ObjectiveTo construct and validate a clinical prediction model for Qi deficiency and blood stasis syndrome in chronic heart failure （CHF），aiming to assist clinical diagnosis and provide tools and methods for individualized treatment of CHF. MethodsThe clinical data of patients with chronic heart failure treated at Dongzhimen Hospital of Beijing University of Chinese Medicine from January 2022 to January 2024 were retrospectively collected. The patients were randomly divided into a training group and a validation group with a ratio of 7∶3. First， the least absolute shrinkage and selection operator （LASSO） regression analysis was used to preliminarily screen the predictive factors affecting the diagnosis of Qi deficiency and blood stasis syndrome in CHF. Subsequently， the Logistic regression method was applied to conduct a more in-depth and detailed analysis of these factors. Variables with P<0.05 in the results of the multi-factor Logistic regression were carefully selected and included. Based on the regression coefficients obtained from this analysis， a model was constructed， and a nomogram was accurately drawn. Using R software，the receiver operating characteristic （ROC） curve，calibration curve，and decision curve analysis （DCA） were precisely drawn. These analyses were used to comprehensively evaluate the model from three crucial aspects： discrimination，calibration，and clinical applicability. Additionally， the accuracy，specificity，sensitivity，positive predictive value，and negative predictive value of the model were meticulously calculated to conduct a more all-round and comprehensive assessment. ResultsIn total， 168 cases were successfully obtained in the training group， and 71 cases were included in the validation group. After a thorough comparison， it was found that there were no statistically significant differences in the baseline data between the two groups. After being rigorously screened by the LASSO-multivariate logistic regression method， dark red tongue，smoking history，cardiac troponin I，and N-terminal pro-B-type natriuretic peptide （NT-ProBNP） were identified as the influencing factors for diagnosing patients with the Qi deficiency and blood stasis syndrome in CHF. The constructed model demonstrated an area under the curve （AUC） of 0.812 in the training group and 0.719 in the validation group. The calibration curve showed that the predicted curve of the model was close to the actual observed curve. DCA indicated that the model could provide substantial clinical benefits for patients at the decision thresholds ranging from 0.2 to 0.9. ConclusionThe clinical prediction model for Qi deficiency and blood stasis syndrome in chronic heart failure constructed in this study shows good performance. It has certain application value in clinical practice， which may contribute to the improvement of the diagnosis and treatment of CHF patients with this syndrome.

Skeletal muscle dysfunction is a common extrapulmonary comorbidity of chronic obstructive pulmonary disease (COPD) and is associated with decreased quality-of-life and survival in patients. The autophagy lysosome pathway is one of the proteolytic systems that significantly affect skeletal muscle structure and function. Intriguingly, both promoting and inhibiting autophagy have been observed to improve COPD skeletal muscle dysfunction, yet the mechanism is unclear. This paper first reviewed the effects of macroautophagy and mitophagy on the structure and function of skeletal muscle in COPD, and then explored the mechanism of autophagy mediating the dysfunction of skeletal muscle in COPD. The results showed that macroautophagy- and mitophagy-related proteins were significantly increased in COPD skeletal muscle. Promoting macroautophagy in COPD improves myogenesis and replication capacity of muscle satellite cells, while inhibiting macroautophagy in COPD myotubes increases their diameters. Mitophagy helps to maintain mitochondrial homeostasis by removing impaired mitochondria in COPD. Autophagy is a promising target for improving COPD skeletal muscle dysfunction, and further research should be conducted to elucidate the specific mechanisms by which autophagy mediates COPD skeletal muscle dysfunction, with the aim of enhancing our understanding in this field.
Pulmonary Disease, Chronic Obstructive/physiopathology* ; Autophagy/physiology* ; Humans ; Muscle, Skeletal/pathology* ; Mitophagy ; Animals ; Mitochondria/metabolism* ; Lysosomes

