The Proctor's reporting guideline for implementation strategies represents a landmark framework in the field of implementation science, aiming to address the issue of inconsistent reporting in implementation research by standardizing the naming, definition, and operationalization of implementation strategies, thereby enhancing the credibility and utility of research findings. This paper provides an in-depth interpretation of the core connotations of this reporting guideline and illustrates its application in developing interview outlines and specifying implementation strategies, using a brief smoking cessation intervention project as a case study. Through this reporting guideline, abstract recommendations for implementation are systematically transformed into clear, multidimensional operational guides, significantly improving the transparency of strategy connotations and the replicability of actual execution. Meanwhile, the case study highlights the flexibility of the guideline, which allows researchers to adapt the content and format of strategies based on local resources and cultural contexts, thus enhancing practical adaptability while maintaining scientific rigor. However, the application of Proctor's reporting guideline still faces challenges, primarily manifested in the potential confusion surrounding the constructs of temporality and dose in practice, as well as the challenges that the inherent flexibility of the guideline may pose to the assessment of fidelity and effectiveness. Despite these limitations, the reporting guideline remains a vital tool for implementation research; future efforts should focus on optimizing its application—through refining operational guidelines, standardizing flexible adaptations, and involving stakeholders—to better guide implementation studies and continuously promote high-quality development in the field.

Objective To investigate the prognostic value of optic nerve sheath diameter(ONSD)measured by critical care ultrasound combined with serum biomarkers[S100 calcium-binding protein β(S100β)and neuron-specific enolase(NSE)]in patients with severe traumatic brain injury.Methods A total of 103 adult severe traumatic brain injury patients admitted to the intensive care unit of this hospital from A-pril 1,2023,to April 1,2024 were enrolled.All patients underwent invasive intracranial pressure monitoring after admission,alongside bedside critical care ultrasound measurement of ONSD at 3 mm behind the globe and serum biomarker testing.Baseline data and Glasgow outcome scale(GOS)scores at 90 days after dis-charge were recorded.Patients were divided into the survival and the non-survival groups based on GOS scores.Receiver operating characteristic(ROC)curve analysis and area under the curve(AUC)were used to evaluate the predictive performance of ONSD and serum biomarkers for poor prognosis in severe traumatic brain injury patients.Results Ninety-six patients were ultimately included,with 52(54.1％)in the survival group and 44(45.9％)in the non-survival group.Significant differences were observed in blood glucose,Glas-gow coma scale(GCS)score,acute physiology and chronic health evaluation Ⅱ(APACHE Ⅱ)score,ONSD,NSE,and S100β levels(P＜0.05)between the two groups.Multivariate analysis identified ONSD(OR=4.962,95％CI:3.473-6.254),NSE(OR=2.704,95％CI:1.987-3.033),S100β(OR=2.983,95％CI:1.843-4.571),and APACHE Ⅱ score(OR=3.726,95％CI:2.837-4.592)as independent predictors of mortality in severe traumatic brain injury patients(P＜0.05).The combination of ONSD,NSE,and S100β yielded an AUC of 0.840 for predicting poor prognosis,with a specificity of 88.3％and sensitivity of 98.6％.Conclusion ONSD and serum brain injury biomarkers(NSE,S100β)are associated with in-hospital prognosis in severe traumatic brain injury patients.Their combined detection can effectively predict a poor outcome.

