OBJECTIVE: To review the latest research advancements in surgical techniques for the treatment of limb lymphedema. METHODS: The relevant literature at home and abroad in recent years was extensively reviewed, and the research on the treatment of limb lymphedema by surgical techniques were summarized and analyzed. RESULTS: Lymphovenous anastomosis has demonstrated good effectiveness for early to mid-stage limb lymphedema, however its long-term effectiveness and applicability for late-stage limb lymphedema still require further validation. Autologous lymphatic/venous grafting has shown clinical feasibility in the treatment of secondary limb lymphedema. Research on tissue-engineered lymphatic scaffolds remains insufficient, primarily due to the complexity of lymphatic anatomical structures and the technical challenges involved. Nevertheless, its potential application is promising. Vascularized lymph node flap transplantation has shown significant effectiveness in treating limb lymphedema, particularly yielding good outcomes in upper limb cases. However, it can not guarantee a complete cure for the condition. Charles' operation is the most effective treatment option for patients with late-stage limb lymphedema, but its extensive incision and severe postoperative complications limit its application. Liposuction has the advantages such as minimal invasiveness, high safety, and repeatability. It is suitable for patients with late-stage limb lymphedema who have failed conservative treatment or developed adiposity. However, its effectiveness is limited in patients with significant limb fibrosis. CONCLUSION Current treatments for limb lymphedema require further improvement, and there is considerable debate regarding treatment strategies for different stages of the condition. Future high-quality, multi-system combined treatment approaches are anticipated to guide clinical practice.
Humans ; Lymphedema/surgery* ; Surgical Flaps/blood supply* ; Lymphatic Vessels/surgery* ; Anastomosis, Surgical/methods* ; Lymph Nodes/transplantation* ; Lipectomy/methods* ; Extremities/surgery* ; Treatment Outcome ; Tissue Engineering ; Tissue Scaffolds ; Veins/transplantation*

Objective:To investigate whether neoadjuvant therapy can improve the prognosis of patients with pancreatic cancer.Methods:A retrospective case-control study analyzed data from the Surveillance, Epidemiology, and End Results (SEER) database on 12, 103 patients who underwent surgical treatment between January 1, 2010, and December 31, 2021. Patients were divided into the neoadjuvant therapy group ( n=3 276) and the upfront surgery group ( n=8 827) based on whether they received neoadjuvant treatment. The neoadjuvant therapy group included 2 342 patients receiving neoadjuvant chemotherapy and 934 patients receiving neoadjuvant chemoradiotherapy. The upfront surgery group consisted of 4 335 patients receiving adjuvant chemotherapy, 1 987 patients receiving adjuvant chemoradiotherapy, 63 patients receiving adjuvant radiotherapy, and 2 442 patients undergoing surgery alone. Propensity score matching was used to eliminate group differences and create a cohort with no statistical differences in other clinicopathological features except for the grouping variable. Variables such as age, gender, tumor location, race, population of residence, tumor diameter, household income, TNM stage, and information on radiotherapy and chemotherapy were used for 1∶1 case matching. T stage, N stage, and the use of radiotherapy or chemotherapy were matched exactly. After matching, 1 182 patients were included in each group: the neoadjuvant therapy group contained 1 155 patients receiving neoadjuvant chemoradiotherapy and 27 receiving neoadjuvant chemotherapy, while the upfront surgery group comprised 848 patients receiving adjuvant chemotherapy and 334 receiving adjuvant chemoradiotherapy. TNM staging was reported according to the 7th edition of the AJCC guidelines. The primary outcome was overall survival. Measurement data with skewed distributions were expressed as M( Q1, Q3), and intergroup comparisons were conducted using the Wilcoxon rank-sum test. Categorical data were compared using the chi-square test or the Fisher′s exact test. The Log-rank test and subgroup analyses to assess interactions between neoadjuvant therapy and subgroup in COX regression models were used to compare survival benefits across variables. Landmark analysis was performed to create segmented survival curves, studying the impact of neoadjuvant therapy on prognosis during different follow-up periods. Results:The neoadjuvant therapy group had a higher proportion of T 4 tumor involving celiac axis, superior mesenteric artery, and/or common hepatic artery compared to the upfront surgery group (14.7% vs 2.8%, P<0.001). Additionally, significant differences were observed between groups in terms of race, location, population of