Objective To investigate the effect of pelvic floor muscle training based on timing theory in patients undergoing robot-assisted laparoscopic radical prostatectomy.Methods A total of 112 patients undergoing robot-assisted laparoscopic radical resection of prostate cancer in the First Affiliated Hospital of Fujian Medical University were selected as the study subjects from August 2021 to August 2022.57 patients in control group were given routine intervention measures,and 55 patients in experimental group were given pelvic floor muscle intervention based on timing theory on the basis of routine intervention measures.The intervention lasted for 1 year.The intervention effects of urinary control ability,urinary incontinence recovery rate and pelvic floor function rehabilitation were compared between two groups in each period after surgery.Results 24h after catheter removal,3 months and 6 months after the intervention,the experimental group had more advantages in urinary control score,urinary incontinence recovery rate and pelvic floor function recovery score(P＜0.05),but there was no statistical significance in the above aspects between the two groups at 12 months after the operation(P＞0.05).Conclusion The pelvic floor muscle training method based on the timing theory is scientific and feasible to a certain extent,and the intervention starts before surgery and lasts until 1 year after surgery,which significantly improves the postoperative urinary incontinence symptoms of patients with robot-assisted laparoscopic radical prostatectomy within the baseline level,improves the recovery rate of urinary incontinence,and helps the early rehabilitation of patients with postoperative urinary control ability.

Objective:Analyze the impact of smoking on the mortality and life expectancy of residents in Tianjin in 2019.Methods:Use mortality case-control study method to collect all cause of death cases of residents in Tianjin in 2019 for analysis. After adjusting for the 5-years-old age group, education level, and marital status, the smoking attributed deaths from different diseases of different genders, smoking attributed deaths in different age groups, and their impact on life expectancy were analyzed.Results:The total number of deaths in 2019 was 75 254, with 42 201 males (56.1%). Among male deaths, 3 215 (9.9%) were attributed to smoking, of which 2 157 (50.2%) lung cancer deaths were attributed to smoking; The risk of lung cancer death among smokers was 3.075 times higher than that of non-smokers (95% CI: 2.812-3.364); Among the 33 053 female deaths (43.9%), 1 396 (5.8%) were caused by smoking, with 744 (29.1%) lung cancer deaths attributed to smoking. The age group with the highest number of deaths attributed to smoking for women was the 75-<80 years old age group, followed by the 70-<75 and 80-<85 years old age groups. The age group with the highest proportion of deaths attributed to smoking for men was the 55-<60 years old age group. In addition, smoking accounts for more than 60% of deaths in the 60-<65, 45-<50, 55-<60, and 65-<70 years old age groups. In 2019, the loss of life expectancy attributed to smoking deaths among all residents in Tianjin was 1.13 years, with a loss of 1.15 years for males and 0.57 years for females. The expected life expectancy excluding deaths caused by smoking was 82.92 years, 80.77 years for males and 84.61 years for females. Conclusions:Smoking remains one of the important risk factors for death among residents. Promoting effective measures to reduce smoking rates is an effective way to increase life expectancy.

Background and purpose:The overexpression of carnitine palmitoyl transferase 1A(CPT1A)is related to the poor prognosis of breast cancer,and it can promote the utilization of fatty acids by mitochondria and maximize triphosphate(ATP)production.However,the role of CPT1A in breast cancer metastasis is still unclear.This study aimed to explore the mechanism that mitochondrial dysfunction and CPT1A/extracellular signal-regulated kinase(ERK)signaling pathway in breast cancer jointly regulate the malignant behavior of breast cancer.Methods:The lentivirus system and shRNA tools were used to overexpress or knock down CPT1A in human breast cancer cell lines MDA-MB-231 and MCF7,and the cells were divided into NC group,CPT1A group and shCPT1A group.The invasion ability of cells was detected by transwell assay,and the protein expressions of peroxisome proliferator-activated receptor γ coactivator-1α(PGC-1α),ERK1/2 and CPT1A were analyzed by Western blot.The mitochondrial morphology of MDA-MB-231 and MCF7 cell lines was analyzed using mitochondrial red staining,and mitochondrial respiratory capacity was analyzed by oxygen consumption rate.Results:Compared with cells expressing control vector,overexpression of CPT1A resulted in enhanced invasion abilities of MCF7 cells and MDA-MB-231 cells(P＜0.05),while knockdown of shCPT1A resulted in decreased invasion abilities of cells(P＜0.05).Compared with NC group,the length of mitochondrial branches in MDA-MB-231 and MCF7 cells in CPT1A group was significantly shorter(P＜0.05),and the expressions of ERK1/2 and PGC-1α increased significantly(P＜0.05).In shCPT1A group,the length of mitochondrial branches in MDA-MB-231 and MCF7 cells increased significantly(P＜0.05),and the expressions of ERK1/2 and PGC-1α decreased significantly(P＜0.05).In addition,compared with NC group,the cellular basis,maximum respiratory capacity and ATP production of MDA-MB-231 in CPT1A group increased significantly(P＜0.05),while the cellular basis,maximum respiratory capacity and ATP production of MDA-MB-231 in shCPT1A group decreased significantly(P＜0.05).Conclusion:ERK1/2-PGC-1α activated by CPT1A Signaling pathway plays a key role in mitochondrial division mediated breast cancer cell metastasis.