Objective To explore the effect of evening primrose oil(EPO)on aortic endothelial damage in rats with polycystic ovary syndrome(PCOS),using network pharmacology and in vivo experiments.Methods The potential targets of EPO for improving aortic endothelial injury in PCOS rats were predicted by network pharmacology,and the selected core targets and renin-angiotensin signaling(RAS)pathway were verified by experiments.Fifty-eight female SD rats were divided randomly into a blank group(n=10)and a modeling group(n=48).Rats in the blank group were fed a normal diet and rats in the modeling group received a high-fat diet for 8 weeks.The PCOS model was prepared at week 6 by administration of letrozole(1 mg/(kg·d))for 21 days.Blood was taken from the tail vein after modeling and serum was collected to detect hormone levels.The model rats were then divided randomly into four groups and treated with the corresponding drugs for 6 weeks.Blood,blood vessels,and ovaries were then collected.Tissue morphology was examined by hematoxylin and eosin staining and serum levels of luteinizing hormone(LH),testosterone(T),follicle-stimulating hormone(FSH),endothelin(ET-1),and tumor necrosis factor(TNF-α)were detected by enzyme-linked immunosorbent assay(ELISA).Serum levels of nitric oxide(NO)were determined by spectrophotometry.Protein expression levels of core targets and RAS pathway-related factors were assessed by western blotting and immunohistochemistry.Results Twenty-five intersection targets of EPO and PCOS were identified by network pharmacological analysis.Kyoto encyclopedia of genes and genomes analysis showed that EPO improved vascular injury in PCOS rats via multiple pathways,including RAS.Serum levels of ET-1,FSH,LH,and T measured by ELISA were significantly decreased after EPO treatment,compared with the model group(P＜0.01).EPO significantly decreased the expression levels of Ang Ⅰ,VEGF-B,AT2R,ET-1,and TNF-α proteins in the aorta(P＜0.01)and significantly increased expression levels of Ang Ⅱ,CD31,and endothelial NO synthase proteins(P＜0.01).Conclusions EPO may ameliorate vascular endothelial injury in PCOS model rats by inhibiting the RAS signaling pathway and by overactivation of the ACE/Ang Ⅱ/AT1 axis.

Objective To observe the effects of acupuncture at"Jiaji"on angiogenesis in rats with lumbar muscle aging based on AMPK/SIRT1/PGC-1α signaling pathway;To explore its possible mechanism of improving lumbar muscle aging atrophy.Methods Totally 30 SPF male SD rats were randomly divided into model group,acupuncture group and non-acupoint group,with 10 rats in each group.Subcutaneous injection of D-galactose(300 mg/kg)into the neck and back of rats was used to prepare a subacute lumbar muscle aging rat model.Another 10 rats were selected as the blank group,and an equal amount of normal saline was subcutaneously injected into the neck and back.Intervention began in the 9th week of modeling.The acupuncture group received acupuncture at bilateral L3-L5"Jiaji",while the non-acupoint group received bilateral non-meridian and non-acupoint acupuncture,each time for 30 minutes,once a day,6 times a week,for 4 consecutive weeks.β-galactosidase staining was used to observe the morphology of rat lumbar muscle tissue;TUNEL staining was used to detect apoptosis of lumbar muscle tissue cells;ELISA was used to detect the contents of nitric oxide(NO)and endothelin-1(ET-1)in lumbar muscle tissue;immunofluorescence staining was used to detect CD31 expression and microvascular density in lumbar muscle tissue;Western blot was used to detect protein expressions of p-AMP activated protein kinase(AMPK),silencing information regulatory factor 1(SIRT1)and peroxisome proliferator activated receptor gamma co activator factor 1α(PGC-1α)in lumbar muscle tissue.Results Compared with the blank group,the positive cells of β-galactosidase staining in lumbar muscle tissue of the model group increased significantly,the apoptosis rate significantly increased(P<0.001),the NO content in lumbar muscle tissue significantly decreased(P<0.001),the ET-1 content significantly increased(P<0.001),the expression of CD31 and microvascular density significantly decreased(P<0.001),and the protein expressions of p-AMPK,SIRT1 and PGC-1α significantly decreased(P<0.01,P<0.001).Compared with the model group,the positive cells of β-galactosidase staining in lumbar muscle tissue of rats in the acupuncture group was significantly reduced,the apoptosis rate was significantly decreased(P<0.001),NO content significantly increased(P<0.001),ET-1 content was significantly reduced(P<0.01),CD31 expression and microvascular density significantly increased(P<0.01,P<0.001),and the protein expressions of p-AMPK,SIRT1,PGC-1α significantly increased(P<0.05,P<0.01).Conclusion Acupuncture at"Jiaji"can promote angiogenesis in lumbar skeletal muscle,and then improve the aging atrophy of lumbar muscle,and its mechanism may be related to the activation of AMPK/SIRT1/PGC-1α signaling pathway.