residence, age, tumor diameter, tumor stage, and adjuvant therapy regimen ( P<0.05). The median overall survival time in the neoadjuvant therapy group was 30 months, compared to 22 months in the upfront surgery group ( P<0.001). In the neoadjuvant therapy group, the median survival was 30 months for both neoadjuvant chemotherapy and chemoradiotherapy patients; in the upfront surgery group, it was 26 months for both adjuvant chemotherapy and chemoradiotherapy patients, 17 months for adjuvant radiotherapy patients, and 12 months for surgery-only patients. After propensity score matching, there were no differences in the distribution of clinical characteristics between groups ( P>0.05), and all patients in the matched cohort had received chemotherapy. The matched neoadjuvant therapy group had a longer median overall survival compared to the upfront surgery group (30 months vs 27 months, P<0.001). Subgroup interaction analysis revealed that T stage had a significant interaction with neoadjuvant therapy, both before (T 4 stage: HR=0.382, 95% CI: 0.319-0.458; T 2-T 3 stages: HR=0.696, 95% CI: 0.656-0.738; T 1 stage: HR=1.199, 95% CI: 0.867-1.657; interaction P<0.001) and after matching (T 4 stage: HR=0.581, 95% CI: 0.414-0.814; T 2-T 3 stages: HR=0.827, 95% CI: 0.734-0.931; T 1 stage: HR=1.320, 95% CI: 0.716-2.433; interaction P=0.043). Subgroup interaction analysis indicated that T 1 patients did not benefit from neoadjuvant therapy; survival curves plotted for matched T 1 patients showed no difference in survival between the neoadjuvant therapy group and the upfront surgery group ( P=0.323). Conversely, non-T 1 (T 2-T 4) stage patients showed significant survival benefits in both unmatched and matched cohorts ( P<0.001). Landmark analysis showing that the survival benefits occurred mainly in the early postoperative period of up to 3 years ( P<0.001), but there was no difference in overall survival between the neoadjuvant therapy group and the upfront surgery group of >3 years ( P>0.05). Patients with Arterial invasion (T 4 stage compared to T 1-T 3 stages) showed a similarly significant interaction with the benefit of neoadjuvant therapy in both the pre-matching cohort (interaction P<0.001) and the post-matching cohort (interaction P=0.037). Patients with T 4 stage disease in the neoadjuvant therapy group had longer overall survival compared to the upfront surgery group (median overall survival in pre-matching cohort: 30 months vs 13 months, P<0.001; median overall survival in post-matching cohort: 28 months vs 18 months, P=0.001). Among T 4 stage patients in the post-matching cohort, neoadjuvant therapy provided significant survival benefits during the early postoperative period of up to 3 years ( P=0.001). However, there was no difference in overall survival between the neoadjuvant therapy group and the direct surgery group beyond 3 years( P=0.729). Conclusions:The prognosis in the neoadjuvant therapy group was better than in the upfront surgery group. Propensity score matching and subgroup interaction analysis showed that non-T 1 and T 4 stage patients benefited more from neoadjuvant therapy, with benefits mainly seen in the early postoperative period (≤3 years).

BACKGROUND:Scaffold materials serve as platforms that provide space and structure,playing a crucial role in the regeneration of cartilage tissue.Scholars from around the world are exploring different approaches to fabricate more ideal scaffold materials. OBJECTIVE:To review the design principles and preparation methods of cartilage scaffolds,and to further explore the advantages and limitations of various preparation methods. METHODS:Literature searches were conducted on the databases of CNKI,WanFang Data,PubMed,and FMRS from 1998 to 2023.The search terms were"cartilage repair,cartilage tissue engineering,cartilage scaffold materials,preparation"in Chinese and English.A total of 57 articles were ultimately reviewed. RESULTS AND CONCLUSION:(1)The articular cartilage has a unique structure and limited self-repair capacity after injury.Even if self-repair occurs,the newly formed cartilage is typically fibrocartilage,which is far inferior to normal articular cartilage in terms of structure and mechanical properties.It is difficult to maintain normal function and often leads to degenerative changes.Currently,the design and fabrication of scaffold materials for cartilage repair need to consider the following aspects:biocompatibility and biodegradability,suitable pore structure and porosity,appropriate mechanical properties,and bioactivity.(2)Research on the preparation of cartilage scaffolds has made significant progress,continuously introducing new preparation methods and optimization strategies.These methods have their advantages and disadvantages,providing more possibilities for customized preparation and functional design of cartilage scaffolds according to specific requirements.

