The accuracy of medical imaging diagnosis will directly impact the clinical forensic evaluation's scientific validity and objectivity.This study systematically analyzed the primary causes of misdiagnosis and missed diagnosis in imaging examinations,focusing on representative cases,including rib fractures,traumatic subarachnoid hemorrhage,joint injuries with ligament damage,nasal fractures,congenital skeletal variations,and epiphyseal injuries.Key contributing factors encompassed limitation of imaging technologies,the insufficient interpretive experience of examiners,the complexity of injury mechanisms,and inadequate post-traumatic dynamic imaging follow-up.To address these issues,improvement strategies are proposed,which were establishing standardized imaging review protocols,implementing multimodal imaging approaches,rigorous evaluation of original imaging data,and enhancing professional knowledge regarding anatomical variations and injury differentiation.These measures aim to elevate the quality of forensic imaging diagnosis,providing more precise and reliable strategies for forensic clinical identifications.

N7-methylguanosine(m7G)modification occurs at the 5'cap of mRNA in eukaryotes,and is also found at specific sites on tRNA and rRNA,showing wide conservation across various biological organisms.Aberrant m7G modification is involved in the dysregulation of gene expression and serves as a biomarker for multiple cancers,with significant potential for applications in tumor diagnosis and therapy.This review summarizes the biological functions and regulatory mechanisms of m7G modification,and outlines its potential clinical applications.It also highlights the oncogenic roles of aberrant m7G modification and its association with prognosis,providing a detailed discussion of the role and molecular mechanisms of abnormal m7G modification in regulating drug resistance in various cancers.

In recent years, more and more studies have shown that autophagy is closely related to female reproductive process. Autophagy is a widespread and highly conserved degradation system in eukaryotes that can be activated under conditions such as hypoxia, starvation, lack of nutrients, or extreme pH. In terms of reproductive health, autophagy can improve reproductive dysfunction by removing damaged organelles and regulating cell growth and metabolism. Appropriate regulation of autophagy helps to improve oocyte quality, delay ovarian aging, fine-regulate endometrial growth, and ensure successful implantation of embryos. However, the abnormality of autophagy pathway may cause problems such as activation of pelvic inflammatory cytokines, reduced endometrial receptivity, abnormal follicle development, and weakened invasion ability of trophoblast cells, thus leading to the occurrence and development of reproductive disorders such as endometriosis, chronic endometritis, polycystic ovary syndrome, early-onset ovarian insufficiency, and recurrent spontaneous abortion. This article reviews the mechanism and therapeutic targets of autophagy in female reproductive diseases, providing clinical ideas and diagnosis and treatment strategies for improving female reproductive health.

Renal cancer is a common and increasingly prevalent malignancy with a complex pathogenesis influenced by genetics,smoking,and obesity.Current treatment mainly involves surgery with adjunctive chemotherapy,radiation,and immunotherapy,but high rates of recurrence and metastasis indicate its limited effectiveness,emphasizing the need for better therapeutic targets.Growing evidence indicates that epigenetic modifications,particularly RNA modifications,play a critical role in renal cancer development and progression.This review highlights recent advances in renal cancer epigenetics,focusing on RNA modifications such as N6-methyladenosine(m6 A),N7-methylguanosine(m7G),5-methylcytosine(m5C),N1-methyladenosine(m1A),adenosine-to-inosine(A-to-I),N6,2'-O-dimethyladenosine(m6Am),and N4-acetylcytidine(ac4C),along with their regulatory factors.It also explores the diagnostic and therapeutic potential of targeting RNA modifications and associated proteins.

Neutrophils are the most abundant white blood cells in the human body and play different roles in various diseases.The studies have shown that inflammation is closely related to the occurrence and development of tumors.As an important component of the tumor microenvironment(TME),neutrophils play a crucial role in tumors and have a dual effect of promoting and inhibiting tumor growth.This article deeply discusses the recruitment and subtypes of neutrophils,as well their dual effects on tumors.Meanwhile,it illustrates the role and clinical significance of neutrophils in gliomas.The therapeutic approach of targeting neutrophils in tumors provides a new direction for subsequent tumor treatment.Especially for central nervous system tumors,neutrophils as carriers can transport chemotherapeutic drugs across the blood-brain barrier to reach the tumor tissue,offering new hope for the subsequent treatment of brain tumors.

