As a vital component of clinical medicine, transfusion medicine was officially recognized as a secondary clinical discipline (code 320.32) in 2016 through Amendment No. 2 to the national standard GB/T 13745-2009 Classification and Code of Disciplines. However, the current Catalogue of Diagnosis and Treatment Subjects for Medical Institutions has not yet established "Transfusion Medicine" as a formal subject. This omission has left transfusion departments in medical institutions across the country without a legitimate basis for clinical practice, creating an institutional dilemma in which departments bear statutory responsibilities and operate as substantive clinical units yet lack a corresponding diagnosis and treatment subject. This predicament severely constrains legal compliance in clinical practice, the development of the disciplinary workforce, education and training, research and innovation, and the enhancement of clinical service capacity. This article systematically reviews the necessity, policy basis, and disciplinary framework for establishing transfusion medicine as a formal diagnosis and treatment subject, aiming to provide evidence-based references for the National Health Commission to revise the Catalogue of Diagnosis and Treatment Subjects for Medical Institutions, and to promote the comprehensive transformation of China's transfusion medicine from a "blood storage and distribution" model toward a "clinically engaged, therapy-oriented" paradigm.

ObjectiveTo conduct sarcopenia-related screening and assessment among community-dwelling elderly patients with type 2 diabetes mellitus (T2DM) in Changning District of Shanghai, to analyze the current status and influencing factors of suspected sarcopenia in this population, and to provide references for the early prevention and treatment of sarcopenia. MethodsUsing a stratified random sampling method, elderly T2DM patients under management in the Chronic Disease Health Management System of Changning District in Shanghai were selected as the study subjects. Patients were screened for sarcopenia and underwent related health examinations according to the Chinese Expert Consensus on Diagnosis and Treatment of Sarcopenia in the Elderly (2021). Self-designed questionnaires were used to collect basic information, lifestyle habits and health status, and the Montreal Cognitive Assessment (MoCA) was employed to evaluate cognitive function. ResultsAmong 758 elderly patients with T2DM [average age: (72.19±6.19) years old], 214 patients were identified as having suspected sarcopenia,accounting for 28.23%. The proportion of suspected sarcopenia was higher in females (30.94%) than in males (24.08%) (χ²=4.20, P=0.040), and higher in older patients (χ²=22.26, P<0.001). Higher proportions of suspected sarcopenia were also observed among patients who followed a vegetarian diet (39.77%) (χ²=73.28, P=0.011), had diabetic foot (59.09%) (χ²=10.65, P=0.001), reported feeling fatigued most of the time (37.11%) (χ²=4.33, P=0.037), or had mild cognitive impairment (χ²=3.95, P=0.047). The duration of T2DM in the suspected sarcopenia group [(12.86±10.07) years old] was longer than that in the non-sarcopenia group [(9.73±8.63) years old] (t=3.79, P<0.001), and the average body mass index (BMI) in the suspected sarcopenia group [(22.17±2.45) kg⋅m^-²)] was lower than that in the non-sarcopenia group [(25.11±3.26) kg⋅m^-²)] (t=-11.41, P<0.001). Multivariate logistic regression analyses showed that older age (OR=1.08, 95%CI:1.047‒1.110) and longer duration of T2DM (OR=1.02, 95%CI:1.005‒1.043) were associated with a higher risk of suspected sarcopenia in elderly T2DM patients. Female elderly T2DM patients had a higher risk of suspected sarcopenia (OR=1.89, 95%CI:1.310‒2.733) than males, and those with diabetic foot (OR=3.66, 95%CI:1.341‒9.990) had a higher risk than those without diabetic foot. ConclusionThe proportion of elderly T2DM patients with suspected sarcopenia was relatively high. In community-based integrated health management, healthcare providers should pay more attention to elderly T2DM patients who are older, have longer disease duration, are female, or have diabetic foot, so as to identify risks early and implement targeted comprehensive interventions and health management.