Objective:To preliminarily investigate the risk factors for distant metastasis and prognosis, and construct a prognostic nomogram in T 4 stage pancreatic cancer. Methods:A retrospective case-control study was conducted using data from the Surveillance, Epidemiology, and End Results (SEER) database for pancreatic patients from January 1, 2010, to December 31, 2021. Based on whether the tumor invaded the celiac axis, superior mesenteric artery, and/or common hepatic artery, 38 759 patients were divided into an arterial invasion group (T 4 stage, n=7 471) and a non-arterial invasion group (non-T 4 stage, n=31 288). Clinical and pathological data, including demographic characteristics, treatment information, and tumor data were collected. The primary outcome was overall survival. Categorical data were expressed as numbers (percentages), and intergroup comparisons were made using the chi-square test. Survival benefits were measured using the Log-Rank test. A multivariate logistic model was used to identify high-risk factors for metastasis in T 4 stage pancreatic cancer. Patients were randomly divided into training ( n=5 232) and validation ( n=2 239) sets at a 7∶3 ratio. A nomogram model was created based on independent prognostic factors from the multivariate Cox regression analysis, and the model′s predictive ability was evaluated using the C-index and calibration curves. Results:The overall metastasis rate in the arterial invasion group was higher than that in the non-arterial invasion group (32.8% vs 29.0%, P<0.001), with fewer patients showing no metastasis or single-organ metastasis (86.3% vs 89.7%, P<0.001) and higher rates of lung metastasis ( P<0.001), distant lymph node metastasis ( P<0.001), and other metastases excluding liver, lung, brain, bone, and distant lymph node metastases ( P<0.001). However, no significant difference was found between groups for liver, brain, or bone metastasis rates ( P>0.05). Surgical rates for T 4 stage patients were significantly lower than for non-T 4 stage patients (all patients: 10.7% vs 38.4%, P<0.001; M 0 stage patients: 15.0% vs 52.4%, P<0.001; M 1 stage patients: 2.1% vs 4.1%, P<0.001). Additionally, significant differences were observed in age, race, radiotherapy, chemotherapy, tumor location, tumor size, and tumor stage ( P<0.05). The median survival for patients with arterial invasion was 8 months, significantly lower than the 10-month median survival for non-arterial invasion patients ( P<0.001). The median survival for surgical patients with arterial invasion was 22 months, lower than the 24-month median for non-T 4 stage patients underwent surgery ( P<0.001) but significantly higher than for patients without surgery (T 4 stage patients without surgery: 8 months, P<0.001; non-T 4 stage patients without surgery: 6 months, P<0.001). For lymph node metastasis, patients with or without positive local lymph node metastasis had similar overall survival ( P>0.05). However, Patients with distant lymph node metastasis had significantly lower overall survival than that in patients without distant lymph node metastasis ( P<0.001). The multivariate logistic model indicated that tumor location in the body and tail ( OR=2.591, 95% CI: 2.343-2.867), positive regional lymph nodes ( OR=2.033, 95% CI: 1.836-2.252), and age <70 years old ( OR=1.183, 95% CI: 1.067-1.312) were risk factors for distant metastasis in arterial invasion patients. The multivariate Cox model showed that surgery ( HR=0.451, 95% CI: 0.405-0.503), radiotherapy ( HR=0.729, 95% CI: 0.677-0.784), chemotherapy ( HR=0.277, 95% CI: 0.258-0.297), tumor location in the body and tail ( HR=0.928, 95% CI: 0.874-0.985), and household income ≥$80, 000 ( HR=0.908, 95% CI: 0.853-0.968) were independent protective factors for prognosis in arterial invasion patients. Living in areas with a population ≤1 million ( HR=1.109, 95% CI: 1.044-1.178), age ≥70 years old ( HR=1.220, 95% CI: 1.150-1.296), larger tumor size (>2 cm but ≤4 cm: HR=1.124, 95% CI: 0.954-1.323; >4 cm: HR=1.310, 95% CI: 1.114-1.541), and having a metastatic burden (lung metastasis: HR=1.049, 95% CI: 0.869-1.267; distant lymph node metastasis: HR=1.179, 95% CI: 0.910-1.527; bone metastasis: HR=1.419, 95% CI: 0.854-2.359; brain or other metastasis: HR=1.519, 95% CI: 1.350-1.709; liver metastasis: HR=1.737, 95% CI: 1.600-1.886; two types of metastasis: HR=1.913, 95% CI: 1.689-2.168; three or more types: HR=2.436, 95% CI: 1.947-3.048) were independent risk factors for prognosis. The nomogram based on these prognostic factors had a C-index of 0.749 in the training set and 0.745 in the validation set; calibration curves in both sets were near the 45° line. Conclusions:High metastasis rates and low surgery rates are characteristic of pancreatic cancer with arterial invasion. Investigating the risk factors for distant metastasis and developing a prognostic nomogram incorporating metastatic burden hold significant clinical value for T 4 stage pancreatic cancer.

