PURPOSE: Hidden blood loss (HBL) during the perioperative period significantly impacts postoperative recovery and complications, yet it is frequently disregarded. This study aimed to investigate the effects of tip-apex distance (TAD) and calcar-referenced tip-apex distance (calTAD) on HBL in the treatment of intertrochanteric fractures utilizing proximal femoral nail antirotation (PFNA). The study also seeks to evaluate the possible decrease in HBL subsequent to PFNA treatment by optimizing nail positioning. METHOD: A historical cohort study was conducted from January 2020 to December 2022. Patients diagnosed with unilateral acute closed femoral intertrochanteric fracture and who underwent PFNA internal fixation surgery met the inclusion criteria, and were grouped according to the value of calTAD and TAD. The participants were divided into low TAD group (TAD<20 mm) and high TAD group (TAD≥20 mm); low calTAD group (calTAD<7.625 mm) and high calTAD group (calTAD≥7.625 mm), respectively. The primary outcome measures were intraoperative blood loss (including HBL, overt blood loss, and total blood loss). Continuous data were analyzed using an independent sample t-test or Mann-Whitney U test, and categorical data were analyzed using the Pearson Chi-square test. Univariate analysis was used to evaluate the association between various indicators and perioperative HBL. A stepwise multiple linear regression analysis model was used to determine the independent factors affecting perioperative HBL. A p value less than 0.05 was considered statistically significant. RESULTS: A total of 131 patients were initially included, of which 80 were assigned to the calTAD group (with 61 in the high calTAD group and 19 in the low calTAD group), and 80 were assigned to the TAD group (with 34 in the high TAD group and 46 in the low TAD group). The average HBL for the low TAD group was 772.85 mL, whereas for the high TAD group it was 919.68 mL (p>0.05). The average HBL for the low calTAD group was 611.42 mL, whereas for the high calTAD group it was 904.97 mL (p<0.05). Subsequent analysis revealed that the patient's height, preoperative hemoglobin levels, changes in hemoglobin and hematocrit levels from pre- to post-surgery, and calTAD are independent risk factors influencing HBL. CONCLUSION In summary, our investigation revealed a significant correlation between the positioning of nails in PFNA and HBL during the perioperative period. By optimizing the placement of the cephalic nail, specifically by ensuring a calTAD of less than 7.625 mm, a significant decrease in HBL can be attained. Additionally, we identified that height, preoperative hemoglobin, differences in preoperative and postoperative hemoglobin and hematocrit, and the positioning of the cephalic nail were independent risk factors for HBL.
Humans ; Retrospective Studies ; Male ; Blood Loss, Surgical/prevention & control* ; Female ; Hip Fractures/surgery* ; Aged ; Fracture Fixation, Intramedullary/methods* ; Bone Nails ; Perioperative Period ; Middle Aged ; Aged, 80 and over

Cancer cachexia is a complex syndrome caused by multiple factors,which seriously affects the quality of life and prognosis of patients.Its overall pathogenesis is related to the deficiency of spleen qi,insufficiency of kidney essence,internal generation of turbid toxins,and the obstruction of the production of qi,blood and essential qi,which cannot nourish the muscles and bones.Under the guidance of the dynamic diagnosis and treatment system of"spleen and kidney exhaustion as the root cause and internal accumulation of turbid toxins as the manifestation",the overall regulation is carried out from four dimensions:opening and closing the spleen and stomach,nourishing the kidney and promoting transportation,transforming turbid toxins and detoxification,and tonifying qi and nourishing yin.It has shown unique value in the intervention of cancer cachexia and can provide ideas and references for the clinical practice of TCM in treating cancer cachexia.

As a non-invasive biomarker, circulating tumor DNA (ctDNA) can sensitively identify minimal residual disease (MRD), offering a novel approach for prognosis prediction and efficacy evaluation in patients with colorectal cancer liver metastasis (CRLM), thereby aiding in the formulation of personalized treatment strategies. This article summarized the progress in the application of ctDNA detection for MRD in CRLM and provided insights into its future directions.