ObjectiveMigraine is a leading neurological disorder and the fourth most common cause of years lived with disability worldwide, affecting nearly 116 million individuals. Although pharmacological treatments are available, their efficacy is often limited by side effects and variable response rates. Repetitive transcranial magnetic stimulation (rTMS) over the dorsolateral prefrontal cortex (DLPFC) offers a safe, non-invasive alternative for migraine management. However, the neurophysiological mechanisms, particularly how rTMS modulates local cortical excitability and distributed pain-related circuits, remain poorly understood. Elucidating these mechanisms is essential for optimizing treatment protocols and improving clinical outcomes. MethodsThis study employed concurrent transcranial magnetic stimulation and electroencephalography (TMS-EEG) to investigate neuroplastic and neurocircuitry mechanisms of DLPFC-rTMS in migraine. Study 1 compared 30 migraineurs and 28 healthy controls to identify abnormalities in TMS-evoked potentials (TEPs) and significant current density (SCD) within sensory-discriminative regions including the primary somatosensory cortex (S1) and posterior insula (pINS), cognitive-affective regions including the anterior insula (aINS) and midcingulate cortex (MCC), and a descending modulatory region, the periaqueductal gray (PAG). Study 2 used a single-blind, crossover, sham-controlled design in 34 healthy participants. Each participant received both active (10 Hz, 80% RMT, 1 500 pulses) and sham DLPFC-rTMS in counterbalanced order. TMS-EEG and cold pain tolerance were assessed before and after each session. ResultsIn Study 1, migraineurs showed a significantly less negative N120 amplitude compared to healthy controls (P=0.027, Cohen’s d=0.60), indicating local intracortical disinhibition. No group differences were observed for N40, P60, or P180 components. At the source level, migraineurs exhibited significantly higher SCD in the S1, pINS, aINS, and MCC (allQ<0.05), but not in the ventroposterior thalamus (vpTHAL), mediodorsal thalamus (mdTHAL), or PAG. In Study 2, active rTMS significantly reduced SCD from pre- to post-stimulation in the S1, aINS, and MCC (all Q<0.05). Sham stimulation also reduced SCD in the S1 (Q<0.05) but not in the aINS or MCC. Although no significant group-level analgesic effect was observed between active and sham conditions (P=0.107), correlation analyses revealed that greater SCD reductions in the S1 and MCC were significantly associated with higher post-rTMS pain tolerance (R=-0.487 and -0.495, both Q<0.01) and larger improvements in pain tolerance(R=-0.487 and -0.451, both Q<0.05). No such correlations were found following sham stimulation, suggesting that the behavioural relevance of neural changes is specific to active rTMS. ConclusionThis study provides novel evidence that migraineurs exhibit both local neuroplastic abnormalities (reduced N120 amplitude) and hyperactivity in key pain-processing regions (S1, pINS, aINS, MCC). A single session of DLPFC-rTMS reduced hyperactivity in the aINS, MCC, and S1. Notably, greater reductions in the S1 and MCC were associated with improved pain tolerance. These findings identify distinct cortical circuitries, particularly within the cognitive-affective pain network, that may serve as potential biomarkers for optimizing rTMS treatment in migraine and other chronic pain conditions. Future studies should validate these results in patient populations experiencing spontaneous migraine attacks and explore multi-session or accelerated rTMS protocols.

Objective: To investigate the current status of personnel structure and service development of blood transfusion departments/blood banks in medical institutions across China, and to provide evidence for discipline construction. Methods: A questionnaire survey was conducted among 3 117 medical institutions in 31 provinces via the Chinese Medical Doctor Association-Blood Transfusion Physician Branch. Data on department naming, staff composition, professional titles, background, and services were analyzed descriptively. Results: Overall, 71.9% of departments were named "Blood Transfusion Department", while 26.4% were still "Laboratory/Blood Bank". Technicians accounted for 86%, physicians only 9%, and nurses 3%. The average number of physicians per tertiary hospital was 0.92, compared to 0.12 in secondary hospitals, with marked regional disparities. Among physicians, 44.5% had a laboratory background and 43.9% clinical background; 3.3% of physicians switched to technician due to promotion barriers. Basic serological tests (ABO/RhD:99.4%; antibody screening:96.2%) were widely available, but advanced tests (antibody identification:18.7%; platelet antibody: 18.2%) remained insufficient. Overall, 70.5% of departments offered therapeutic procedures, mainly autotransfusion (24.5%) and platelet-rich plasma (PRP) collection (20.4%); plasma exchange was only 15.9%, and 29.5% performed no therapeutic services. Conclusion: Transfusion departments in China are still in the early stage of transitioning from traditional medical technology departments to clinical disciplines. The development of the discipline is constrained by administrative disciplinary positioning, talent construction and internal service capacity. Meanwhile, emerging services including transfusion consultations and specialized outpatient clinics have gained initial momentum.