ObjectiveTo explore the effect and mechanism of Sishenjian on synovial lesions induced by monosodium iodoacetate （MIA） in rats with knee osteoarthritis （KOA）. MethodSixty female Sprague-Dawley （SD） rats were randomly divided into the following six groups： normal group， model group， celecoxib group， and high-， medium-， and low-dose Sishenjian group. The KOA rat model was established by intra-articular injection of MIA. Celecoxib （18 mg·kg^-1） and Sishenjian （14.4， 7.2， 3.6 g·kg^-1） were administered by gavage according to the groups. All rats were euthanized after four weeks of continuous administration. The transverse diameter of the bilateral knee joints of rats was measured， and gross observation of the knee joint was performed. Pathological changes in knee joint synovial tissue were observed by hematoxylin-eosin （HE） staining and picrosirius red staining. Immunohistochemistry （IHC） was used to detect the expression of vascular endothelial growth factor A （VEGFA） in synovial tissue. The levels of inflammatory cytokines in the joint synovial fluid were detected by enzyme-linked immunosorbent assay （ELISA）. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were used to detect the expression of mRNA and proteins related to the transforming growth factor-β₁ （TGF-β₁）/Smad2/3 pathway in knee joint synovium. ResultCompared with the normal group， the transverse diameter of the knee joint in the model group significantly increased （P<0.01）. Compared with the model group， the transverse diameter of the knee joint in rats of each Sishenjian group significantly decreased （P<0.01）. Compared with the normal group， the expression levels of interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） in the knee joint synovial fluid of model group significantly increased （P<0.01）. Compared with the model group， the expression levels of IL-1β and TNF-α in the knee joint synovial fluid of rats in each Sishenjian group significantly decreased （P<0.01）. Compared with the normal group， the expression levels of TGF-β₁， Smad2/3， phosphorylation（p）-Smad2/3， type Ⅰ collagen α1 （ColⅠ_α1）， type Ⅲ collagen α1 （ColⅢ_α1）， VEGFA proteins and TGF-β₁， Smad2/3， ColⅠ_α1， ColⅢ_α1 mRNA in knee joint synovium of model group significantly increased （P<0.01）. Compared with the model group， the expression levels of TGF-β₁， Smad2/3， phosphorylation （p）-Smad2/3， ColⅠ_α1， ColⅢ_α1， VEGFA proteins and TGF-β₁， Smad2/3， ColⅠ_α1， ColⅢ_α1 mRNA in knee joint synovium of rats in each Sishenjian group significantly decreased （P<0.05， P<0.01）. ConclusionSishenjian can inhibit synovial inflammation and angiogenesis， and may become a potential drug for treating synovial lesions in KOA by regulating the TGF-β₁/Smad2/3 pathway.

Objective:Based on the needs of advanced nursing practice development, to establish an indicator system of role function of position of oncology genetic nurses suitable for our national condition, and to provide a basis for position establishing of nocology genetic nurses.Methods:Initial indexes were generated through the literature review and semi-structured interviews. From September to December 2022, two rounds of expert consultations and analytic hierarchy process were conducted to establish the evaluation index for role function of position of oncology genetic nurses.Results:A total of 43 experts were included in the study, the response rates of 2 rounds were 93.62%(44/47) and 97.73%(43/44), and the authority coefficients of the experts were 0.821 and 0.853. The Kendall′s coefficients of concordance for the 2 rounds of consultations were 0.100-0.150 (all P<0.01) and 0.101-0.237 (all P<0.01). Finally, the role function system of position for oncology genetic nurses was formed, which consisted of 5 first-level indexes, 17 second-level indexes and 86 third-level indexes. Conclusions:The system of role function of position for oncology genetic nurses is reasonable, scientific and reliable, professional and specific, which can provide a theoretical reference for the development of advanced nursing practice on hereditary oncology in China.

