Biomolecular condensates are formed through phase separation of biomacromolecules such as proteins and RNAs. These condensates exhibit liquid-like properties that can futher transition into more stable material states. They form complex internal structures via multivalent weak interactions, enabling precise spatiotemporal regulations. However, the use of inconsistent and non-standardized terminology has become increasingly problematic, hindering academic exchange and the dissemination of scientific knowledge. Therefore, it is necessary to discuss the terminology related to biomolecular condensates in order to clarify concepts, promote interdisciplinary cooperation, enhance research efficiency, and support the healthy development of this field.

Fibrosis, the pathological scarring of vital organs, is a severe and often irreversible condition that leads to progressive organ dysfunction. It is particularly pronounced in organs like the liver, kidneys, lungs, and heart. Despite its clinical significance, the full understanding of its etiology and complex pathogenesis remains incomplete, posing substantial challenges to diagnosing, treating, and preventing the progression of fibrosis. Among the various molecular players involved, platelet-derived growth factor-C (PDGF-C) has emerged as a crucial factor in fibrotic diseases, contributing to the pathological transformation of tissues in several key organs. PDGF-C is a member of the PDGFs family of growth factors and is synthesized and secreted by various cell types, including fibroblasts, smooth muscle cells, and endothelial cells. It acts through both autocrine and paracrine mechanisms, exerting its biological effects by binding to and activating the PDGF receptors (PDGFRs), specifically PDGFRα and PDGFRβ. This binding triggers multiple intracellular signaling pathways, such as JAK/STAT, PI3K/AKT and Ras-MAPK pathways. which are integral to the regulation of cell proliferation, survival, migration, and fibrosis. Notably, PDGF-C has been shown to promote the proliferation and migration of fibroblasts, key effector cells in the fibrotic process, thus accelerating the accumulation of extracellular matrix components and the formation of fibrotic tissue. Numerous studies have documented an upregulation of PDGF-C expression in various fibrotic diseases, suggesting its significant role in the initiation and progression of fibrosis. For instance, in liver fibrosis, PDGF-C stimulates hepatic stellate cell activation, contributing to the excessive deposition of collagen and other extracellular matrix proteins. Similarly, in pulmonary fibrosis, PDGF-C enhances the migration of fibroblasts into the damaged areas of lungs, thereby worsening the pathological process. Such findings highlight the pivotal role of PDGF-C in fibrotic diseases and underscore its potential as a therapeutic target for these conditions. Given its central role in the pathogenesis of fibrosis, PDGF-C has become an attractive target for therapeutic intervention. Several studies have focused on developing inhibitors that block the PDGF-C/PDGFR signaling pathway. These inhibitors aim to reduce fibroblast activation, prevent the excessive accumulation of extracellular matrix components, and halt the progression of fibrosis. Preclinical studies have demonstrated the efficacy of such inhibitors in animal models of liver, kidney, and lung fibrosis, with promising results in reducing fibrotic lesions and improving organ function. Furthermore, several clinical inhibitors, such as Olaratumab and Seralutinib, are ongoing to assess the safety and efficacy of these inhibitors in human patients, offering hope for novel therapeutic options in the treatment of fibrotic diseases. In conclusion, PDGF-C plays a critical role in the development and progression of fibrosis in vital organs. Its ability to regulate fibroblast activity and influence key signaling pathways makes it a promising target for therapeutic strategies aiming at combating fibrosis. Ongoing research into the regulation of PDGF-C expression and the development of PDGF-C/PDGFR inhibitors holds the potential to offer new insights and approaches for the diagnosis, treatment, and prevention of fibrotic diseases. Ultimately, these efforts may lead to the development of more effective and targeted therapies that can mitigate the impact of fibrosis and improve patient outcomes.