The dysregulation of cyclin-dependent kinase 12 (CDK12), which may result from genomic alterations or modulation by upstream effectors, is implicated in cancer oncogenesis and progression. CDK12 overexpression or activation is sufficient to induce tumor initiation, recurrence, and therapeutic resistance. However, CDK12 may also exert tumor-suppressive functions in a context-dependent manner. Therefore, caution is warranted when targeting CDK12 in future clinical trials. A comprehensive elucidation of the dual roles and underlying mechanisms of CDK12 in carcinogenesis is urgently needed to advance precision oncology. This review provides an overview of the current understanding of the dysregulation and biological roles of CDK12 in cancer. Subsequently, we systematically summarize the functions and mechanisms of the oncogenic and tumor-suppressive roles of CDK12 in different contexts. Finally, we discuss the potential of CDK12 as a novel therapeutic target and its implications in clinical oncology, offering insights into future directions for innovative cancer treatment strategies.

Objective: To compare quality control (relative purity and specific activity) and process control [plasminogen (Pg) antigen recovery and potency recovery] indexes of samples before and after adding the Q chromatography step to the full chromatography process of human Pg, thereby determining whether the addition of this step could improve Pg recovery by affinity chromatography. Methods: A Q chromatography step was added before the Pg affinity chromatography in the original Pg chromatography process. The loading solution, flow through solution and eluate of Q chromatography and Pg affinity chromatography were collected. The potency of coagulation factor Ⅱ (FⅡ), Ⅶ (FⅦ), Ⅷ (FⅧ), Ⅸ (FⅨ), and Ⅹ(FⅩ) were detected by the coagulation method, the total protein content was detected by the BCA method, and the Pg potency was detected by the chromogenic substrate method. The content of specific plasma proteins was detected by immunoturbidimetry, the potency recovery of coagulation factors was calculated, and the flow direction of coagulation factors was analyzed. The recovery of different plasma protein antigens were calculated, and the distribution of impurity proteins was analyzed. The relative purity and specific activity of Pg, antigen content, and potency recovery in the target fractions were calculated and compared with the original process indicators, so as to determine the effect of adding Q chromatography on the original process. Furthermore, the reproducibility after process modification was assessed. Results: 100% of FⅡ, FⅩ, and FⅨ, 87.81% of FⅧ, and 40.44% of FⅦ in filtered plasma were removed by Q chromatography. The residual FⅦ (53.26%) and FⅧ (13.30%) in Q flow-through fraction were completely removed by Pg affinity chromatography. In both the original process (without Q-chromatography) and the modified process (with Q-chromatography), non-target plasma proteins mainly existed in the flow-through fraction of Pg affinity chromatography. The antigen recovery of IgM, ceruloplasmin (CER), and fibronectin (FNC) in Q-chromatography flow-through fraction were reduced. In contrast, antigen recovery of other plasma proteins [IgG, IgA, Pg, albumin (AlB), alpha-1-antitrypsin (AAT), and fibrinogen (Fg)] were all >90%, which were consistent with the protein composition and proportion in the original affinity chromatography loading solution. Compared with the recovery rate of Pg antigen in the original process (74.4%), the total recovery of Pg antigen in the modified process was significantly increased (89.97%). Compared with the recovery of IgG (97.48%) and Fg (95.32%) in the Pg affinity flows-through fraction of the original process, the modified process resulted in a slight reduction in the recovery of IgG (94.60%), while the recovery of Fg was not affected (95.05%). The potency recovery rate, specific activity, and relative purity of Pg after Q chromatography were 99.3%, 0.016 U/mg, and 0.15%. These values were the same as those of Pg affinity chromatography loading solution by the original process, indicating that introduction of Q chromatography did not affect subsequent Pg affinity chromatography. Compared with the recovery of Pg antigen in three batches of the original process (66.49±1.02)%, the recovery of Pg antigen in the affinity chromatography eluent of the modified process [five batches; (77.43±4.43)%] was significantly improved. Furthermore, the potency recovery was (86.80±4.28)%, the relative purity was (81.99±1.25)%, the specific activity was (8.679±1.073)U/mg, and the process was reproducible. Conclusion: The addition of Q chromatography could improve the recovery of Pg affinity chromatography in the full chromatography process.