Objective:To investigate the effects and its related mechanism of placenta-derived mesenchymal stem cells(PMSCs)on the lipopolysaccharides(LPS)damaged astrocytes.Methods:Primary astrocytes were isolated from the cerebral cortex of neonatal rats.The expression of glial fibrillary acidic protein(GFAP)was identified using immu-nofluorescence staining to evaluate the purity of the primary astrocytes.PMSCs were cocultured with LPS-treated astro-cytes.The expression levels of factors related to inflammation including interleukin-1β(IL-1β),inducible nitric oxide synthase(iNOS),tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),arginase-1(Arg-1),S100 calcium-bind-ing protein A10(S100A10),and TGF-β/Smad signaling pathway-related proteins such as transforming growth factor beta 1(TGF-β1),transforming growth factor beta type I receptor(TβRⅠ),transforming growth factor beta type II re-ceptor(TβRⅡ),phospho-Smad2 and phospho-Smad3(p-Smad2,p-Smad3)in astrocytes from each group were detec-ted using real time RT-PCR or Western blot techniques.Results:Astrocytes at the third passage exhibited an 80%pos-itivity rate for GFAP.After treated with 10 μg/ml LPS,the astrocytes expression levels of pro-inflammatory factors IL-1β,iNOS,IL-6,and TNF-α were significantly increased(P<0.05),while their expression levels of the anti-inflam-matory factors of Arg-1 and S100A10 were significantly decreased(P<0.05).Meanwhile,their expression levels of TGF-β/Smad signaling pathway related proteins of TGF-β1,TβRⅠ,TβRⅡ,p-Smad2 and Smad3 were increased(P<0.05).After the LPS damaged astrocytes were cocultured with PMSCs,their expression levels of pro-inflammatory factors IL-1β,iNOS,IL-6,and TNF-α were significantly decreased(P<0.05),while their expression levels of the anti-inflammatory factors of Arg-1 and S100A10 were significantly increased(P<0.05).Also,their expression levels of TGF-β/Smad signaling pathway related proteins of TGF-β1,TβRⅠ,TβRⅡ,p-Smad2,and Smad3 were decreased(P<0.05).Conclusion:PMSCs may inhibit the activation of A1 astrocytes through the TGF-β/Smad signaling path-way,by which reducing the astrocytic activation.

Objective To explore the effect of evening primrose oil(EPO)on aortic endothelial damage in rats with polycystic ovary syndrome(PCOS),using network pharmacology and in vivo experiments.Methods The potential targets of EPO for improving aortic endothelial injury in PCOS rats were predicted by network pharmacology,and the selected core targets and renin-angiotensin signaling(RAS)pathway were verified by experiments.Fifty-eight female SD rats were divided randomly into a blank group(n=10)and a modeling group(n=48).Rats in the blank group were fed a normal diet and rats in the modeling group received a high-fat diet for 8 weeks.The PCOS model was prepared at week 6 by administration of letrozole(1 mg/(kg·d))for 21 days.Blood was taken from the tail vein after modeling and serum was collected to detect hormone levels.The model rats were then divided randomly into four groups and treated with the corresponding drugs for 6 weeks.Blood,blood vessels,and ovaries were then collected.Tissue morphology was examined by hematoxylin and eosin staining and serum levels of luteinizing hormone(LH),testosterone(T),follicle-stimulating hormone(FSH),endothelin(ET-1),and tumor necrosis factor(TNF-α)were detected by enzyme-linked immunosorbent assay(ELISA).Serum levels of nitric oxide(NO)were determined by spectrophotometry.Protein expression levels of core targets and RAS pathway-related factors were assessed by western blotting and immunohistochemistry.Results Twenty-five intersection targets of EPO and PCOS were identified by network pharmacological analysis.Kyoto encyclopedia of genes and genomes analysis showed that EPO improved vascular injury in PCOS rats via multiple pathways,including RAS.Serum levels of ET-1,FSH,LH,and T measured by ELISA were significantly decreased after EPO treatment,compared with the model group(P＜0.01).EPO significantly decreased the expression levels of Ang Ⅰ,VEGF-B,AT2R,ET-1,and TNF-α proteins in the aorta(P＜0.01)and significantly increased expression levels of Ang Ⅱ,CD31,and endothelial NO synthase proteins(P＜0.01).Conclusions EPO may ameliorate vascular endothelial injury in PCOS model rats by inhibiting the RAS signaling pathway and by overactivation of the ACE/Ang Ⅱ/AT1 axis.