This paper aimed to investigate the therapeutic effect and mechanism of action of the Yiqi Fumai Formula(YQFM), a kind of traditional Chinese medicine(TCM), on mice with experimental heart failure based on the "heart-gut axis" theory. Based on the network pharmacology integrated with the group collaboration algorithm, the active ingredients were screened, a "component-target-disease" network was constructed, and the potential pathways regulated by the formula were predicted and analyzed. Next, the model of experimental heart failure was established by intraperitoneal injection of adriamycin at a single high dose(15 mg·kg~(-1)) in BALB/c mice. After intraperitoneal injection of YQFM(lyophilized) at 7.90, 15.80, and 31.55 mg·d~(-1) for 7 d, the protective effects of the formula on cardiac function were evaluated using indicators such as ultrasonic electrocardiography and myocardial injury markers. Combined with inflammatory factors in the cardiac and colorectal tissue, as well as targeted assays, the relevant indicators of potential pathways were verified. Meanwhile, 16S rDNA sequencing was performed on mouse fecal samples using the Illumina platform to detect changes in gut flora and analyze differential metabolic pathways. The results show that the administration of injectable YQFM(lyophilized) for 7 d significantly increased the left ventricular end-systolic internal diameter, fractional shortening, and ejection fraction of cardiac tissue of mice with experimental heart failure(P<0.05). Moreover, markers of myocardial injury were significantly decreased(P<0.05), indicating improved cardiac function, along with significantly suppressed inflammatory responses in cardiac and intestinal tissue(P<0.05). Additionally, the species of causative organisms was decreased, and the homeostasis of gut flora was improved, involving a modulatory effect on PI3K-Akt signaling pathway-related inflammation in cardiac and colorectal tissue. In conclusion, YQFM can affect the "heart-gut axis" immunity through the homeostasis of the gut flora, thereby exerting a therapeutic effect on heart failure. This finding provides a reference for the combination of TCM and western medicine to prevent and treat heart failure based on the "heart-gut axis" theory.
Animals ; Drugs, Chinese Herbal/administration & dosage* ; Heart Failure/microbiology* ; Mice ; Mice, Inbred BALB C ; Male ; Disease Models, Animal ; Gastrointestinal Microbiome/drug effects* ; Heart/physiopathology* ; Humans ; Signal Transduction/drug effects*

OBJECTIVE: To assess the efficacy of Qingda Granule (QDG) in ameliorating hypertension-induced cardiac damage and investigate the underlying mechanisms involved. METHODS: Twenty spontaneously hypertensive rats (SHRs) were used to develope a hypertension-induced cardiac damage model. Another 10 Wistar Kyoto (WKY) rats were used as normotension group. Rats were administrated intragastrically QDG [0.9 g/(kg•d)] or an equivalent volume of pure water for 8 weeks. Blood pressure, histopathological changes, cardiac function, levels of oxidative stress and inflammatory response markers were measured. Furthermore, to gain insights into the potential mechanisms underlying the protective effects of QDG against hypertension-induced cardiac injury, a network pharmacology study was conducted. Predicted results were validated by Western blot, radioimmunoassay immunohistochemistry and quantitative polymerase chain reaction, respectively. RESULTS: The administration of QDG resulted in a significant decrease in blood pressure levels in SHRs (P<0.01). Histological examinations, including hematoxylin-eosin staining and Masson trichrome staining revealed that QDG effectively attenuated hypertension-induced cardiac damage. Furthermore, echocardiography demonstrated that QDG improved hypertension-associated cardiac dysfunction. Enzyme-linked immunosorbent assay and colorimetric method indicated that QDG significantly reduced oxidative stress and inflammatory response levels in both myocardial tissue and serum (P<0.01). CONCLUSIONS Both network pharmacology and experimental investigations confirmed that QDG exerted its beneficial effects in decreasing hypertension-induced cardiac damage by regulating the angiotensin converting enzyme (ACE)/angiotensin II (Ang II)/Ang II receptor type 1 axis and ACE/Ang II/Ang II receptor type 2 axis.
Animals ; Drugs, Chinese Herbal/therapeutic use* ; Hypertension/pathology* ; Renin-Angiotensin System/drug effects* ; Rats, Inbred SHR ; Oxidative Stress/drug effects* ; Male ; Rats, Inbred WKY ; Blood Pressure/drug effects* ; Myocardium/pathology* ; Rats ; Inflammation/pathology*

