pain sensitization in mice.Methods Chronic constriction injury (CCI) of the sciatic nerve was used to establish a mouse model of neuropathic pain (NeP).A total of 20 male C57BL/6 mice (6～8 weeks old,weighing 20～30 g)were randomly divided into sham group,and CCI-7,-14 and CCI-21 d groups.Paw withdrawal mechanical threshold (PWMT)was measured,and the changes in mtDNA content in the spinal cord were detected with quantitative real-time PCR (qPCR).After mtDNA was extracted from human neuroblastoma cells (SH-SY5Y)treated with H2O2,U87 cells were treated with mtDNA at a dose of 0～1 ng/μL.CCK-8 assay was utilized to detect cell viability,and the appropriate concentration was selected according to the results.Then U87 cells were divided into:control group,mtDNA group,mtDNA+GRP75 inhibitor (MKT-0771 μg/mL)group,mtDNA+calcium chelator (BAPTA-AM10 μmol/L)group,and mtDNA+MKT-077+BAPTA-AM group.MKT-077 and BAPTA-AM were pre-treated in 2 h before mtDNA treatment,respectively.Western blotting was employed to assess the expression of glucose-regulated protein 75 (GRP75) protein,and endoplasmic reticulum-mitochondrial colocalization staining was conducted to observe the endoplasmic reticulum-mitochondrial junction.Calcium ion fluorescent probe was used to measure mitochondrial Ca2+levels.The oxidative stress and function of mitochondria were evaluated by reactive oxygen species (ROS)and mitochondrial membrane potential.PI fluorescent labeling was employed to examine apoptotic rate of U87 cells.Results Compared with the sham group,the cytochrome C oxidase I (CO1)and nicotinamide adenine dinucleotide dehydrogenase 1 (ND1),which were utilized to measure mtDNA content in the spinal cord of mice in the CCI-21 group,were increased (1.01±0.20 vs 2.22±0.26,P<0.05,1.00±0.12 vs 1.79±0.07,P<0.05).CCK-8 assay showed that mtDNA (1 ng/μL) inhibited U87 cell viability (P<0.01).mtDNA (0.2 ng/μL) up-regulated the expression of GRP75 protein (P<0.05),promoted endoplasmic reticulum-mitochondrial coupling,and consequently increased mitochondrial Ca2+level (109.4±62.6 vs 540.3±150.3,P<0.05)and production of ROS (P<0.05).After MKT-077 or/and BAPTA-AM treatment,the level of mitochondrial Ca2+was decreased,the mitochondrial membrane potential was improved,and the apoptotic rate of U87 cells was reduced by PI assays (mtDNA vs mtDNA+MKT-077:18.39±2.09 vs 13.22±1.42,P<0.05;mtDNA vs mtDNA+BAPTA-AM:18.39±2.09 vs 12.09±1.53,P<0.05;mtDNA vs mtDNA+MKT-077+BAPTA-AM:18.39±2.09 vs 11.65±2.09,P<0.05).Conclusion Damaged nerve-derived mtDNA can up-regulate the expression of GRP75,interfere with mitochondrial Ca2+level and exacerbate mitochondrial oxidative stress to induce apoptosis in U87 cells,which may be a novel mechanism involved in NeP formation.

Objective UPLC-Q-TOF-MS integrated molecular network strategy was used to rapidly analyze and identify the chemical components of Yuye detoxification Particle. Methods The secondary mass spectrometry data of compounds were obtained using mass spectrometry scanning in both positive and negative ion mode. The similarity of MS/MS fragmentation patterns was calculated to create the global natural product social molecular networking (GNPS) platform. The major components in Yuye detoxification Particle were quickly identified according to the molecular clusters with similar structures in GNPS. Manual analysis and identification of other compounds were performed according to the mass fragment ion information of the primary and secondary mass spectrum data and related references by using the molecular feature extraction (MFE) function of Agilent Masshunter Qualitative Analysis workstation and traditional Chinese Medicine composition database (TCM-DATA). Results A total of 89 compounds in Yuye detoxification Particle were identified by LC-MS,including 22 phenoliacids,21 flavonoids and their glycosides,6 iridoid glycosides,28 triterpenoid saponins and 12 other types of ingredients. Conclusion UPLC-Q-TOF-MS/MS integrated molecular network technology can be used for rapid and systematic identification of chemical components of Yuye detoxification Particle,which provides theoretical basis for its quality control and clinical application. The established molecular network can provide reference for rapid qualitative analysis of components of traditional Chinese medicine compound.