Objective:To evaluate the effect of age factor on preoperative sedative potency of midazolam oral solution in pediatric patients with inguinal hernia undergoing high ligation of the hernial sac.Methods:This was a prospective study. American Society of Anesthesiologists Physical Status classification I or Ⅱ pediatric patients of either sex with inguinal hernia, aged 1-6 yr, with preoperative Parental Separation Anxiety Scale score ≥3, undergoing elective laparoscopic high ligation of the hernia sac with general anesthesia, were divided into group A (1 yr ≤ age < 4 yr) and group B (4 yr ≤ age ≤ 6 yr) based on age. The trial was performed using a sequential method, with an initial midazolam oral solution set at 0.50 mg/kg. If the response was positive, the dose was increased by 0.05 mg/kg in the next patient, or conversely if negative, the dose was decreased by 0.05 mg/kg in the next patient. The child who preceded the one that exhibited a positive response served as the first case, and this process was repeated until 7 turning points were reached. A positive response was defined as a PSAS score of ≥3 measured at 30 min after oral administration of midazolam oral solution. The probit method was used to calculate the median-effective dose (ED 50) and 95% confidence interval ( CI) of midazolam oral solution for preoperative sedation in pediatric patients with inguinal hernia undergoing high ligation of the hernial sac in both groups. Results:A total of 49 children were ultimately included in this study, with 24 in group A and 25 in group B. The ED 50 of midazolam oral solution for preoperative sedation was 0.628 mg/kg (95% CI 0.614-0.643 mg/kg) in group A and 0.385 mg/kg (95% CI 0.361-0.412 mg/kg) in group B. The ED 50 was significantly higher in group A than in group B ( P≤0.05). Conclusions:The potency of midazolam oral solution for preoperative sedation in pediatric patients aged 4-6 yr is superior to that in pediatric patients aged 1-<4 yr with inguinal hernia undergoing high ligation of the hernial sac.

Objective:To evaluate the effect of age factor on preoperative sedative potency of midazolam oral solution in pediatric patients with inguinal hernia undergoing high ligation of the hernial sac.Methods:This was a prospective study. American Society of Anesthesiologists Physical Status classification I or Ⅱ pediatric patients of either sex with inguinal hernia, aged 1-6 yr, with preoperative Parental Separation Anxiety Scale score ≥3, undergoing elective laparoscopic high ligation of the hernia sac with general anesthesia, were divided into group A (1 yr ≤ age < 4 yr) and group B (4 yr ≤ age ≤ 6 yr) based on age. The trial was performed using a sequential method, with an initial midazolam oral solution set at 0.50 mg/kg. If the response was positive, the dose was increased by 0.05 mg/kg in the next patient, or conversely if negative, the dose was decreased by 0.05 mg/kg in the next patient. The child who preceded the one that exhibited a positive response served as the first case, and this process was repeated until 7 turning points were reached. A positive response was defined as a PSAS score of ≥3 measured at 30 min after oral administration of midazolam oral solution. The probit method was used to calculate the median-effective dose (ED 50) and 95% confidence interval ( CI) of midazolam oral solution for preoperative sedation in pediatric patients with inguinal hernia undergoing high ligation of the hernial sac in both groups. Results:A total of 49 children were ultimately included in this study, with 24 in group A and 25 in group B. The ED 50 of midazolam oral solution for preoperative sedation was 0.628 mg/kg (95% CI 0.614-0.643 mg/kg) in group A and 0.385 mg/kg (95% CI 0.361-0.412 mg/kg) in group B. The ED 50 was significantly higher in group A than in group B ( P≤0.05). Conclusions:The potency of midazolam oral solution for preoperative sedation in pediatric patients aged 4-6 yr is superior to that in pediatric patients aged 1-<4 yr with inguinal hernia undergoing high ligation of the hernial sac.