Probiotics are natural systems bridging synthetic biology, physical biotechnology, and immunology, initiating innate and adaptive anti-tumor immune activity. We previously constructed an all-in-one engineered food-grade probiotic Lactococcus lactis (FOLactis) which could boost the crosstalk among different immune cells such as dendritic cells (DCs), natural killer cells, and T cells. Herein, considering the limited clinical efficacy of naked personalized neoantigen peptide vaccines, we decorate FOLactis with tumor antigens by employing a Plug-and-Display system comprising membrane-inserted peptides. Intranodal injection of FOLactis coated with neoantigen peptides (Ag-FOLactis) induces robust DCs presentation and neoantigen-specific cellular immunity. Notably, Ag-FOLactis not only triggers a 45-fold rise in the quantity of locally reactive neoantigen-specific T cells but also induces epitope spreading in both subcutaneous and metastatic tumor-bearing models, leading to potent inhibition of tumor growth. These findings imply that Ag-FOLactis represents a powerful platform to rapidly and easily display antigens, facilitating the development of a bio-activated platform for personalized therapy.

Superior vena cava syndrome(SVCS)is a group of clinical syndromes caused by obstruction of the superior vena cava and its major branches from various causes.Pulmonary artery stenosis(PS)is a complication of lung cancer or mediastinal tumours.SVCS combined with PS due to pulmonary metastases from bladder cancer is extremely rare and has not been reported in the literature.Here we reported an old male patient with pulmonary metastases from bladder cancer presenting with swelling of the head,neck and both upper limbs.SVCS combined with PS was clarified by pulmonary artery computed tomography angiography(CTA)and digital subtraction angiography(DSA).Endovascular stenting was used to treat SVCS.Angiography also showed that PS had not caused pulmonary hypertension and did not need to be treated.The swelling of the patient's head,neck and upper limbs was gradually reduced after the procedure.

Objective This study aims to investigate the application of the Plan-Do-Check-Act(PDCA)cycle in the Di-agnosis Related Group(DRG)payment system for oncological diseases.Methods We analyzed the factors influencing DRG pay-ment and incorporated the PDCA Cycle in the oncological diseases at a tertiary hospital in Tianjin.The baseline data of cases partic-ipating in DRG payment from April 2022 to September 2022 were compared with the settlement data of cases participating in DRG payment from October 2022 to March 2023.SPSS 20.0 was used to evaluate the impact of data quality in medical record documenta-tion on DRG admission rate,average hospitalization costs,average length of stay,Case Mix Index(CMI)value,and DRG settle-ment rate,so as to assess the effectiveness of the PDCA cycle in DRG payment within the oncological diseases at the hospital.Re-sults Following the PDCA cycle,the DRG admission rate increased from 84.03%to 89.98%,and the cases ineligible for inclu-sion decreased by 22.78%due to mismatched main diagnosis and procedures."Violations of the reporting and coding principles that do not require reporting"and"omission of primary surgical procedure codes"were no longer observed as reasons for failed DRG inclusion.Ambiguous cases with both average hospitalization costs and average length of stay higher than those of normal inclu-sion cases,leading to an increase in the average hospitalization cost from 22 496.56 yuan to 24714.92 yuan,and the average length of stay increased from 7.50 days to 8.13 days.The CMI value increased from 0.96 to 1.08,and the DRG settlement rate increased from 107.93%to 130.67%.Conclusion The PDCA cycle can effectively enhance the quality of medical record documentation,leading to improved quality in medical insurance settlement lists and DRG admission rates.It can help identify operational issues within the de-partment and promote the smooth implementation of DRG payment reform in the oncological department.