Ghrelin is a hormone produced by the stomach that regulates energy metabolism after acting on the central nervous system.Cocaine amphetamine-regulated transcriptional peptide(CART)neurons participate in the regulation of feeding behavior and energy balance.It is known that CART neurons are influenced by hormones to regulate energy homeostasis,but whether ghre-lin exerts its pro-appetite function by influencing CART neurons is unknown.Therefore,this study focuses on the role of VMHCART neurons in the regulation of feeding and relative body weight by ghrelin.Firstly,the whole brain expression of CART was determined by immunofluorescence.Then the effect of intraperitoneal injection of ghrelin on the expression of DMHCART neurons was evalua-ted.Finally,the ghrelin was delivered to DMH and the changes of food intake and relative body weight of mice were measured.CART immunoreactive neurons were detected in medial preoptic nucleus(MPA),arcuate nucleus(ARC),dorsomedial hypothalamic nucleus(DMH),thalamic pa-raventricular nucleus(PVT)and raphe nucleus(ROb).Compared with the control group,periph-eral injection of ghrelin significantly increased the expression of DMHC ART immunoreactive neurons(P=0.037 3).DMH long-term injection of ghrelin resulted in an increase in body weight(P=0.004 0)and feed intake(P=0.023 1).The results provide anatomical evidence for the whole brain distribution of CART,which proves that ghrelin affects feed intake and body weight of mice through CART neurons in DMH,suggesting that specific neuron types and regional specificity are involved in ghrelin regulation of feed intake and energy homeostasis.

Vesicular glutamate transporter 2(VGlut2)is expressed in the PVN of the hypothalamic paraventricular nucleus(PVNVG1ut2)as an excitatory neurotransmitter,which regulates food intake and energy metabolism and plays an important role in maintaining homeostasis.However,it is not clear that the upstream and downstream projection network of PVNVGut2 neurons hinders the anal-ysis of glutamatergic neuron circuit function.Anterograde and retrograde tracer viruses were injec-ted into the PVN of VGlut2 mice by stereotactic brain injection technique to find the input and output nuclei of PVNVGlut2 neurons.Anterograde tracing results showed that PVNVGlut2 neurons pro-jected to the downstream medial amygdala(MeAD)and arcuate nucleus(ARC).Retrograde trac-ing results showed that PVNVGlut2 received input from the prefrontal nucleus(Pr),the reticular tegmental nucleus(RtTg),and the hypoglossal nucleus(12N).In addition,VGlut2 was found to be co-expressed with neuronal nitric oxide synthase(nNOS)neurons in the PVN.The anatomical net-work of PVNVG1ut2 neurons was analyzed by virus tracking tool,which laid the anatomical founda-tion for further study on the functional regulation of PVNVGlut2.

Purpose/Significance To analyze the multidimensional interaction between the characteristics of traditional Chinese and western medicine in patients with type 2 diabetes mellitus and its influence on traditional Chinese medicine(TCM)syndrome differentia-tion.Method/Process Based on the real-world electronic medical record(EMR)data,the traditional association rule algorithm is im-proved,and the important TCM syndromes are screened out as dependent variables by increasing the respect index,and the logistic regres-sion algorithm is used to explore the influence of traditional Chinese and western medicine indexes on TCM syndromes.Result/Conclusion Based on 688 patients,112 association rules are obtained,of which 12 includes TCM syndromes.The respect of association rules between middle-earth stagnation syndrome and overweight/obesity is the highest,moreover,overweight/obesity patients have a higher prevalence rate of middle-earth stagnation syndrome.There is a strong correlation between middle-earth stagnation syndrome,peripheral neuropathy or hypertension and overweight/obesity.Patients with diabetic nephropathy are more likely to have qi and yin deficiency syndrome.