Objective:To investigate the effects and its related mechanism of placenta-derived mesenchymal stem cells(PMSCs)on the lipopolysaccharides(LPS)damaged astrocytes.Methods:Primary astrocytes were isolated from the cerebral cortex of neonatal rats.The expression of glial fibrillary acidic protein(GFAP)was identified using immu-nofluorescence staining to evaluate the purity of the primary astrocytes.PMSCs were cocultured with LPS-treated astro-cytes.The expression levels of factors related to inflammation including interleukin-1β(IL-1β),inducible nitric oxide synthase(iNOS),tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),arginase-1(Arg-1),S100 calcium-bind-ing protein A10(S100A10),and TGF-β/Smad signaling pathway-related proteins such as transforming growth factor beta 1(TGF-β1),transforming growth factor beta type I receptor(TβRⅠ),transforming growth factor beta type II re-ceptor(TβRⅡ),phospho-Smad2 and phospho-Smad3(p-Smad2,p-Smad3)in astrocytes from each group were detec-ted using real time RT-PCR or Western blot techniques.Results:Astrocytes at the third passage exhibited an 80%pos-itivity rate for GFAP.After treated with 10 μg/ml LPS,the astrocytes expression levels of pro-inflammatory factors IL-1β,iNOS,IL-6,and TNF-α were significantly increased(P<0.05),while their expression levels of the anti-inflam-matory factors of Arg-1 and S100A10 were significantly decreased(P<0.05).Meanwhile,their expression levels of TGF-β/Smad signaling pathway related proteins of TGF-β1,TβRⅠ,TβRⅡ,p-Smad2 and Smad3 were increased(P<0.05).After the LPS damaged astrocytes were cocultured with PMSCs,their expression levels of pro-inflammatory factors IL-1β,iNOS,IL-6,and TNF-α were significantly decreased(P<0.05),while their expression levels of the anti-inflammatory factors of Arg-1 and S100A10 were significantly increased(P<0.05).Also,their expression levels of TGF-β/Smad signaling pathway related proteins of TGF-β1,TβRⅠ,TβRⅡ,p-Smad2,and Smad3 were decreased(P<0.05).Conclusion:PMSCs may inhibit the activation of A1 astrocytes through the TGF-β/Smad signaling path-way,by which reducing the astrocytic activation.

Objective This study mainly focuses on the relationship between the serum glycoprotein non-metastatic melanoma protein B(GPNMB)concentration and the degree of neurological damage and prognosis in patients with acute ischemic stroke(AIS),and screens potential biomarkers to provide a reference for clinical diagnosis and treatment.Methods A total of 105 AIS patients hospitalized in the Department of Neurology of the Hospital 2 of Nantong University from June 2023 to March 2024 were selected as the sample group.In this study,the patients were divided into mild group(n=42)and moderate to severe group(n=63)according to the National Institutes of Health Strobe Scale(NIHSS)score within 24 hours of admission.The Modified Rankin Scale(mRS)was used to evaluate the functional recovery 3 months after discharge.The samples were subdivided into good prognosis group(n=34)and poor prognosis group(n=71).The serum GPNMB protein level was detected by ELISA,and the correlation between serum GPNMB protein level and NIHSS and mRS scores was analyzed.The binary Logistic regression model was used to evaluate the predictive value and prognostic evaluation value of serum GPNMB protein level for AIS neurological function damage.Results The serum GPNMB protein concentration in patients with moderate to severe neurological impairment and poor prognosis was significantly lower than that in patients with mild and good prognosis(P<0.05).The serum GPNMB protein level was significantly negatively correlated with the NIHSS score(r=-0.196,P<0.05)and the mRS score(r=-0.334,P<0.05).Multivariate regression analysis showed that GPNMB was still a key independent risk factor for AIS(P<0.05).The evaluation results obtained based on the receiver operating characteristic curve(ROC)showed that the serum GPNMB protein level had diagnostic value in predicting neurological impairment and poor prognosis(sensitivity reached 55.6%,specificity was 81.8%,and the overall accuracy was 63.81%,P<0.05).Conclusion There is a significant positive correlation between the decrease in serum GPNMB protein concentration and the degree of neurological damage in AIS patients,and it is likely to become an important biological indicator for measuring the severity of the disease and long-term prognosis.