The importance of evaluating the oxygen supply system of the medical aircraft was introduced.With considerations on the characteristics of the oxygen supply system of the medical aircraft during its development and application,an oxygen supply system effectiveness evaluation method was proposed based on the analytic hierarchy process and the experience of experts in the field of medical aircraft,which involved in seven evaluation indexes of total oxygen supply,pipeline airtight-ness,single-nozzle flow adjustment characteristics,single-nozzle outlet pressure adjustment characteristics,disassembly and assembly,mechanical operation and fixation ability.The effectiveness evaluation method proposed was of significance for accurately grasping the changes in the performance of the oxygen supply system.References were provided for the ground maintenance of the oxygen supply system of the medical aircraft.[Chinese Medical Equipment Journal,2024,45(1):89-92]

Objective:Obesity related glomerulopathy(ORG)is induced by obesity,but the pathogenesis remains unclear.This study aims to investigate the expression of early growth response protein 3(EGR3)in the renal cortex tissues of ORG patients and high-fat diet-induced obese mice,and to further explore the molecular mechanism of EGR3 in inhibiting palmitic acid(PA)induced human podocyte inflammatory damage. Methods:Renal cortex tissues were collected from ORG patients(n=6)who have been excluded from kidney damage caused by other diseases and confirmed by histopathology,and from obese mice induced by high-fat diet(n=10).Human and mouse podocytes were intervened with 150 μmol/L PA for 48 hours.EGR3 was overexpressed or silenced in human podocytes.Enzyme linked immunosorbent assay(ELISA)was used to detcet the levels of interleukin-6(IL-6)and interleukin-1β(IL-1β).Real-time RT-PCR was used to detect the mRNA expressions of EGR3,podocytes molecular markers nephrosis 1(NPHS1),nephrosis 2(NPHS2),podocalyxin(PODXL),and podoplanin(PDPN).RNA-seq was performed to detect differentially expressed genes(DEGs)after human podocytes overexpressing EGR3 and treated with 150 μmol/L PA compared with the control group.Co-immunoprecipitation(Co-IP)combined with liquid chromatography tandem mass spectrometry(LC-MS)was used to detect potential interacting proteins of EGR3 and the intersected with the RNA-seq results.Co-IP confirmed the interaction between EGR3 and protein arginine methyltransferases 1(PRMT1),after silencing EGR3 and PRMT1 inhibitor intervention,the secretion of IL-6 and IL-1β in PA-induced podocytes was detected.Western blotting was used to detect the expression of phosphorylated signal transducer and activator of transcription 3(p-STAT3)after overexpression or silencing of EGR3. Results:EGR3 was significantly upregulated in renal cortex tissues of ORG patients and high-fat diet-induced obese mice(both P<0.01).In addition,after treating with 150 μmol/L PA for 48 hours,the expression of EGR3 in human and mouse podocytes was significantly upregulated(both P<0.05).Overexpression or silencing of EGR3 in human podocytes inhibited or promoted the secretion of IL-6 and IL-1β in the cell culture supernatant after PA intervention,respectively,and upregulated or downregulated the expression of NPHS1,PODXL,NPHS2,and PDPN(all P<0.05).RNA-seq showed a total of 988 DEGs,and Co-IP+LC-MS identified a total of 238 proteins that may interact with EGR3.Co-IP confirmed that PRMT1 was an interacting protein with EGR3.Furthermore,PRMT1 inhibitors could partially reduce PA-induced IL-6 and IL-1β secretion after EGR3 silencing in human podocytes(both P<0.05).Overexpression or silencing of EGR3 negatively regulated the expression of PRMT1 and p-STAT3. Conclusion:EGR3 may reduce ORG podocyte inflammatory damage by inhibiting the PRMT1/p-STAT3 pathway.

Human brain banks use a standardized protocol to collect,process and store post-mortem human brains and related tissues,along with relevant clinical information,and to provide the tissue samples and data as a resource to foster neuroscience research according to a standardized operating protocols(SOP).Human brain bank serves as the foundation for neuroscience research and the diagnosis of neurological disorders,highlighting the crucial rule of ensuring the consistency of standardized quality for brain tissue samples.The first version of SOP in 2017 was published by the China Human Brain Bank Consortium.As members increases from different regions in China,a revised SOP was drafted by experts from the China Human Brain Bank Consortium to meet the growing demands for neuroscience research.The revised SOP places a strong emphasis on ethical standards,incorporates neuropathological evaluation of brain regions,and provides clarity on spinal cord sampling and pathological assessment.Notable enhancements in this updated version of the SOP include reinforced ethical guidelines,inclusion of matching controls in recruitment,and expansion of brain regions to be sampled for neuropathological evaluation.