BACKGROUND:The repair process of myocardial injury involves complex cellular and molecular mechanisms,especially mitochondrial calcium homeostasis,macrophage autophagy and pyroptosis pathways.Traditional Chinese medicine(TCM)has shown significant clinical efficacy in improving myocardial injury,but its mechanism of action needs to be thoroughly investigated. OBJECTIVE:To investigate the role of mitochondrial calcium homeostasis-mediated macrophage autophagy and pyroptosis pathways in myocardial injury,and to summarize the progress of TCM in this field. METHODS:A computerized search was performed for relevant literature from the database inception to March 2024 in the Web of Science,PubMed and CNKI.The search terms were"mitochondrial calcium homeostasis,macrophage autophagy,macrophage pyroptosis,traditional Chinese medicine,myocardial injury,myocardial injury reperfusion"in Chinese and English.Through literature review,we analyzed the relationship between mitochondrial calcium homeostasis and macrophage autophagy and pyroptosis,explored the mechanism of their roles in myocardial injury,and summarized the pathways of multi-targeted,multi-pathway effects of TCM. RESULTS AND CONCLUSION:The maintenance of mitochondrial calcium homeostasis has been found to be closely related to the normal function of cardiomyocytes.Macrophages can participate in the repair process of myocardial injury through autophagy and pyroptosis pathways.Autophagy contributes to cell clearance and regulation of inflammatory response,while pyroptosis affects myocardial repair by releasing inflammatory factors.TCM regulates mitochondrial calcium homeostasis and macrophage function through multiple mechanisms.For example,astragalosid regulates calcium homeostasis by lowering mitochondrial membrane potential and inhibiting cytochrome C,and epimedium glycoside plays a role in reducing β-amyloid deposition.In addition,herbal compounds and single drugs promote myocardial repair by activating or inhibiting specific signaling pathways,such as PI3K/AKT and nuclear factor-κB signaling pathways.Future studies should focus on the interactions between mitochondrial calcium homeostasis,autophagy and pyroptosis pathways,as well as how TCM can exert therapeutic effects through these pathways to provide new strategies and drugs for the treatment of myocardial injury.

Objective:To discussed the regulation role of calcium/calmodulin dependent protein kinase(CaMK4)on γδT cells in the pathogenesis of lupus nephritis.Methods:The proportion of γδT cells in peripheral blood of LN patients and healthy con-trols were compared by flow cytometry.Magnetic bead was used to separation LN patients and healthy controls of gamma delta T cells in peripheral blood.RNA-SEQ analysis were performed in γδT cells of peripheral blood from LN patients and healthy controls.Real-time PCR and western blot were used to verify the expression level of differential gene CaMK4.The expression levels of CD80,CD86 and CD40L on γδT cells treated with CaMK4 inhibitor were detected by flow cytometry.ELISA was used to measure the level of IL-17 secreted by γδT cells after CaMK4 inhibitor treatment.Results:The proportion of γδT cells in the peripheral blood of LN patients was lower than that of healthy control group.A total of 28 differential genes related to LN were screened by RNA-SEQ sequencing,among which CaMK4 had significant by differences at molecular level and protein level.After γδT cells from LN patients were treated with CaMK4 inhibitor,KN-93,the expressions of surface costimulatory molecules CD80,CD86 and CD40L was decreased,and the level of IL-17 also was decreased.Conclusion:CaMK4 regulates γδT cells to participate in the pathogenesis of LN by IL-17 secretion and the expression of costimulatory molecules.Inhibition of CaMK4 may become a new target for the treatment of LN.

Progressive myoclonic epilepsy (PME) is a rare epileptic syndrome closely associated with genetic factors. The disease is primarily inherited in an autosomal recessive manner, although there are rare cases that demonstrate autosomal dominant or mitochondrial inheritance. Common clinical features include myoclonus, multiple seizure types, and progressive decline in neurological and cognitive function. PME typically manifests in late childhood or adolescence but can occur at any age. It accounts for approximately 1% of epileptic syndromes among children and adolescents worldwide. In recent years, in addition to antiseizure medications, numerous non-pharmacological treatments have emerged, including dietary therapy, neuromodulatory therapy, immunomodulatory therapy, enzyme replacement therapy, gene therapy, etc. This article aims to review the research progress in the treatment of PME.