To investigate the protective effect of Lycium barbarum glycopeptide(LbGp)on testicu-lar injury induced by D-galactose(D-gal)in aging rats,male SD rats were randomly divided into 6 groups:the blank control group(Control),aging model group(Model),positive control group(β-nicotinamide mononucleotide,NMN),low dose LbGp group(LLbGp),medium dose LbGp group(MLbGp)and high dose LbGp group(HLbGp).The testicular mass of rats was counted,the morphological changes of testicular tissue were observed by hematoxylin-eosin(HE)staining,the testicular senescence was detected by β-galactosidase(SA-β-gal)staining,and the levels of testos-terone(T),luteinizing hormone(LH)and follicle stimulating hormone(FSH)in serum were de-tected.The levels of oxidative factors such as glutathione peroxidase(GSH-Px),superoxide dis-mutase(SOD),malondialdehyde(MDA),catalase(CAT)and inflammatory factors such as tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-6(IL-6)in rat tissues were measured.TUNEL staining was used to detect the apoptosis of testicular cells,epididymal sperm quality,and the expression of Keap1,Nrf2 and Nqo1 mRNA were analyzed.The results showed that compared with the Model group,the testicular coefficient of Lycium barbarum glycopeptide rats in MLbGp and HLbGp groups increased(P＜0.01),the level of T in serum and sperm quality increased(P＜0.05),the structural degeneration and aging of testicular tissue decreased(P＜0.01),the level of antioxidant factors increased,and the levels of inflammatory factors and apopto-sis decreased(P＜0.05).The expression of Keap1 decreased significantly(P＜0.01),while the ex-pression of Nrf2 and Nqo1 mRNA increased(P＜0.05).The above results indicate that Lycium barbarum glycopeptide can improve D-gal-induced testicular senescence,attenuate oxidative stress,reduce inflammatory response,decrease apoptosis,and exert a protective effect on testicular injury in rats due to senescence through the Keap1-Nrf2 signaling pathway.

Objectives:To analyze the cardiac involvement of patients with Fabry disease(FD)in Anhui region.Methods:This retrospective analysis included 48 previously and currently diagnosed FD patients(25 males)in Anhui region,overall patient and gender specific cardiac involvement was analyzed.Results:The median age of FD patients is 28.0(19.0,46.0)years.The cardiac manifestations of patients with FD were most commonly characterized by palpitations/arrhythmias(13/42 cases)and exertional dyspnea(11/42 cases),electrocardiographic changes were most commonly characterized by T-wave inversion(22/42 cases),ST-segment depression(16/42 cases),and left ventricular hypervoltage(18/42 cases),cardiac structural and functional changes were most common in papillary muscle hypertrophy(29/36 cases),bilateral sign(22/37 cases)and left ventricular hypertrophy(21/46 cases),as well as reduced left ventricular global longitudinal strain(26/39 cases).Neuropathic pain(28/43 cases)was the most common extracardiac manifestation of FD patients.FD patients of different gender differed in age at diagnosis(P=0.018),alpha galactosidase A activity(P<0.001),globotriaosylsphingosine(lyso-GL3)levels(P<0.001),enzyme replacement therapy rate(P=0.043),dyshidrosis(P<0.01),and the incidence of angiokeratoma(P=0.004).Correlation analysis showed that genotype was not correlated with enzyme activity or Lyso-GL-3 levels,whereas the Sokolow-Lyon index was positively correlated with Lyso-GL-3 levels(ρ=0.423,P=0.008),and the Sokolow-Lyon indices(septal thickness:ρ=0.562,P<0.001;left ventricle posterior wall thickness:ρ=0.569,P<0.001)and QRS duration(septal thickness:ρ=0.543,P<0.001;left ventricle posterior wall thickness:ρ=0.557,P<0.001)were positively correlated with left ventricular wall thickness.Conclusions:Cardiac involvement in patients with FD in the Anhui region is characterised by palpitations or arrhythmias,accompanied by nonspecific electrocardiographic changes.Echocardiography frequently reveals papillary muscle hypertrophy.The manifestation of cardiac involvement in patients of different genders is similar.