ObjectiveTo characterize the systemically absorbed components of Zhengqi prescription （ZQP） and investigate its therapeutic effects and mechanisms against cancer-related fatigue （CRF） through an integrated approach of network pharmacology and animal experiments. MethodsThe systemically absorbed components of ZQP were identified by ultra-performance liquid chromatography coupled with quadrupole-Orbitrap mass spectrometry （UPLC-Q-Exactive Orbitrap MS）. Network pharmacology was employed to predict the potential targets and signaling pathways involved in the anti-CRF effects of ZQP. A mouse model of paclitaxel-induced CRF， mimicking breast cancer-related fatigue， was established. Mice were administered different doses of ZQP extract. The therapeutic efficacy was evaluated based on fatigue-related indicators， behavioral test results， and energy metabolism parameters. Western blot analysis was conducted to validate the regulation of core signaling pathways. ResultsA total of 48 systemically absorbed components were identified. Network pharmacology analysis revealed 124 intersecting targets （including Akt1） and implicated signaling pathways such as phosphatidylinositol 3-kinase/protein kinase （PI3K/Akt）. Pharmacodynamic studies with the established CRF model demonstrated that ZQP alleviated fatigue symptoms. Specifically， ZQP-treated mice exhibited increased exhaustive swimming time （P<0.05）， prolonged struggling time in the tail suspension test， and enhanced movement duration and distance in the open field test （P<0.05， P<0.01）. Furthermore， ZQP treatment decreased serum lactate and blood urea nitrogen levels （P<0.05， P<0.01）， increased liver and muscle glycogen content （P<0.05， P<0.01）， and upregulated the expression of phosphorylated （p）-Akt and p-PI3K in the gastrocnemius muscle （P<0.05， P<0.01）. ConclusionZQP exerts significant therapeutic effects on paclitaxel-induced breast cancer-related fatigue by regulating the PI3K/Akt signaling pathway. Furthermore， this study provides a preliminary foundation for subsequent quality control of the formula and further investigation into its mechanism against CRF.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

The anterior cruciate ligament (ACL), anterolateral complex (ALC) and lateral meniscus (LM) maintain the anterolateral rotatory stability of the knee and control the internal rotation of the tibia. Anterolateral rotatory instability (ALRI) of the knee is not uncommon in clinic, and its main injury mechanism is non-contact injury. A pivot shift test or a tibial internal rotation test can indicate ALRI while X-ray, CT, MRI and ultrasound can assist in its diagnosis and differential diagnosis. For acute ALRI, good technique of ACL reconstruction is the basis to avoid postoperative residual ALRI, and anterolateral ligament reconstruction and extra-articular tenodesis are optional as appropriate. For chronic cases, however, both anterolateral ligament reconstruction and extra-articular tenodesis are effective. This article reviews the progress in research on the diagnosis and treatment of ALRI of the knee, hoping to provide references for its clinical diagnosis and treatment.

BACKGROUND:In recent years,increasing studies have focused on the abnormal proliferation and differentiation of acinous cells in the meibomian gland,suggesting that this process is closely related to the occurrence and development of dry eye.Structural and functional abnormalities such as blockage of the lumen of the meibomian gland and atrophy of the glands can cause or exacerbate dry eye.Therefore,the study of changes in the meibomian glands in dry eyes is important for understanding the pathogenesis of dry eyes in depth and finding new targets for the treatment and prevention of dry eyes. OBJECTIVE:To investigate the changes of the meibomian gland in a mouse model of aqueous deficient dry eyes. METHODS:Thirty-two female C57/B6 mice at 6-8 weeks were selected and randomly divided into experimental and control groups with 16 mice in each group.The mice in the experimental group were constructed by removing both the extra-orbital and intra-orbital lacrimal glands,while those in the control group were not treated.After 2 weeks of normal feeding,the corneal changes of both groups were observed under a slit lamp,and the tear secretion of both groups was measured.The meibomian glands of the two groups of mice were removed after decapitation.The changes in the gross morphology of the meibomian glands were observed and the meibomian glands were made into frozen sections.Hematoxylin-eosin staining was used to observe the structure of the meibomian glands,oil red staining was used to evaluate the function of the meibomian glands,and immunofluorescence staining and RT-qPCR were used to observe the expression of cytokeratin 14,Ki67 and abnormally differentiated small proline-rich protein 1B in the meibomian glands of mice. RESULTS AND CONCLUSION:Two weeks after modeling,lamellar defects were seen in the corneas of the experimental mice,and neovascularization of the limbal corneal was generated and invaded the central cornea.(2)Tear secretion volume was significantly reduced in the experimental group compared with the control group(P<0.05).Microscopic findings showed that the ducts of the meibomian glands in the experimental group were interrupted and atrophied,and their arrangement was disorganized.Hematoxylin-eosin staining results showed a significant increase in lipid vacuoles in the meibomian glands of the experimental mice compared with the control group.Lipid deposition was seen in oil red staining in the experimental group.Immunofluorescence and RT-qPCR results showed a significant increase in the expression of cytokeratin 14,Ki67 and small proline-rich protein 1B in the meibomian glands of mice in the experimental group compared with the control group(P<0.05).To conclude,aqueous deficient dry eye can lead to compensatory hypertrophy,increased proliferation,and abnormal lipid metabolism in the meibomian gland,as well as abnormal differentiation of the meibomian gland.

