Objective:To identify and validate secreted effector proteins of Chlamydia psittaci ( C. psittaci) through bioinformatic prediction and experimental verification, and to characterize their subcellular localization in host cells. Methods:Potential effector proteins were predicted using bioinformatics tools. Candidate effectors were fused to β-lactamase through the constructed expression vectors, and these vectors were transformed into C. psittaci. The secretion of these candidate effectors was evaluated by β-lactamase translocation assays. Eukaryotic expression vectors of confirmed effectors were transfected into host cells to determine their intracellular localization patterns. Results:Bioinformatic analysis identified 29 candidate effector proteins. Experimental validation confirmed the secretion of five effectors, with four exhibiting cytoplasmic localization and one displaying nuclear localization in host cells.Conclusion:This study characterizes five novel C. psittaci secreted effector proteins, providing critical insights for investigating the molecular pathogenesis of psittacosis.

Diabetic cardiomyopathy(DCM)is one of the complications of diabetes.The onset of DCM is hidden and easy to be ignored.Myocardial injury is serious in the later stage and the prognosis is poor.At present,symptomatic treatment is the main clinical treatment.Cuproptosis is a novel cell death mode caused by imbalanced copper ion concentration in the body,leading to mitochondrial metabolic abnormalities,which is one of the important mechanisms of DCM.Targeted cuproptosis pathway therapy for DCM is currently a focus and hotspot of research.The"Qi Luo Theory"is one of the disciplinary branches of the theory of collateral diseases,which mainly operates the meridian Qi system.The syndrome and treatment system of collateral diseases cardiovascular diseases have important guiding significance for the treatment of DCM.Traditional Chinese medicine believes that deficiency and stagnation of Qi that in the collaterals are the root causes of DCM,with stasis and toxin obstructing collaterals and damage to the heart collaterals being the core of the disease.The ultimate outcome is the deficiency and decline of Qi,Blood,Yin,and Yang in the heart.The"Qi Luo Theory"and cuproptosis have similarities in physiological functions and pathological processes,and cuproptosis can be said to be one of the microscopic manifestations of the"Qi Luo theory".Based on this,the staged treatment principle of tonifying deficiency and promoting stagnation as the norm,attacking and supplementing simultaneously as the principle,and strengthening the body and consolidating the core has been proposed,in order to provide theoretical reference for the clinical treatment of DCM.

Triple-negative breast cancer (TNBC) represents a distinctive subtype, characterized by the absence of estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2 (HER2). Due to its high inter-tumor and intra-tumor heterogeneity, TNBC poses significant chanllenges for personalized diagnosis and treatment. The advant of clustered regular interspaced short palindromic repeats (CRISPR) technology has profoundly enhanced our understanding of the structure and function of the TNBC genome, providing a powerful tool for investigating the occurrence and development of diseases. This review focuses on the application of CRISPR/Cas technology in the personalized diagnosis and treatment of TNBC. We begin by discussing the unique attributes of TNBC and the limitations of current diagnostic and treatment approaches: conventional diagnostic methods provide limited insights into TNBC, while traditional chemotherapy drugs are often associated with low efficacy and severe side effects. The CRISPR/Cas system, which activates Cas enzymes through complementary guide RNAs (gRNAs) to selectively degrade specific nucleic acids, has emerged as a robust tool for TNBC research. This technology enables precise gene editing, allowing for a deeper understanding of TNBC heterogeneity by marking and tracking diverse cell clones. Additionally, CRISPR facilitates high-throughput screening to promptly identify genes involved in TNBC growth, metastasis, and drug resistance, thus revealing new therapeutic targets and strategies. In TNBC diagnostics, CRISPR/Cas was applied to develop molecular diagnostic systems based on Cas9, Cas12, and Cas13, each employing distinct detection principles. These systems can sensitively and specifically detect a variety of TNBC biomarkers, including cell-specific DNA/RNA and circulating tumor DNA (ctDNA). In the realm of precision therapy, CRISPR/Cas has been utilized to identify key genes implicated in TNBC progression and treatment resistance. CRISPR-based screening has uncovered potential therapeutic targets, while its gene-editing capabilities have facilitated the development of combination therapies with traditional chemotherapy drugs, enhancing their efficacy. Despite its promise, the clinical translation of CRISPR/Cas technology remains in its early stages. Several clinical trials are underway to assess its safety and efficacy in the treatment of various genetic diseases and cancers. Challenges such as off-target effects, editing efficiency, and delivery methods remain to be addressed. The integration of CRISPR/Cas with other technologies, such as 3D cell culture systems, human induced pluripotent stem cells (hiPSCs), and artificial intelligence (AI), is expected to further advance precision medicine for TNBC. These technological convergences can offer deeper insights into disease mechanisms and facilitate the development of personalized treatment strategies. In conclusion, the CRISPR/Cas system holds immense potential in the precise diagnosis and treatment of TNBC. As the technology progresses and becomes more costs-effective, its clinical relevance will grow, and the translation of CRISPR/Cas system data into clinical applications will pave the way for optimal diagnosis and treatment strategies for TNBC patients. However, technical hurdles and ethical considerations require ongoing research and regulation to ensure safety and efficacy.

