Age-related sarcopenia is a progressive, systemic skeletal muscle disorder associated with aging. It is primarily characterized by a significant decline in muscle mass, strength, and physical function, rather than being an inevitable consequence of normal aging. Despite ongoing research, there is still no globally unified consensus among physicians regarding the diagnostic criteria and clinical indicators of this condition. Nonetheless, regardless of the diagnostic standards applied, the prevalence of age-related sarcopenia remains alarmingly high. With the global population aging at an accelerating rate, its incidence is expected to rise further, posing a significant public health challenge. Age-related sarcopenia not only markedly increases the risk of physical disability but also profoundly affects patients’ quality of life, independence, and overall survival. As such, the development of effective prevention and treatment strategies to mitigate its dual burden on both societal and individual health has become an urgent and critical priority. Skeletal muscle regeneration, a vital physiological process for maintaining muscle health, is significantly impaired in age-related sarcopenia and is considered one of its primary underlying causes. Skeletal muscle satellite cells (MSCs), also known as muscle stem cells, play a pivotal role in generating new muscle fibers and maintaining muscle mass and function. A decline in both the number and functionality of MSCs is closely linked to the onset and progression of sarcopenia. This dysfunction is driven by alterations in intrinsic MSC mechanisms—such as Notch, Wnt/β‑Catenin, and mTOR signaling pathways—as well as changes in transcription factors and epigenetic modifications. Additionally, the MSC microenvironment, including both the direct niche formed by skeletal muscle fibers and their secreted cytokines, and the indirect niche composed of extracellular matrix proteins and various cell types, undergoes age-related changes. Mitochondrial dysfunction and chronic inflammation further contribute to MSC impairment, ultimately leading to the development of sarcopenia. Currently, there are no approved pharmacological treatments for age-related sarcopenia. Nutritional intervention and exercise remain the cornerstone of therapeutic strategies. Adequate protein intake, coupled with sufficient energy provision, is fundamental to both the prevention and treatment of this condition. Adjuvant therapies, such as dietary supplements and caloric restriction, offer additional therapeutic potential. Exercise promotes muscle regeneration and ameliorates sarcopenia by acting on MSCs through various mechanisms, including mechanical stress, myokine secretion, distant cytokine signaling, immune modulation, and epigenetic regulation. When combined with a structured exercise regimen, adequate protein intake has been shown to be particularly effective in preventing age-related sarcopenia. However, traditional interventions may be inadequate for patients with limited mobility, poor overall health, or advanced sarcopenia. Emerging therapeutic strategies—such as miRNA mimics or inhibitors, gut microbiota transplantation, and stem cell therapy—present promising new directions for MSC-based interventions. This review comprehensively examines recent advances in MSC-mediated muscle regeneration in age-related sarcopenia and systematically discusses therapeutic strategies targeting MSC regulation to enhance muscle mass and strength. The goal is to provide a theoretical foundation and identify future research directions for the prevention and treatment of this increasingly prevalent condition.

ObjectiveMicrotube associated protein-2 （MAP-2）， alpha-tubulin （α-tubulin）， and synaptophysin （SYP） are important proteins in neuronal signal communication. This paper observed the effects of modified Zhigancao Tang on the expression of serum α-Synuclein （α-Syn） and its oligomers， MAP-2， α-tubulin， and SYP of patients with liver and kidney deficiency of Parkinson's disease （PD）， analyzed their correlation， and evaluated the therapeutic effect of modified Zhigancao Tang in patients with liver and kidney deficiency of PD based on α-Syn transmission pathway mediated by neuronal communication in vivo. MethodsA total of 60 patients with PD who met the inclusion criteria were randomly divided into a treatment group （30 cases） and a control group （30 cases）. Both groups were treated on the basis of PD medicine， and the treatment group was treated with modified Zhigancao Tang. Both groups were treated for 12 weeks. The changes in UPDRS score， TCM syndrome score， and expression of serum α-Syn and its oligomers， MAP-2， α-tubulin， and SYP were observed before and after 12 weeks of treatment in each group. The correlation between the above-mentioned serum biological indexes and the levels of serum α-Syn and its oligomers was analyzed. ResultsAfter treatment， the TCM syndrome score， UPDRS score， UPDRS-Ⅱ score， and UPDRS-Ⅲ score of the treatment group were significantly decreased （P<0.05， P<0.01）. The UPDRS score， UPDRS-Ⅱ score， and UPDRS-Ⅲ scores in the treatment group were significantly decreased compared with those in the control group after treatment （P<0.05）. After treatment， the total effective rate of the control group was 63.3% （19/30）， and that of the treatment group was 86.7% （26/30）. The clinical effect of the observation group was better than the control group （Z=-2.03， P<0.05）. The total effective rate of the observation group was better than that of the control group， and the difference was statistically significant （χ²=5.136， P<0.05）. After treatment， the oligomer level of serum α-Syn and MAP-2 level in the treatment group were significantly decreased （P<0.05， P<0.01）. The levels of serum α-Syn and its oligomers， as well as α-tubulin in the treatment group， were significantly decreased compared with those in the control group after treatment （P<0.05， P<0.01）. Serum α-Syn was correlated with serum MAP-2 and α-Syn oligomer in patients with PD （P<0.05， P<0.01） but not correlated with serum SYP . Serum α-Syn oligomers of patients with PD were correlated with serum MAP-2 and α-tubulin （P<0.05， P<0.01） but not correlated with serum SYP level. Serum SYP of patients with PD was correlated with serum MAP-2 （P<0.05）. ConclusionModified Zhigancao Tang has a therapeutic effect on patients with liver and kidney deficiency of PD by inhibiting the production of α-Syn oligomers and intervening α-Syn microtubule transport pathway in vivo.