Objective:To explore the incidence, clinical characteristics, imaging features, clinical outcome and prognosis of indeterminate pulmonary nodules (IPN) in patients with osteosarcoma.Methods:A total of 69 patients of osteosarcoma with IPN in lung treated in the Bone tumor Center of Eastern Theater General Hospital from January 2011 to January 2021 were collected retrospectively, there were 47 males and 22 females, with a median age of 19 years old (range 7-60 years old). The clinical characteristics including disease-free interval, the chemotherapy response, with recurrence/non-pulmonary, IPN presence before / during / after chemotherapy and imaging features of IPN including number of IPN, location of IPN, density of IPN, boundary clarity of IPN and outcome. The patients were divided into the metastasis pulmonary nodules group and the benign nodules group according to the final outcome of IPN. Further, χ 2 test was performed for comparison of the clinical and imaging characteristics between the two groups. The survival of patients was counted and the correlation between single factor and survival was compared by Kaplan-Meier test, and multivariate survival analyses were performed using Cox proportional hazards regression models. Results:Sixty-nine cases occurred IPN in 211 patients with osteosarcoma, with an incidence of 32.7%. Of the 69 patients, 45 patients (65.2%) with IPN were diagnosed as metastases, and 24 patients (34.8%) with IPN were diagnosed as benign nodules. Follow-up length ranged from 1 to 124 months, with the median follow up time 43 months. To the end of follow-up, 41 patients (59.4%) remained alive and 28 patients (40.6%) had died. The median survival time was 41.0 (20.0, 65.0) months and the median survival time after diagnosis of IPN was 25.0 (10.0, 43.0) months. There were significant differences in lung nodule density ( P<0.001), boundary ( P=0.002), history of recurrence/extra-pulmonary metastasis ( P=0.023) and chemotherapeutic effect ( P<0.001) between the metastasis pulmonary nodules group and the benign nodules group. Multivariate survival analysis showed that chemotherapeutic effect was an independent factor affecting the overall survival of patients [ HR=0.048, 95% CI (0.01, 0.26)]. Boundary definition [ HR=0.12, 95% CI (0.02, 0.93)] and chemotherapeutic effect [ HR=0.06, 95% CI (0.01, 0.29)] were independent factors influencing survival after diagnosis of IPN. Conclusion:Osteosarcoma patients with IPN have a poor prognosis. The poor effect of chemotherapy is an independent risk factor for the overall survival time of those patients and the survival time after diagnosis of IPN. The boundary definition of IPN is an independent risk factor for the survival time after diagnosis of IPN.

Objective:To compare outcomes between standardized and misdiagnosis and mistreatment of osteosarcoma.Methods:A retrospective analysis of patients with high-grade osteosarcoma who received appropriate surgical treatment and chemotherapy (299 cases, control group) and those who were misdiagnosed (benign or infective) and received mistreatment (23 cases, study group) between January 2009 and December 2021. Gender, age, first operation mode, recurrence time, recurrence interval, metastasis time, metastasis interval, total survival time (months), survival status in the two group and tumor site reoperation mode in the study group were statistically analyzed. Further, chi-square test was performed for comparison of the clinical between two groups. The survival analysis was performed using Kaplan-Meier test and Log-rank test.Results:All the 322 patients were followed up. In the control group, the average follow-up time was 42 months (1-137 months), the average age was 24 years (3-80 years), male 184 cases, female 115 cases, and limb salvage rate was 85.3% (255/299). Seven patients underwent amputation, and the amputation rate was 17.7% (44/299). The recurrence rate was 8.4% (25/299), the average recurrence interval was 22.8 months (7-36 months), and the metastasis rate was 28.1% (85/299), the average metastasis time was 32.7 months (0-58 months). In the study group, the average of follow-up time was 30 months (9-117 months), the average age was 36 years (5-67 years), 17 males and 6 females. Among them, eleven patients were treated with limb salvage in the second stage, and the limb salvage rate was 47.8% (11/23). Seven patients underwent amputation, and the amputation rate was 30.4% (7/23). The recurrence rate was 26.1% (6/23), the average recurrence interval was 11 months (1-42 months), and the metastasis rate was 43.4% (10/23), the average metastasis time was 20.3 months (1-44 months). The 5-year survival rate was 50.7% in the study group and 56.1% in the control group. There was no significant difference between the two groups (χ 2=0.09, P=0.760). Conclusion:The overall prognosis of patients with high-grade osteosarcoma who receive active treatment after mistreatment is similar to that of patients with standardized treatment, but the recurrence and metastasis rate is higher, the recurrence time is earlier, and the amputation rate is higher.

In recent years, "Internet+" medical treatment has gradually become an important form of medical care in China. Especially affected by the COVID-19, China′s maternal and child health care institutions have closely integrated "Internet+" technology with maternal health care to meet maternal health needs and reduce maternal risk. Based on a comprehensive analysis of Chinese literature on "Internet+" maternal health care in CNKI, Wanfang database, VIP, CBM in recent five years, this paper introduces the main forms, contents and effects of " Internet+" maternal health care in China, and points out the direction of clinical practice and scientific research in the future, which can be used for reference by the general colleagues.

Women′s health is the cornerstone of national health. During the 70 years since the founding of New China, under the leadership of the Communist Party of China, a legal system and related policies including more than 100 laws and regulations have been established to fully protect women′s rights and health, and women′s rights and health throughout their life cycle have been effectively protected. The health status of Chinese women has been significantly improved, the form and accessibility of women′s health care services have been continuously improved, and the building of women′s health care teams has been continuously strengthened. All of these achievements demonstrate the original intention of the Communist Party of China to put people′s health first and action of forging ahead.