Objective:To explore the impact of childhood trauma on drug relapse tendency, as well as the mediating role of post-traumatic stress disorder (PTSD).Methods:From March to May 2017, a total of 403 compulsory drug rehabilitation personnel were selected for a cross-sectional study and then were investigated by the general demography scale, drug relapse risk scale, childhood trauma questionnaire (CTQ), and PTSD checklist for DSM-5(PCL-5).SPSS 27.0 software and PROCESS 4.1 macro program were used for correlation analysis, regression analysis and Bootstrap-based mediation analysis.Results:The scores of negative emotions subscale of drug relapse risk scale, emotional abuse and emotional neglect subscales of CTQ had no significant gender differences(all P>0.05).There were gender differences in relapse tendency, childhood trauma, and PTSD total scores as well as other dimensions ( t/ Z=2.08-4.67, all P<0.05).There were pairwise positive correlations among the total score of the drug relapse risk scale(31.68±9.79), CTQ(39.90±12.13), and PCL-5(11(3, 24)) for compulsory isolation and rehabilitation personnel ( r=0.28, 0.36, 0.37, P<0.05).After controlling for gender, childhood trauma could significantly and positively predict drug relapse tendency( β=0.34, t=7.24, P<0.01), and PTSD played a mediating role between childhood trauma and drug relapse tendency, with the indirect effect of 0.11(95% CI=0.06-0.16). Conclusion:Childhood trauma can affect drug relapse tendency directly, and indirectly through PTSD.

Cholesterol (CH) plays a crucial role in enhancing the membrane stability of drug delivery systems (DDS). However, its association with conditions such as hyperlipidemia often leads to criticism, overshadowing its influence on the biological effects of formulations. In this study, we reevaluated the delivery effect of CH using widely applied lipid microspheres (LM) as a model DDS. We conducted comprehensive investigations into the impact of CH on the distribution, cell uptake, and protein corona (PC) of LM at sites of cardiovascular inflammatory injury. The results demonstrated that moderate CH promoted the accumulation of LM at inflamed cardiac and vascular sites without exacerbating damage while partially mitigating pathological damage. Then, the slow cellular uptake rate observed for CH@LM contributed to a prolonged duration of drug efficacy. Network pharmacology and molecular docking analyses revealed that CH depended on LM and exerted its biological effects by modulating peroxisome proliferator-activated receptor gamma (PPAR-γ) expression in vascular endothelial cells and estrogen receptor alpha (ERα) protein levels in myocardial cells, thereby enhancing LM uptake at cardiovascular inflammation sites. Proteomics analysis unveiled a serum adsorption pattern for CH@LM under inflammatory conditions showing significant adsorption with CH metabolism-related apolipoprotein family members such as apolipoprotein A-V (Apoa5); this may be a major contributing factor to their prolonged circulation in vivo and explains why CH enhances the distribution of LM at cardiovascular inflammatory injury sites. It should be noted that changes in cell types and physiological environments can also influence the biological behavior of formulations. The findings enhance the conceptualization of CH and LM delivery, providing novel strategies for investigating prescription factors' bioactivity.

Sonodynamic therapy（SDT）has garnered significant attention in cancer treatment modalities due to its superior tissue penetration capabilities，non-invasive approach，and controllability. SDT operates by utilizing sonosensitizers and ultrasound-responsive devices to induce the production of reactive oxygen species（ROS）under ultrasound stimulation，thereby eliciting immunogenic cell death（ICD）in tumor cells and the release of damage-associated molecular patterns，which in turn trigger an immune response against the tumor.However，the tumor microenvironment often results in a relatively weak immune response post-cancer treatment. To address this issue，extensive research is being conducted on combining SDT with immunotherapy，particularly focusing on immune checkpoint blockade（ICB）therapies. This review synthesizes the mechanisms of SDT，its integration with immunotherapy，especially ICB therapies，and the current state of research，with the objective of providing strategic guidance for the advancement of sonodynamic immunotherapy.