[摘 要] 目的：探讨甲状腺滤泡癌（FTC）组织中程序性死亡蛋白1（PD-1）和NOD样受体蛋白3（NLRP3）的表达及其与患者临床病理特征和预后的关系。方法：收集2015年1月至2020年6月福建医科大学附属第二医院手术切除的60例FTC患者的癌和配对癌旁组织标本，采用免疫组织化学染色法检测癌及癌旁组织中PD-1和NLRP3的阳性表达率，χ²检验或者Fisher精确检验法分析PD-1和NLRP3表达与FTC患者临床病理特征的关系，Pearson相关性分析PD-1与NLRP3表达的关系，Kaplan-Meier生存和Logistic回归分析PD-1和NLRP3表达与患者预后的关系。结果：在60例FTC组织中，PD-1和NLRP3均有较高的阳性表达率（46.67%与63.33%）。PD-1表达与FTC患者肿瘤分期、肿瘤大小、血管侵犯、复发与否具有显著相关性（均P<0.05），NLRP3表达与患者肿瘤大小、血管侵犯、甲状腺外浸润以及复发具有显著相关性（均P<0.05）。PD-1与NLRP3的表达成负相关，前者与患者更好的预后相关，后者是FTC复发的独立风险因素。结论：PD-1和NLRP3在FTC组织中有较高的阳性表达率，前者与患者更好的预后相关，后者是FTC复发的独立风险因素，且两者的表达呈负相关。

Food wastes are rich in nutrients and can be used for producing useful chemicals through biotransformation. Some oleaginous microorganisms can use food wastes to produce lipids and high value-added metabolites such as polyunsaturated fatty acids, squalene, and carotenoids. This not only reduces the production cost, but also improves the economic value of the products, thus has large potential for commercial production. This review summarized the advances in food waste treatment, with a focus on the lipid production by oleaginous microorganisms using food wastes. Moreover, challenges and future directions were prospected with the aim to provide a useful reference for related researchers.
Biofuels ; Biotransformation ; Food ; Lipids ; Refuse Disposal

Objective To investigate the clinicopathological characteristics of colon cancer patients with different mismatch repair gene (MMR) status and evaluate the value of MMR status combined with preoperative blood neutrophil-lymphocyte ratio (NLR) in predicting postoperative recurrence of colon cancer. Methods We retrospectively analyzed the pathological MMR immunohistochemistry results of 125 colon cancer patients after radical resection. Patients were divided into deficient mismatch repair (dMMR) group (n=55) and proficient mismatch repair (pMMR) group (n=70), and further divided into four groups according to MMR status and NLR level. Results Compared with the pMMR group, the patients in the dMMR group had younger onset age, larger tumor size, lower differentiation and more nerve invasion, and were more likely to occur in the right hemicolon (P < 0.05). According to the ROC curve, the NLR threshold was determined as 3. The proportion of low NLR in dMMR group was significantly higher than that in pMMR group (P < 0.05). The 3-year recurrence-free survival rate of the dMMR with low NLR group was 85.0%, significantly higher than those of the other three groups (P < 0.05); Survival analysis showed a significant advantage of the dMMR with low NLR group comparing with the pMMR with high NLR group. Conclusion dMMR colon cancer has unique clinicopathological characteristics. MMR status combined with NLR value can be used to evaluate the postoperative recurrence risk of colon cancer patients.

Objective Comparison of induction time on the proliferation of induced adipose-derived stem cells (ADSC) to differentiate into Schwann-like cells (iSC).Methods From March,2017 to October,2018,ADSCs were isolated from inguinal adipose tissue of healthy adult female SD rats.Flow cytometry was performed to detect ADSC positive markers CD29,CD90 and negative marker CD45.iSC induction medium was used to culture ADSC.S-100 and GFAP were detected by immunofluorescence staining to confirm that ADSC had differentiated into iSC.Morphological changes of cells were observed by inverted microscope on day 1st,4th,7th,10th,13rd,16th and 19th after induction.MTS assay was used to evaluate cell proliferation ability.Tunel staining was applied to assess cell apoptosis.Results Both S100 and GFAP were expressed in iSC.On day 7th,the cell proliferation rate was significantly slower than that before induction (A value was 0.330±0.020 vs.0.400±0.004,P＜0.05).It was negatively correlated with induction time.On day 19th,the proliferation rate of iSC was lower than 50％ of the proliferation rate before induction (A value was 0.016±0.003 vs.0.400±0.004,P＜0.05).Apoptosis of iSC was more obvious than ADSC at the same time point.Conclusion The proliferation ability of ADSC-induced iSC is optimal within 7 days after induction.