P21-activated kinase 5 (PAK5) belongs to the PAK-II subfamily, which is an important regulator of cell survival, adhesion, and motility. However, the functions of PAK5 in endometriosis remain unclear. Here, PAK5 is strikingly upregulated in endometriosis. Furthermore, the knockdown of PAK5 or its inhibitor GNE 2861 blocks the development of endometriosis, which is equally demonstrated in PAK5-knockout mice. In addition, PAK5 promotes glycolysis by enhancing the protein stability of pyruvate kinase 2 (PKM2) in endometriotic cells, which is a key enzyme for glucose metabolism. Moreover, the phosphorylation of PKM2 at Ser519 by PAK5 mediates endometriosis cell proliferation and metastasis. Collectively, PAK5 plays an indispensable role in endometriosis. Our findings demonstrate that PAK5 is an important target for the treatment of endometriosis.
Endometriosis/genetics* ; Female ; Animals ; p21-Activated Kinases/genetics* ; Mice ; Phosphorylation ; Glycolysis ; Humans ; Thyroid Hormone-Binding Proteins ; Membrane Proteins/genetics* ; Carrier Proteins/genetics* ; Cell Proliferation ; Mice, Knockout ; Thyroid Hormones/metabolism* ; Pyruvate Kinase/genetics*

OBJECTIVE: To study the molecular epidemiology of thalassemia in Jiaxing area of Zhejiang province and provide a basis for prenatal diagnosis, genetic counseling and prevention and control of birth defects. METHODS: A total of 24 003 pregnant women who presented at the Jiaxing Maternal and Child Health Care Hospital from April 2017 to September 2021 were enrolled. Capillary hemoglobin electrophoresis in combination with routine blood test were used for primary screening for carriers of thalassemia-associated mutations, and those with positive results were subjected to fluorescence quantitative PCR assay. Prenatal diagnosis was provided for couples with a risk of giving birth to children with intermediate or severe thalassemia. RESULTS: Among the 24 003 pregnant women, 1 211 cases were suspected as carriers of thalassemia-associated mutations, among whom 443 (36.58%) were confirmed by genetic testing. Among these, carriers of α-, β- and α-complex β-globin gene mutations have accounted for 27.31% (121/443), 70.65% (313/443) and 2.04% (9/443), respectively. The result of prenatal diagnosis for an at-risk couple was --SEA/αCSα, and the fetus was predicted to have intermediate or severe thalassemia. Termination of the pregnancy was recommended. CONCLUSION Hemoglobin electrophoresis combined with routine blood test during pregnancy may be used as a preliminary screening measure for carriers of thalassemia-associated variants. Combined with genetic testing, this will be of great significance for the control of thalassemia in this region.
Female ; Humans ; Pregnancy ; Electrophoresis, Capillary ; Genetic Counseling ; Genetic Testing ; Mutation ; Prenatal Diagnosis ; Thalassemia/genetics*

Objective:To investigate the clinical and electrophysiological characteristics of patients with sudden unexpected death of epilepsy (SUDEP).Methods:Using "epilepsy" as the keyword, the relevant cases entered from October 2011 to March 2012 were searched in the database of the Electroencephalogram (EEG) Monitoring Center, Xijing Hospital, the Air Force Military Medical University. Telephone follow-up was conducted for all confirmed epilepsy patients, and for the death cases confirmed by telephone follow-up, the patients identified as consistent with SUDEP diagnosis were included in this study based on their past medical history, clinical data, death details, etc, and their clinical and neuroelectrophysiological characteristics were summarized and analyzed.Results:Among the 1 232 patients who underwent 24-hour video-EEG monitoring during the study period, 354 patients were successfully followed up by telephone interview, of whom 17 patients were died (4.8%), 12 individuals met the diagnosis of SUDEP (7 men, 5 women). The duration of the disease in 9 patients exceeded 10 years. Eight cases presented with focal-bilateral tonic clonic seizures. Nine patients were treated with anti-seizure drug monotherapy. All the 24-hour video EEG of 12 patients were abnormal. There were 8 occasions when the EEG occipital α background rhythm slowed down compared with the standard frequency of peers or was dominated by slow waves. Interictal epileptic discharge (IED) located in temporal lobe were found in 12 EEG records, of which 9 EEG records were found with frontal IED. One of the 12 cases received 24-hour video EEG twice within 6 years, and his EEG background rhythm was significantly slower and the IED region was expanded compared with the first EEG record. At the third year after reexamination of EEG, SUDEP developed in this patient.Conclusions:SUDEP patients have a long course of disease and bilateral tonic-clonic seizure. The interictal EEG shows occipital slow α activity and temporofrontal epileptiform discharges, which may increase the risk of SUDEP.