The chemical constituents in dried roots of Atractylodes macrocephala were investigated in this study. Through utilizing normal-phase silica gel and ODS column chromatography, TLC, and semi-preparative HPLC, 4 new sesquiterpenoids were purified from the ethyl acetate extract of A. macrocephala. By various spectroscopic techniques, such as 1D and 2D NMR, HR-ESI-MS, IR, UV, and CD, their structures were identified as atractylmacron A (1), 9β-hydroxyasterolide (2), atractylenolide H (3), atractylenolide J (4). Compound 1 possesses a rare 6/7 bicyclic skeleton.

Objective To investigate the genetic causes of auditory neuropathy with optic atrophy in a family.Methods The proband's medical history and family history were inquired in detail,and relevant clinical examina-tions were performed to confirm the diagnosis of auditory neuropathy with optic atrophy,and the genetic pedigree of the family was drawn.Peripheral blood of proband(Ⅲ-7)was collected for whole exome sequencing,and the patho-genicity of the detected mutations were interpreted.Blood samples of proband's wife(Ⅲ-8),eldest daughter(Ⅳ-7),second daughter(Ⅳ-9)and son(Ⅳ-10)were tested for mutation sites by Sanger sequencing.Combined with clinical manifestations and examination results,the family was studied.Results The genetic pattern of this family was autosomal dominant.The proband showed decreased visual acuity at the age of 19,bilateral sensorineural deaf-ness at the age of 30,and decreased speech recognition rate.Among 20 members of the family of 5 generations,10(2 deceased)showed similar symptoms of hearing and visual impairment.Proband(Ⅲ-7),eldest daughter(Ⅳ-7)and son(Ⅳ-10)underwent relevant examination.Pure tone audiometry showed bilateral sensorineural deafness.ABR showed no response bilaterally.The 40 Hz AERP showed no response in both ears.OAE showed responses in some or all of the frequencies.No stapedial reflex was detected.The eye movement of Ⅲ-7 and Ⅳ-10 were reasona-ble in all directions,and color vision was normal.Ocular papilla atrophy was observed in different degrees in fundus examination.OCT showed thinning of optic disc nerve fibers in both eyes,and visual evoked potential showed pro-longed P100 wave peak.They were diagnosed as hereditary auditory neuropathy with optic atrophy.A mutation of the OPA1 gene c.1334G＞A(p.Arg445His,NM_015560.2)at a pathogenic locus on chromosome 3 was detected by whole exon detection in Ⅲ-7.The results of generation sequencing analysis showed that the OPA1 gene c.1334G＞A(p.Arg445His,NM_015560.2)mutation of chromosome 3 was also found in Ⅳ-7 and Ⅳ-10.Meanwhile,the gen-otypes of Ⅲ-8 and Ⅳ-9 were wild homozygous,that is,no mutation occurred.Conclusion The OPA1 c.1334G＞A(p.Arg445His,NM_015560.2)mutation site might be the pathogenic mutation in this family.