Diabetic cardiomyopathy(DCM)is one of the complications of diabetes.The onset of DCM is hidden and easy to be ignored.Myocardial injury is serious in the later stage and the prognosis is poor.At present,symptomatic treatment is the main clinical treatment.Cuproptosis is a novel cell death mode caused by imbalanced copper ion concentration in the body,leading to mitochondrial metabolic abnormalities,which is one of the important mechanisms of DCM.Targeted cuproptosis pathway therapy for DCM is currently a focus and hotspot of research.The"Qi Luo Theory"is one of the disciplinary branches of the theory of collateral diseases,which mainly operates the meridian Qi system.The syndrome and treatment system of collateral diseases cardiovascular diseases have important guiding significance for the treatment of DCM.Traditional Chinese medicine believes that deficiency and stagnation of Qi that in the collaterals are the root causes of DCM,with stasis and toxin obstructing collaterals and damage to the heart collaterals being the core of the disease.The ultimate outcome is the deficiency and decline of Qi,Blood,Yin,and Yang in the heart.The"Qi Luo Theory"and cuproptosis have similarities in physiological functions and pathological processes,and cuproptosis can be said to be one of the microscopic manifestations of the"Qi Luo theory".Based on this,the staged treatment principle of tonifying deficiency and promoting stagnation as the norm,attacking and supplementing simultaneously as the principle,and strengthening the body and consolidating the core has been proposed,in order to provide theoretical reference for the clinical treatment of DCM.

The pregnant woman was 39 years old，G2P1，a fetal goiter was found at 25 weeks at the Second Xiangya Hospital of Central South University，and thyroid function was normal during the pregnancy. Amniocentesis revealed the presence of two DUOX2 mutations in fetal DNA：c.3340delC（P.L1114Sfs56）in exon 25 and c.2654G＞A（p.R885Q）in exon 20，which were determined to be heritable by familial genetic testing. Many fetal and neonatal ultrasounds have shown goiter，rich blood flow in the parenchyma and low postnatal thyroid hormone levels led to the diagnosis of congenital hypothyroidism. The patient was given L-thyroxine 30 μg/d. After 3 months of follow-up，the thyroid function was normal without developmental problems.

Objective:To identify and validate secreted effector proteins of Chlamydia psittaci ( C. psittaci) through bioinformatic prediction and experimental verification, and to characterize their subcellular localization in host cells. Methods:Potential effector proteins were predicted using bioinformatics tools. Candidate effectors were fused to β-lactamase through the constructed expression vectors, and these vectors were transformed into C. psittaci. The secretion of these candidate effectors was evaluated by β-lactamase translocation assays. Eukaryotic expression vectors of confirmed effectors were transfected into host cells to determine their intracellular localization patterns. Results:Bioinformatic analysis identified 29 candidate effector proteins. Experimental validation confirmed the secretion of five effectors, with four exhibiting cytoplasmic localization and one displaying nuclear localization in host cells.Conclusion:This study characterizes five novel C. psittaci secreted effector proteins, providing critical insights for investigating the molecular pathogenesis of psittacosis.