ObjectiveTo investigate the potential mechanism of Qingguangan Ⅱ Formula （青光安Ⅱ号方， QGAⅡ） in the treatment of glaucoma from the perspectives of oxidative stress and the cyclic adenosine monophosphate/ protein kinase A （cAMP/PKA） signaling pathway. MethodsForty SD rats were randomly assigned to a medicated serum group （n=30）， which received QGAⅡby intragastric administration at 6.741 g/（kg·d）， and a blank group （n=10）， which received normal saline at 10 ml/（kg·d）. After 7 consecutive days of administration， medicated serum and blank serum were prepared. The optimal concentration of medicated serum for R28 cell intervention was determined using CCK-8 assay. An in vitro glaucoma model was established by exposing R28 cells to continuous hydrostatic pressure combined with oxygen-glucose deprivation （OGD） for 24 h to simulate the pathological microenvironment of glaucomatous optic nerve injury. The experiment set a control group （complete medium）， model group （glucose-free medium + tri-gas incubator）， medicated serum group （selected concentration of QGA-medicated serum + glucose-free medium + tri-gas incubator）， and blank serum group （blank serum + glucose-free medium + trigas incubator）. The total culture medium volume in each culture dish was 5 ml. After 24 h of culture， cell proliferation was assessed using the EdU immunofluorescence assay， and apoptosis was determined by flow cytometry. Malondialdehyde （MDA） content and superoxide dismutase （SOD） activity were measured using biochemical assays. Western Blotting was performed to detect the expression of oxidative stress-related proteins including 4-hydroxynonenal （4-HNE） and heme oxygenase-1 （HO-1）， apoptosis-related proteins including B-cell lymphoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， and cleaved caspase-3 （C-caspase-3）， and cAMP/PKA signaling pathway-related proteins including protein kinase A （PKA）， phosphorylated PKA （p-PKA）， cAMP response element-binding protein （CREB）， and phosphorylated CREB （p-CREB）. Intracellular cyclic adenosine monophosphate （cAMP） levels were determined by ELISA. In addition， a forskolin （agonist） group， an H89 （inhibitor） group， and a 7.5% medicated serum plus inhibitor group were established to further investigate the effects of QGAⅡ-medicated serum on oxidative stress and the cAMP/PKA signaling pathway in R28 cells. ResultsA concentration of 7.5% QGAⅡ-medicated serum was identified as the optimal concentration for subsequent experiments. Compared to the control group， the model group exhibited significantly decreased cell proliferation， SOD activity， Bcl-2 protein expression， p-PKA/PKA ratio， p-CREB/CREB ratio， and cAMP content， as well as increased apoptosis rate， MDA content， and the protein expression levels of 4-HNE， HO-1， Bax， and C-caspase-3 （P＜0.01）. Compared to the model group， the 7.5% medicated serum group showed significant improvements in all of the above parameters （P＜0.01）. In the forskolin group， the apoptosis rate and the expression levels of C-caspase-3 and Bax significantly decreased， whereas Bcl-2 expression and the p-PKA/PKA and p-CREB/CREB ratios increased compared to those in the model group （P＜0.01）. Compared to the 7.5% medicated serum group， the 7.5% medicated serum plus inhibitor group exhibited significantly increased expression of C-caspase-3 and Bax， together with significantly decreased Bcl-2 expression and reduced p-PKA/PKA and p-CREB/CREB ratios （P＜0.01）. ConclusionUnder continuous hydrostatic pressure and OGD-induced injury conditions， QGAⅡ- containing serum effectively mitigates oxidative stress in R28 cells， activates the cAMP/PKA signaling pathway， and inhibits apoptosis， thereby exerting a neuroprotective effect on retinal ganglion cells

Ovulatory dysfunction (OD) is one of the main causes of infertility in women of childbearing age, which not only affects their reproductive ability, but also physical and mental health. Traditional treatment strategies have limited efficacies, and the emergence of biomedicines provides a promising alternative solution via the strategies of combining engineered design with modern advanced technology. This review explores the pathophysiological characteristics and related induction mechanisms of OD, and evaluates the current cutting-edge advances in its treatments. It emphasizes the potentials of biomedicines strategies such as hydrogels, nanoparticles and extracellular vesicles in improving therapeutic precision and efficacy. By mimicking natural physiological processes, and achieving controlled drug release, these advanced drug carriers are expected to address the challenges in ovarian microenvironment reprogramming, tissue repair, and metabolic and immune regulation. Despite the promising progress, there are still challenges in terms of biomedical complexity, differences between animal models and human physiology, and the demand for intelligent drug carriers in the therapy of OD. Future researches are mainly dedicated to developing precise personalized biomedicines in OD therapy through interdisciplinary collaboration, promoting the development of reproductive regenerative medicine.