BACKGROUND:Current rehabilitation programs are effective in treating post-stroke sequelae,but the treatment cycle is long and the labor cost is high.Brain-computer interface technology can be used for the treatment of post-stroke patients by extracting signals from the brain's neural activity through special equipment and converting this signal into commands that can be recognized by a computer. OBJECTIVE:To analyze and summarize the application of brain-computer interface technology in the upper limb motor function rehabilitation of stroke patients in recent years and to explore the clinical value of brain-computer interface technology in the upper limb function rehabilitation of stroke patients. METHODS:CNKI and PubMed were retrieved for relevant literature published from 2000 to 2022.The keywords were"stroke,electroencephalogram,brain-computer interface,upper limb,virtual reality technology,functional electrical stimulation,exoskeleton"in Chinese and"stroke,brain-computer interface,computer assistance,upper limb,virtual reality technology,functional electrical stimulation,exoskeleton"in English. RESULTS AND CONCLUSION:The brain-computer interface has shown promise for the restoration of upper limb motor function in stroke patients and has been shown to produce results that are unattainable with conventional treatments,and is well worth further research and promotion,but the mechanisms have not been fully elucidated.Also the ability to accurately decode all degrees of freedom of upper limb movements to provide flexible and natural control remains a challenge from the perspective of brain-computer interface systems that capture electroencephalogram signals from patients.Future research should focus on clarifying the specific neural mechanisms by which brain-computer interface technology facilitates upper limb motor recovery after stroke and identifying rehabilitation options such as brain-computer interfaces combined with external devices to facilitate upper limb motor function recovery in stroke patients.

Objective:To study the in vitro construction of functional and self-renewing cartilage organoids based on cartilage acellular extracellular matrix (ECM) microcarriers.Methods:Fresh porcine articular cartilage was taken. The merely crushed cartilage particles were set as natural cartilage group and ECM microcarriers of appropriate particle size, which were prepared by the acellular method of combining physical centrifugation and chemical extraction, were set as microcarrier group. Cartilage organoids were constructed by loading human umbilical cord mesenchymal stem cells (hUCMSCs) and human chondrocytes (hCho) with a ratio of 3∶1 with microcarriers through a rotating bioreactor. The organoids with different induction times were divided into 0-, 7-, 14-, and 21-day induction groups. The cell residues of the microcarrier group and natural cartilage group were evaluated by 4′, 6-diaminidine 2-phenylindole (DAPI) fluorescence staining and DNA quantitative analysis. The retention of microcarrier components was observed by Safranin O and toluidine blue stainnings, and the collagen and glycosaminoglycan (GAGs) levels in the microcarrier group and the natural cartilage group were determined by colorimetric method and dimethyl-methylene blue (DMMB) method. The microcarriers were further characterized by scanning electron microscopy and energy dispersive spectroscopy. The hUCMSCs cultured with Dulbecco′s Modified Eagle′s Medium (DMEM) supplemented with fetal bovine serum (FBS) in a volume fraction of 10% was used as the control group and the hUCMSCs cultured with the microcarrier extract was used as the experimental group. Subgroups of hUCMSCs cultured at 3 time points: 1, 3 and 5 days were set up in the two groups separately. Cell Counting Kit 8 (CCK-8) was used to detect the biocompatibility of the two groups. The cellular activity of the organoids of the 0-, 7-, 14-, and 21-day induction groups was detected by live/dead staining and the self-renewal ability of the cartilage organoids of the 14-day induced group was identified by Ki67 fluorescence staining. The organoids of the 7-, 14-, and 21-day induction groups were detected by RT-PCR in terms of the expression levels of chondrogenesis-related marker aggrecan (ACAN), type II collagen (COL2A1), SRY-related high mobility group-box gene-9 (SOX9), cartilage hypertrophy-and mineralization-related marker