Objective To establish a stable experimental model of vascularized composite allograft (VCA),which would facilitate us to study of the reaction and intervening measure regarding rejection reaction in the future.Methods From September,2016 to July,2017,30 healthy male New Zealand rabbits,weighted 2.5-3.0 kg each,were chosen.Their ears should be intact without defect or necrosis.All of them were randomly and eaqually divided into 2 groups:transverse amputated group and V-shaped amputated group.In situ ear replantation after the amputation was performed.Histology analysis of skin and cartilage were done through HE and TUNEL staining,in order to compare vital rate of these ears.Results Thirty rabbits underwent ear replantation,including 13 via transverse incision and 17 via V-shaped incision.In transverse group,no ear survived,and some of them encountered vein crisis gradually after operation.The survival time ranged from 1 day to 10 days.There were 2 ears survived in V-shaped group.From HE staining,it was found certain vacuolar degenerated cells within skin and cartilage in failure ears.The rates of cell necrosis and apoptosis were higher than the survived ears.Conclusion Rabbit ear replantation model is viable.However,the rabbit ear replantation model is not suitable to be used in large samples.

Objective:To evaluate the clinical efficacy,toxicity,and prognostic factors of nab-paclitaxel as first-line treatment for elderly patients with advanced lung squamous carcinoma.Methods:This was a prospective study.Forty patients enrolled in the Second Affili-ated Hospital of Fujian Medical University were treated with nab-paclitaxel(260 mg/m2,ivggt d1),and a period of three weeks was considered as one session.The effects were evaluated after two cycles.Results:All 40 patients were followed up and appraised.Two patients achieved complete remission,13 achieved partial remission,13 achieved stable disease,and 12 achieved progressive disease. The objective response rate was 37.5% and the disease control rate was 70.0%.The progression-free survival(PFS),median overall sur-vival,and 1-year survival rate was 6.3 months,12.6 months,and 62.5%,respectively.The main hematologic toxicities were neutrope-nia and anemia,and the main non-hematologic adverse events were fatigue,constipation,nausea,vomiting,muscle aches,and hear-ing loss.Most patients could tolerate these toxic reactions.Moreover,Cox multivariate regression analysis showed that the neoplasm stage,Eastern Cooperative Oncology Group performance status,response rate,and PFS were independent factors for the survival rate (P<0.05),while age was not related to patient prognosis(P>0.05).Conclusions:Nab-paclitaxel as single drug and first-line therapy for elderly patients with advanced lung squamous carcinoma is effective and safe.

OBJECTIVETo investigate the effect of mammalian target of rapamycin(mTOR) inhibitor-rapamycin on cognitive function after chronic cerebral ischemia in mice and its molecular mechanism.

METHODSThe chronic cerebral ischemia model was induced by ligation of right common carotid artery (rUCCAO) in 6-week-old ICR mice. The expressions of mTOR, S6K, S6 and corresponding phosphorylated proteins were detected by Western blotting at different time interval (1 h, 3 h, 6 h, 24 h, 3 d, 7 d, 2 w, 4 w, 6 w) after rUCCAO to determine the changes of mTOR signaling pathway. Rapamycin was administrated i.p. at the dose of 3.0 mg/kg 24 h after rUCCAO. Fluoro Jade B staining was used to detect the apoptotic cells. The expressions of Beclin and LC3-Ⅱ were detected by Western blotting to determine the status of autophagy. Morris water maze test and Y maze test were performed to evaluate cognitive functions.

RESULTSThe mTOR signaling pathway was abnormally activated from 6 h to 6 w after rUCCAO in mouse cortex. The activation of mTOR signaling pathway induced by rUCCAO was reversed by administration of rapamycin, and the apoptotic cell number was significantly decreased (146.1±16.3 vs 84.5±9.6,<0.05). Meanwhile, the elevation of Beclin and LC3-Ⅱ protein induced by rUCCAO was reversed by rapamycin administration. Furthermore, compared with vehicle-treated mice, the latent period[(11.1±2.3) s vs (8.1±1.8) s,<0.05] and swimming distance[(672.8±128.5) cm vs (558.2±124.9) cm,<0.05] were significantly decreased and the number of crossing the platform quadrant in Morris water maze increased(2.8±0.9 vs 5.2±0.8,<0.05) in rapamycin-treated mice. Correct response rate in the Y maze was also increased significantly in rapamycin-treated mice[(38.5±9.2)% vs (64.9±7.9)%,<0.05].

CONCLUSIONSInhibiting mTOR pathway by rapamycin reverses the rUCCAO-induced cognitive impairment partly through the suppression of apoptosis and autophagy.