Loss-of-function variants in CSDE1 have been strongly linked to neuropsychiatric disorders, yet the precise role of CSDE1 in neurogenesis remains elusive. In this study, we demonstrate that knockout of Csde1 during cortical development in mice results in impaired neural progenitor proliferation, leading to abnormal cortical lamination and embryonic lethality. Transcriptomic analysis revealed that Csde1 upregulates the transcription of genes involved in the cell cycle network. Applying a dual thymidine-labelling approach, we further revealed prolonged cell cycle durations of neuronal progenitors in Csde1-knockout mice, with a notable extension of the G1 phase. Intersection with CLIP-seq data demonstrated that Csde1 binds to the 3' untranslated region (UTR) of mRNA transcripts encoding cell cycle genes. Particularly, we uncovered that Csde1 directly binds to the 3' UTR of mRNA transcripts encoding Cdk6, a pivotal gene in regulating the transition from the G1 to S phases of the cell cycle, thereby maintaining its stability. Collectively, this study elucidates Csde1 as a novel regulator of Cdk6, sheds new light on its critical roles in orchestrating brain development, and underscores how mutations in Csde1 may contribute to the pathogenesis of neuropsychiatric disorders.
Animals ; Neurogenesis/genetics* ; Cell Cycle/genetics* ; Mice, Knockout ; Mice ; Neural Stem Cells/metabolism* ; DNA-Binding Proteins/metabolism* ; Cyclin-Dependent Kinase 6/genetics* ; Cell Proliferation ; 3' Untranslated Regions ; Cerebral Cortex/embryology* ; RNA-Binding Proteins ; Mice, Inbred C57BL

BACKGROUND: While emotional distress, encompassing anxiety and depression, has been associated with negative clinical outcomes, its impact across various clinical departments and general hospitals has been less explored. Previous studies with limited sample sizes have examined the effectiveness of specific treatments (e.g., antidepressants) rather than a systemic management strategy for outcome improvement in non-psychiatric inpatients. To enhance the understanding of the importance of addressing mental health care needs among non-psychiatric patients in general hospitals, this study retrospectively investigated the impacts of emotional distress and the effects of early detection and management of depression and anxiety on hospital length of stay (LOS) and rate of long LOS (LLOS, i.e., LOS >30 days) in a large sample of non-psychiatric inpatients. METHODS: This retrospective cohort study included 487,871 inpatients from 20 non-psychiatric departments of a general hospital. They were divided, according to whether they underwent a novel strategy to manage emotional distress which deployed the Huaxi Emotional Distress Index (HEI) for brief screening with grading psychological services (BS-GPS), into BS-GPS ( n = 178,883) and non-BS-GPS ( n = 308,988) cohorts. The LOS and rate of LLOS between the BS-GPS and non-BS-GPS cohorts and between subcohorts with and without clinically significant anxiety and/or depression (CSAD, i.e., HEI score ≥11 on admission to the hospital) in the BS-GPS cohort were compared using univariable analyses, multilevel analyses, and/or propensity score-matched analyses, respectively. RESULTS: The detection rate of CSAD in the BS-GPS cohort varied from 2.64% (95% confidence interval [CI]: 2.49%-2.81%) to 20.50% (95% CI: 19.43%-21.62%) across the 20 departments, with a average rate of 5.36%. Significant differences were observed in both the LOS and LLOS rates between the subcohorts with CSAD (12.7 days, 535/9590) and without CSAD (9.5 days, 3800/169,293) and between the BS-GPS (9.6 days, 4335/178,883) and non-BS-GPS (10.8 days, 11,483/308,988) cohorts. These differences remained significant after controlling for confounders using propensity score-matched comparisons. A multilevel analysis indicated that BS-GPS was negatively associated with both LOS and LLOS after controlling for sociodemographics and the departments of patient discharge and remained negatively associated with LLOS after controlling additionally for the year of patient discharge. CONCLUSION Emotional distress significantly prolonged the LOS and increased the LLOS of non-psychiatric inpatients across most departments and general hospitals. These impacts were moderated by the implementation of BS-GPS. Thus, BS-GPS has the potential as an effective, resource-saving strategy for enhancing mental health care and optimizing medical resources in general hospitals.
Humans ; Retrospective Studies ; Male ; Length of Stay/statistics & numerical data* ; Female ; Middle Aged ; Adult ; Psychological Distress ; Inpatients/psychology* ; Aged ; Anxiety/diagnosis* ; Depression/diagnosis*