type I collagen (COL1A1), Runt-related transcription factor-2 (RUNX2), and osteocalcin (OCN). Colorimetric and DMMB assays were performed to determine the ability of organoids in the 0-, 7-, 14-, and 21-day induction groups to secrete collagen and GAGs.Results:The results of DAPI fluorescent staining showed that the natural cartilage group had a large number of nuclei while the microcarrier group hardly had any nuclei. The DNA content of the microcarrier group was (7.8±1.8)ng/mg, which was significantly lower than that of the natural cartilage group [(526.7±14.7)ng/mg] ( P<0.01). Saffranin O and toluidine blue staining showed that the microcarrier was dark- and uniform-colored and it kept a lot of cartilage ECM components. The collagen and GAGs contents of the microcarrier group were (252.9±1.4)μg/mg and (173.4±0.8)μg/mg, which were significantly lower than those of the natural cartilage group [(311.9±2.2)μg/mg and (241.3±0.7)μg/mg] ( P<0.01). Scanning electron microscopy showed that the surface of the microcarriers had uneven and interleaved collagen fiber network. The results of energy spectrum analysis showed that elements C, O and N were evenly distributed in the microcarriers, indicating that the composition of the microcarrier was uniform. The microcarrier had good biocompatibility and there was no statistical significance in the results of CCK-8 test between the control group and the experimental group after 1 and 3 days of culture ( P>0.05). After 5 days of culture, the A value of the experimental group was 0.53±0.02, which was better than that of the control group (0.44±0.03) ( P<0.05). In the 0-, 7-, 14-, and 21-day induction groups, hUCMSCs and hCho were attached to the surface of the microcarriers, with good cellular activity, and the live/death rates were (70.6±1.1)%, (80.5±0.6)%, (94.5±0.9)%, and (90.8±0.5)% respectively ( P<0.01). There were a large number of Ki67 positive cells in cartilage organoids. RT-PCR showed that the expression levels of ACAN, COL2A1, SOX9, COL1A1, RUNX2 and OCN were 1.00±0.09, 1.00±0.24, 1.00±0.18, 1.00±0.03, 1.00±0.06 and 1.00±0.13 respectively in the 7-day induction group; 4.16±0.28, 5.09±1.25, 5.65±1.05, 0.47±0.01, 1.68±0.02 and 0.21±0.06 respectively in the 14-day induction group; 13.42±0.92, 3.07±0.21, 1.84±1.08, 2.72±0.17, 2.91±0.18 and 3.32±1.20 respectively in the 21-day induction group. Compared with the 7-day induction group, the expression levels of ACAN, COL2A1, SOX9 and RUNX2 in the 14-day group were increased ( P<0.05), but COL1A1 expression level was decreased ( P<0.05), with no significant difference in OCN expression level ( P>0.05). Compared with the 7-day induction group, the expression levels of ACAN, COL1A1 and RUNX2 in the 21-day induction group were significantly increased ( P<0.01), with no significant differences in the expression levels of COL2A1, SOX9 and OCN ( P>0.05). Compared with the 14-day induction group, the expression levels of ACAN, COL1A1, RUNX2 and OCN in the 21-day group were increased ( P<0.05 or 0.01), with no significant difference in the expression level of COL2A1 ( P>0.05), but the expression level of SOX9 was decreased ( P<0.05). The contents of collagen in 0-, 7-, 14-and 21-day induction groups were (219.15±0.48)μg/mg, (264.07±1.58)μg/mg, (270.83±0.84)μg/mg and (280.01±0.48)μg/mg respectively. The GAGs contents were (171.18±1.09)μg/mg, (184.06±1.37)μg/mg, (241.08±0.84)μg/mg and (201.14±0.17)μg/mg respectively. Compared with the 0-day induction group, the contents of collagen and GAGs in 7-, 14-, and 21-day induction groups were significantly increased ( P<0.01), among which the content of collagen was the lowest in 7-day induction group ( P<0.01) but the highest in the 21-day induced group ( P<0.01); the content of GAGs was the lowest in the 7-day induced group ( P<0.01) but the highest in the 14-day induction group ( P<0.01). Conclusions:The microcarriers prepared by combining physical and chemical methods are decellularized successfully, with more matrix retention, uniform composition and on cytotoxicity. By loading microcarriers with hUCMSCs and hCho, cartilage organoids are successfully constructed in vitro, which are characterized by good cell activity, self-renewal ability, strong expression of genes related to chondrogenesis and secretion of collagen and GAGs. The cartilage organoids constructed at 14 days of induction have the best chondrogenic activity.