Although tumor immunotherapy has transformed cancer treatment，its efficacy against solid tumors remains limited by the immunosuppressive tumor microenvironment，inefficient drug delivery，and off-target toxicity. Engineered bacterial therapy has recently attracted considerable interest as a promising therapeutic strategy owing to its capacity for selective tumor colonization and immunomodulation. Meanwhile，ultrasound technology provides a non-invasive，spatially precise，and real-time controllable means to improve the performance and applicability of bacterial-mediated therapies. This review summarizes recent advances in ultrasound-regulated bacterial therapy for cancer immunotherapy. Beginning with an examination of the mechanisms through which engineered bacteria modulate antitumor immunity，it is followed by an elucidation of how ultrasound technology exploits its biological effects and spatiotemporal control capabilities to simultaneously enhance bacterial therapy's safety/efficacy and enable tumor treatment visualization，thereby activating systemic immune responses. Finally，current challenges and future directions for clinical translation are critically discussed. In conclusion，ultrasound-regulated bacterial therapy represents an emerging interdisciplinary approach with the potential to overcome key limitations in solid tumor immunotherapy.

The tumor microenvironment (TME) is the cellular milieu in which tumor cells thrive, comprising interacting cells and associated factors that form a complex network of interactions, directly or indirectly influencing the initiation, progression, and metastasis of lung cancer. Through TCM pattern identification, it has been observed thatphlegm-pathogen is closely associated with disorder in the inflammatory-metabolic-immune microenvironments of lung cancer. This involves three key pathological mechanisms: "phlegm-stasis complicated by toxin, qi deficiency with exuberant phlegm, and phlegm-pathogen impairing healthy qi". Molecular mechanism studies have revealed that phlegm-resolving agents can extensively modulate multiple targets or pathways, thereby remodeling the inflammatory-metabolic-immune microenvironments of lung cancer. Consequently, a comprehensive therapeutic strategy integrating "resolving phlegm, dispelling stasis, and detoxifying; supplementing qi, warming yang, and resolving phlegm; and reinforcing healthy qi, tonifying the lung, and eliminating phlegm" is essential to reshape the lung cancer TME and enhance antitumor efficacy.

Cancer is one of the major diseases of high morbidity and mortality worldwide,and its therapeutic approaches are facing great challenges.Immunotherapy,especially the activation of innate immunity represented by the cGAS-STING signaling pathway,is the current research hotspot in tumor immunotherapy.Activation of innate immune response by gas therapy is the latest development in tumor therapeutic approaches,especially the use of gas signaling molecules(NOx CO,H2S and SO2)to activate the cGAS-STING signaling pathway to induce intrinsic immunity of the organism,which leads to anti-tumor immunotherapy.Although intrinsic immunity activated by gas signaling molecules plays an important role in tumor immunotherapy,few reviews have been reported on its association with the cGAS-STING signaling mechanism.In this paper,we will comprehensively describe how gas signaling molecules damage the mitochondrial matrix and DNA damage through oxidative/nitrosative stress,thereby activating the cGAS-STING signaling pathway and triggering the innate immune cascade,aiming to summarize the process of activation of anti-tumor immune effects by gas signaling molecules,and to provide more references for the gas therapies in the future anti-tumor immunity research.

Objective To investigate the status and influencing factors of type 2 diabetes mellitus(T2DM)patients' fear of complications,and to provide a reference for formulating targeted intervention measures.Methods From April to November 2024,370 patients with T2DM in 2 tertiary general hospitals in Daqing City were selected by convenience sampling method.General data questionnaire,Fear of Complications Questionnaire,Self-Perceived Burden Scale,Psychological Capital Questionnaire,Mishel Uncertainty in Illness Scale and Family Apgar Index Questionnaire were used for investigation.Univariate analysis and binary Logistic regression were performed to analyze the influencing factors.Results A total of 364 valid questionnaires were collected,with an effective recovery rate of 98.38％.The score of Fear of Complications Questionnaire was(23.47±7.47),and the incidence of fear of complications was 22.25％.Logistic regression analysis showed that medical payment methods,the number of complications,positive psychological capital and family care were the influencing factors of FoC in T2DM patients.Conclusion The fear of complications in T2DM patients is at a moderate level.Nursing staff should pay attention to the early assessment of patients' fear of complications,promptly identify and take effective measures to reduce the level of patients' fear of complications,improve their quality of life.