The present study aimed to investigate the effects of eccentric treadmill exercise on adaptive hypertrophy of skeletal muscle in rats. Thirty-two 3-month-old Sprague Dawley (SD) rats were selected and randomly assigned to one of the four groups based on their body weights: 2-week quiet control group (2C), 2-week downhill running exercise group (2E), 4-week quiet control group (4C), and 4-week downhill running exercise group (4E). The downhill running protocol for rats in the exercise groups involved slope of -16°, running speed of 16 m/min, training duration of 90 min, and 5 training sessions per week. Twenty-four hours after the final session of training, all the four groups of rats underwent an exhaustion treadmill exercise. After resting for 48 h, all the rats were euthanized and their gastrocnemius muscles were harvested for analysis. HE staining was used to measure the cross-sectional area (CSA) and diameter of muscle fibers. Transmission electron microscope was used to observe the ultrastructural changes in muscle fibers. Purithromycin surface labeling translation method was used to measure protein synthesis rate. Immunofluorescence double labeling was used to detect the colocalization levels of lysosomal-associated membrane protein 2 (Lamp2)-leucyl-tRNA synthetase (LARS) and Lamp2-mammalian target of rapamycin (mTOR). Western blot was used to measure the protein expression levels of myosin heavy chain (MHC) IIb and LARS, as well as the phosphorylation levels of mTOR, p70 ribosomal protein S6 kinase (p70S6K), and eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1). The results showed that, compared with the 2C group rats, the 2E group rats showed significant increases in wet weight of gastrocnemius muscle, wet weight/body weight ratio, running distance, running time, pre- and post-exercise blood lactate levels, myofibrillar protein content, colocalization levels of Lamp2-LARS and Lamp2-mTOR, and LARS protein expression. Besides these above changes, compared with the 4C group, the 4E group further exhibited significantly increased fiber CSA, fiber diameter, protein synthesis rate, and phosphorylation levels of mTOR, p70S6K, and 4E-BP1. Compared with the quiet control groups, the exercise groups exhibited ultrastructural damage of rat gastrocnemius muscle, which was more pronounced in the 4E group. These findings suggest that eccentric treadmill exercise may promote mTOR translocation to lysosomal membrane, activating mTOR signaling via up-regulating LARS expression. This, in turn, increases protein synthesis rate through the mTOR-p70S6K-4E-BP1 signaling pathway, promoting protein deposition and inducing adaptive skeletal muscle hypertrophy. Although the ultrastructural changes of skeletal muscle are more pronounced, the relatively long training cycles during short-term exercise periods have a more significant effect on promoting gastrocnemius muscle protein synthesis and adaptive hypertrophy.
Animals ; Rats, Sprague-Dawley ; Physical Conditioning, Animal/physiology* ; Rats ; Muscle, Skeletal/metabolism* ; TOR Serine-Threonine Kinases/metabolism* ; Male ; Hypertrophy ; Adaptation, Physiological/physiology* ; Adaptor Proteins, Signal Transducing/metabolism* ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism* ; Intracellular Signaling Peptides and Proteins

This study explores the therapeutic differences and mechanisms of salt-processed Phellodendri Chinensis Cortex in improving insulin resistance(IR) based on network pharmacology, molecular docking, and cellular experiments. The components and intersection targets of Phellodendri Chinensis Cortex in improving IR were collected from databases, and a "drug-component-target-disease" network and protein-protein interaction(PPI) network were constructed to screen core components and targets. A total of 29 active components and 240 intersection targets were identified, of which 13 were core targets. Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses were used to identify key signaling pathways, and molecular docking was performed to validate the binding activity between core components and targets. An IR model in HepG2 cells was induced using insulin combined with high glucose, and the effects of Phellodendri Chinensis Cortex before and after salt-processing on cell glucose consumption were evaluated. The expression of proteins related to the mitogen-activated protein kinase(MAPK) and phosphatidylinositol 3-kinase(PI3K)-protein kinase B(AKT) signaling pathways was detected by Western blot. The cellular experimental results showed that, compared with the model group, glucose consumption in the drug-treated groups was significantly increased(P<0.01), the phosphorylation level of extracellular regulated protein kinase(ERK) was decreased(P<0.05), the phosphorylation levels of PI3K and AKT were increased, and the expression of glucose transporter 4(GLUT4) was also upregulated(P<0.05). Furthermore, the effect of salt-processed Phellodendri Chinensis Cortex was better than that of raw Phellodendri Chinensis Cortex. The study demonstrates that Phellodendri Chinensis Cortex, both before and after salt-processing, improves IR by regulating the expression of related proteins in the MAPK and PI3K-AKT signaling pathways, with enhanced effects after salt-processing.
Humans ; Network Pharmacology ; Phellodendron/chemistry* ; Insulin Resistance ; Drugs, Chinese Herbal/chemistry* ; Hep G2 Cells ; Signal Transduction/drug effects* ; Molecular Docking Simulation ; Protein Interaction Maps/drug effects* ; Proto-Oncogene Proteins c-akt/genetics* ; Phosphatidylinositol 3-Kinases/genetics* ; Glucose/metabolism*