Objective: To analyze the influencing factors of psychological flexibility for cancer-related pain patients, so as to provide insights for improving their psychological flexibility. Methods: Cancer-related pain patients hospitalized in the Oncology Department of Anhui Cancer Hospital were selected as the subjects of the survey. Demographic information and disease information were collected through questionnaires. Pain belief was assessed using the Pain Beliefs and Perceptions Inventory. Alexithymia was assessed using the Twenty-Item Toronto Alexithymia Scale-Ⅱ. Psychological flexibility was assessed using the Psychological Inflexibility in Pain Scale. The influencing factors of psychological flexibility among cancer-related pain patients was analyzed by using a multiple linear regression model. Results: A total of 202 cancer-related pain patients were surveyed, including 114 males (56.44%) and 88 females (43.56%). The mean age was (59.99±11.53) years. The primary tumor type was digestive system cancer, with 121 cases (59.90%). The average pain intensity in the past 24 hours was mainly mild, with 150 cases (74.26%). The median pain beliefs score was -0.19 (interquartile range, 0.39) points. The total score of alexithymia was (66.86±5.60) points. The total score of psychological flexibility in cancer-related pain patients was (66.35±7.23) points. Multiple linear regression analysis showed that pain belief (β'=0.321), alexithymia (β'=0.222), and average pain intensity in the past 24 hours (β'=-0.481) were influencing factors for psychological flexibility in cancer-related pain patients. Conclusion The psychological flexibility of cancer-related pain patients is related to pain beliefs, alexithymia and average pain intensity in the past 24 hours.

ObjectiveSorafenib is a first-line only drug approved for the treatment of advanced hepatocellular carcinoma (HCC). Resistance to sorafenib means that treatment outcomes are often unsatisfactory. Although the mechanism underlying sorafenib resistance remains unclear, resistance may occur through Akt signaling pathway activation in HCC. Dihydrotanshinone (DHT), a lipophilic component of traditional Chinese medicine Salvia miltiorrhiza Bunge, has multiple anti-tumor activities and inhibits Akt activation. The effect and mechanism of DHT combined with sorafenib on HCC have not been investigated. In this study, we investigate whether DHT potentiates the anti-cancer activities of sorafenib against HCC. MethodsIn this study, the effects of sorafenib and DHT on the viability, apoptosis and drug sensitivity of Huh7 and HepG2 cells were verified by Cell Counting Kit-8 (CCK-8) and flow cytometry. Akt, P-Akt, Caspase3, GSK-3β, P-GSK-3β, ribosomal protein S6 kinase (S6K), P-S6K, Cyclin D1, Bcl-xl, Bcl-2, and Bax expression levels were analyzed via Western blot. All data were statistically compared using one-way analysis of variance (ANOVA) and Dunnett test. Statistical analysis using SPSS 20.0 statistical software. ResultsDHT inhibit proliferation and promote apoptosis in HCC cells by reducing Akt activation. DHT inhibits the expression and activation of Akt downstream factors, including GSK-3β and S6K, which regulate the apoptotic response and are activated and upregulated by sorafenib treatment. Both sorafenib and DHT downregulate cyclin D1 expression and DHT upregulates Bax expression and downregulates Bcl-2 and Bcl-xl expression. However, sorafenib had little influence on Bcl-2 family protein expression. ConclusionDHT may enhance the proliferation inhibition and apoptosis induction of sorafenib in HCC cells by inhibiting the activation of Akt signaling pathway, thus enhancing the anticancer effect of sorafenib.

Objective To investigate the clinical characteristics of female migraine patients with patent foramen ovale(PFO)and design a risk prediction model for PFO in female migraine patients(migraineur patients PFO risk prediction model,MPRPM).Methods Female migraine patients who visited Zhongshan Hospital,Fudan University from Jun 1,2019 to Dec 31,2022 were included.Preoperative information and follow-up results after discontinuation of medication were collected.Patients were divided into PFO-positive and PFO-negative groups based on transesophageal echocardiography results.A multivariate Logistic regression model and a random forest model were constructed,and the random forest model was validated multidimensionally.Key features were selected based on the mean decrease accuracy(MDA)to construct MPRPM.Results A total of 305 female patients were included in the study,with 204 patients in the PFO-positive group and 101 patients in the PFO-negative group.Multivariate Logistic regression analysis showed that age at migraine onset,attack frequency,severe impact on life during attacks,exercise-related headaches,menstruation-induced headaches,aura migraines,and a history of cryptogenic stroke were predictive factors for PFO positivity.The random forest model effectively predicted the incidence of PFO in female migraine patients,with an AUC of 0.895(95%CI:0.847-0.943).MPRPM demonstrated a sensitivity of 71.6%and specificity of 91.1%(AUC:0.862,95%CI:0.818-0.906,P<0.001).The optimal cut-off value was 2.5 points.Patients correctly classified by the model showed a higher rate of symptom improvement compared to incorrectly classified patients(94.3%vs.82.0%,P=0.023).Conclusion We identified predictive factors for PFO in migraine patients.MPRPM can provide guidance in the diagnostic process and therapeutic decision-making for female migraine patients,assist in patient triage,and reduce the healthcare burden.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.