Humans ; Arthroplasty, Replacement, Knee ; Follow-Up Studies ; Cohort Studies ; Treatment Outcome ; Minimally Invasive Surgical Procedures ; Knee Joint/surgery* ; Knee Prosthesis ; Osteoarthritis, Knee/surgery*

Objective:Hepatocellular carcinoma(HCC)patients at the same stage exhibit different prognosis,and the underlying molecular mechanism remains unclear.This study aims to identify the key genes impacting the prognosis of HCC patients. Methods:Differentially expressed gene analyses were performed between HCC samples and normal ones,and between patients with long overall survival(OS)and those with short OS,in TCGA-LIHC and GSE14520 datasets.The Kaplan-Meier method with log-rank test was used to evaluate the role of secreted phosphoprotein 2(SPP2)in the prognosis of HCC patients.Gene set enrichment analysis(GSEA)was used to understand the difference of enriched signaling pathways between SPP2-stratified HCC subgroups.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)analyses were performed to predict the potential functional pathways in which SPP2 might participate. Results:SPP2 was significantly down-regulated in tumors when compared with normal tissues,or in tumor samples with short OS when compared with those with long OS[fold change(FC)>2 and false discovery rate(FDR)<0.05].Low expression of SPP2 was associated with worse clinicopathological features like vascular invasion(P=1.6e-05),poor cancer status(with tumor,P=0.021),advanced T stage(T3 or T4,P=4.5e-04),advanced TNM stage(stage Ⅲ or Ⅳ,P=3.1e-04),and with unfavorable prognosis(shorter OS,P= 0.002).Gene enrichment analyses revealed that SPP2 might involve in the metabolic homeostasis of HCC and in the development of liver fibrosis and cirrhosis. Conclusion:SPP2 might inhibit the development of liver fibrosis and cirrhosis and the tumorigenesis of HCC,and analogs of SPP2 might be potential drugs in the prevention of these diseases.

Objective To investigate the association and mechanism between glutathione S-transferase P1(GSTP1) and radiation-induced lung injury.Methods Two effective GSTP1 siRNAs were designed and synthesized.The normal lung epithelial cell line BEAS-2B cells were transfected with GSTP1 siRNA (experimental group,siRNA-1,siRNA-2) and negative control siRNA (negative control group,NC).Western blot was performed to detect the expression levels of GSTP1 protein and EMT-related proteins.CDNB was adopted to evaluate the activity of GSTs.DCFH-DA probe was used for incubation.Flow cytometry was conducted to detect the median fluorescence intensity (MFI) and cellular apoptosis.Annexin-v/PI staining was utilized for incubation.MTT assay was performed to measure the proliferation of BEAS-2B,and the growth curve was drawn based on the results.Results After radiation,compared with the NC group,the ROS level and MFI were significantly higher in experimental group (6774.66±399.60 vs.8759.00±256.96 vs.9967.67±735.11,P＜0.05).In the experimental group,the percentage of cellular apoptosis was remarkably higher than that in the NC group (12.3± 1.16 vs.17.38± 1.65 vs.22.88± 1.20,P＜0.05).MTT assay demonstrated that the OD values in the experimental group were significantly lower than that in the NC group everyday.Further more,the level of EMT process is higher in the experimental group.Conclusions Interfering with the GSTP1 expression in lung epithelial cells can increase the intracellular ROS level,increase the percentage of cellular apoptosis,and reduce the cell proliferation rate following γ-radiation.Besides,it can also promote the epithelial mesenchymal transition in lung epithelial cells.The down-regulation of GSTP1 protein expression level probably aggravates the radiationinduced lung cell injury and promotes the epithelial mesenchymal transition.