Objective: To systematically analyzes the impact of blood donor characteristics on red blood cell (RBC) quality and transfusion outcomes, and to provide a scientific basis for optimizing donor selection criteria and developing personalized transfusion strategies. Methods: A literature search was conducted across electronic databases including CNKI, VIP, Wanfang Data, PubMed, and Embase using combinations of keywords such as "donor characteristics", "blood storage lesion", "blood quality", and "transfusion outcomes" for summary and analysis. Results: Factors associated with the blood donor characteristics including demographic characteristics (sex, age, body mass index), lifestyle habits (smoking, alcohol consumption, exercise), and dietary or pharmacological exposures significantly influence blood storage stability and transfusion efficacy by modulating erythrocyte metabolism, oxidative stress levels, and immune properties. Conclusion: The complexity and diversity of the blood donor characteristics are associated with blood quality and transfusion outcomes. Future efforts should focus on refining donor selection criteria and establishing personalized transfusion strategies to enhance blood product quality and improve patient outcomes.

Objective To investigate the effect of concentrated growth factor(CGF)on angiogenesis in human microvascular endothelial cells(HMEC-1)and explore the underlying mechanisms.Methods HMEC-1 were divided into the control group,CGF group,and CGF+LY294002 group.Cell proliferation,migration,and tubule formation abilities were measured and compared using the Cell Counting Kit-8(CCK-8),Transwell assay,and tube formation assay,respectively.The protein expression levels of phosphoinositide 3-kinase(PI3K),phosphorylated PI3K(p-PI3K),phospho-protein kinase B(Akt),phosphorylated Akt(p-Akt),mam-malian target of rapamycin(mTOR),and phosphorylated mTOR(p-mTOR)were detected and compared by Western blot.Results Compared with the control group,the CGF group exhibited enhanced cell proliferation,migration,and tubule formation abilities(P＜0.05),along with increased expression levels of p-PI3K,p-Akt,and p-mTOR(P＜0.05).Compared with the CGF group,the CGF+LY294002 group demonstrated reduced cell proliferation,migration,and tubule formation abilities(P＜0.05),accompanied by decreased expression levels of p-PI3K,p-Akt,and p-mTOR(P＜0.05).Conclusion CGF promotes the proliferation,migration,and angiogenesis of HMEC-1 via the PI3K/mTOR/Akt pathway.

The dysregulation of cyclin-dependent kinase 12(CDK12),which may result from genomic alterations or modulation by upstream effectors,is implicated in cancer oncogenesis and progression.CDK12 over-expression or activation is sufficient to induce tumor initiation,recurrence,and therapeutic resistance.However,CDK12 may also exert tumor-suppressive functions in a context-dependent manner.Therefore,caution is warranted when targeting CDK12 in future clinical trials.A comprehensive elucidation of the dual roles and underlying mechanisms of CDK12 in carcinogenesis is urgently needed to advance pre-cision oncology.This review provides an overview of the current understanding of the dysregulation and biological roles of CDK12 in cancer.Subsequently,we systematically summarize the functions and mechanisms of the oncogenic and tumor-suppressive roles of CDK12 in different contexts.Finally,we discuss the potential of CDK12 as a novel therapeutic target and its implications in clinical oncology,offering insights into future directions for innovative cancer treatment strategies.