The pregnant woman was 39 years old，G2P1，a fetal goiter was found at 25 weeks at the Second Xiangya Hospital of Central South University，and thyroid function was normal during the pregnancy. Amniocentesis revealed the presence of two DUOX2 mutations in fetal DNA：c.3340delC（P.L1114Sfs56）in exon 25 and c.2654G＞A（p.R885Q）in exon 20，which were determined to be heritable by familial genetic testing. Many fetal and neonatal ultrasounds have shown goiter，rich blood flow in the parenchyma and low postnatal thyroid hormone levels led to the diagnosis of congenital hypothyroidism. The patient was given L-thyroxine 30 μg/d. After 3 months of follow-up，the thyroid function was normal without developmental problems.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, defined by several phases, ranging from benign fat accumulation to non-alcoholic steatohepatitis (NASH), which can lead to liver cancer and cirrhosis. Although NAFLD is a disease of disordered metabolism, it also involves several immune cell-mediated inflammatory processes, either promoting and/or suppressing hepatocyte inflammation through the secretion of pro-inflammatory and/or anti-inflammatory factors to influence the NAFLD process. However, the underlying disease mechanism and the role of immune cells in NAFLD are still under investigation, leaving many open-ended questions. In this review, we presented the recent concepts about the interplay of immune cells in the onset and pathogenesis of NAFLD. We also highlighted the specific non-immune cells exhibiting immunological properties of therapeutic significance in NAFLD. We hope that this review will help guide the development of future NAFLD therapeutics.

The study aimed to investigate the effect of anemoside B4(B4) on fatty acid metabolism in mice with colitis-associated cancer(CAC). The CAC model was established by azoxymethane(AOM)/dextran sodium sulfate(DSS) in mice. Mice were randomly divided into a normal group, a model group, and low-, medium-, and high-dose anemoside B4 groups. After the experiment, the length of the mouse colon and the size of the tumor were measured, and the pathological alterations in the mouse colon were observed using hematoxylin-eosin(HE) staining. The slices of the colon tumor were obtained for spatial metabolome analysis to analyze the distribution of fatty acid metabolism-related substances in the tumor. The mRNA levels of SREBP-1, FAS, ACCα, SCD-1, PPARα, ACOX, UCP-2, and CPT-1 were determined by real-time quantitative PCR(RT-qPCR). The results revealed that the model group showed decreased body weight(P<0.05) and colon length(P<0.001), increased number of tumors, and increased pathological score(P<0.01). Spatial metabolome analysis revealed that the content of fatty acids and their derivatives, carnitine, and phospholipid in the colon tumor was increased. RT-qPCR results indicated that fatty acid de novo synthesis and β-oxidation-related genes, such as SREBP-1, FASN, ACCα, SCD-1, ACOX, UCP-2, and CPT-1 mRNA expression levels increased considerably(P<0.05, P<0.001). After anemoside B4 administration, the colon length increased(P<0.01), and the number of tumors decreased in the high-dose anemoside B4 group(P<0.05). Additionally, spatial metabolome analysis showed that anemoside B4 could decrease the content of fatty acids and their derivatives, carnitine, and phospholipids in colon tumors. Meanwhile, anemoside B4 could also down-regulate the expression of FASN, ACCα, SCD-1, PPARα, ACOX, UCP-2, and CPT-1 in the colon(P<0.05, P<0.01, P<0.001). The findings of this study show that anemoside B4 may inhibit CAC via regulating fatty acid metabolism reprogramming.
Mice ; Animals ; Sterol Regulatory Element Binding Protein 1 ; Colitis-Associated Neoplasms ; PPAR alpha/genetics* ; Colonic Neoplasms/genetics* ; Colon ; Azoxymethane ; RNA, Messenger ; Dextran Sulfate ; Colitis/drug therapy* ; Mice, Inbred C57BL ; Disease Models, Animal