Rectal cancer, which accounts for approximately 40% of colorectal cancers, remains a major clinical concern. Recent advances in diagnostic imaging, surgical techniques, radiotherapy, and systemic treatment have steadily improved rectal cancer outcomes. Considering this, the Korean Rectal Cancer Multidisciplinary (KRCM) Committee has aimed to provide clinicians and policymakers with up-to-date, evidence-based clinical practice guidelines to support optimal decision-making, reflecting current evidence, the Korean healthcare context, and patient values and preferences. The Clinical Practice Guidelines for Rectal Cancer version 2.0 were developed through multidisciplinary collaboration with related academic societies, building upon and updating the KRCM Clinical Practice Guidelines version 1.0 (titled “Multidisciplinary guidelines for the management of rectal cancer”). These consensus guidelines of the KRCM were established based on a comprehensive literature review, evidence synthesis, with recommendation development guided by the GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology, and consideration of applicability in real-world clinical practice under the national health insurance system. Each recommendation has been presented with its strength and level of evidence.

Necrotizing fasciitis (NF) is a rapidly progressive, life-threatening soft tissue infection that rarely involves the periorbital region. We report an unusual case of periorbital NF caused by methicillin-sensitive Staphylococcus aureus (MSSA) in a previously healthy 48-year-old woman, originating from a neglected, recurrent hordeolum—an otherwise benign eyelid condition. The infection resulted in an extensive fullthickness defect of the upper eyelid and adjacent temporal area, presenting major reconstructive challenges. Reconstruction was performed using a radial forearm free flap combined with a buccal mucosal graft to restore both anterior and posterior lamellae, achieving functional eyelid protection and improved visual acuity. This case highlights the potential for seemingly minor, recurrent eyelid infections to progress rapidly to devastating NF even in the absence of systemic symptoms or risk factors. Early recognition and multidisciplinary management were critical to preventing further morbidity. To our knowledge, MSSA has not previously been reported as a causative agent of periorbital NF, underscoring the need for clinical vigilance and timely intervention in common eyelid conditions to avoid catastrophic complications.

Core fucosylation, catalyzed exclusively by fucosyltransferase 8 (FUT8), is an evolutionarily conserved post-translational modification that has emerged as a central regulatory hub linking liver homeostasis, chronic disease progression, and malignant transformation. Liver diseases, particularly hepatocellular carcinoma, remain a leading global health burden characterized by late diagnosis, limited therapeutic options, and poor overall survival. While aberrant glycosylation is now recognized as a hallmark of cancer and inflammatory disorders, existing research on FUT8-mediated core fucosylation in liver diseases remains fragmented: the dynamic functional switch of FUT8 from a homeostatic regulator to a pathological driver across the full disease continuum has not been systematically delineated, and the integrated mechanisms by which core fucosylation modulates oncogenic signaling, metabolic reprogramming, and immune evasion remain poorly understood. This review synthesizes recent advances to establish a unified framework for understanding the dual role of core fucosylation in liver physiology and pathology, and evaluates its translational potential for precision medicine. At the molecular level, FUT8’s unique catalytic specificity makes core fucosylation an irreplaceable modification, as evidenced by the perinatal lethality and severe organ dysfunction in Fut8 knockout mice. In hepatocellular carcinoma, genomic amplification of guanosine 5'-diphosphate-fucose biosynthetic enzymes provides metabolic support for aberrant core fucosylation. FUT8 expression is tightly regulated by a multi-layered network: transcriptional activation via Wnt/β‑catenin and wild-type p53, epigenetic upregulation by lncRNAs, post-transcriptional repression by miR-122-5p and miR-34a, and virus-specific induction by hepatitis B virus/hepatitis C virus. Physiologically, core fucosylation maintains liver homeostasis through four core mechanisms: it acts as a molecular switch for epidermal growth factor receptor/hepatocyte growth factor receptor signaling to enable liver regeneration; directs polarized secretion of hepatocyte-derived glycoproteins into bile ducts; modulates cholesterol metabolism via the hepatocyte nuclear factor 1α-proprotein convertase subtilisin/kexin type 9-low density lipoprotein receptor axis; and regulates aging through insulin‑like growth factor 1 receptor signaling. Pathologically, core fucosylation exhibits context-dependent dual functions: in liver fibrosis, FUT8 upregulation in hepatic stellate cells forms a negative feedback loop that limits excessive fibrogenesis; in hepatocellular carcinoma, however, aberrant FUT8 overexpression drives cell-autonomous malignancy by constitutively activating epidermal growth factor/hepatocyte growth factor receptor, transforming growth factor‑β/Smad, and Wnt/β‑catenin pathways, while simultaneously establishing a multi-layered immune evasion network by stabilizing programmed cell death ligand 1 and cluster of differentiation 47, and impairing natural killer cell homeostasis via interleukin‑2 receptor β glycosylation. Clinically, stage-specific core fucosylation biomarkers enable non-invasive monitoring of liver disease progression: low molecular mass kringle-Fc fusion protein outperforms conventional markers for early fibrosis detection, while alpha-fetoprotein-L3 and novel glycopeptides (α‑2‑macroglobulin N‑linked glycosylation site 1424, lumican core fucosylated peptide) significantly improve early hepatocellular carcinoma diagnosis, especially in alpha-fetoprotein-negative patients. Next-generation detection technologies (chemoenzymatic labeling, site-specific mass spectrometry) overcome the specificity limitations of traditional lectin assays. Therapeutically, four promising strategies are emerging: small-molecule FUT8 inhibitors, afucosylated antibodies with enhanced antibody‑dependent cellular cytotoxicity, Fuc-modified targeted drug delivery systems, and core fucose-specific lectins for NASH treatment. The core challenge for clinical translation lies in FUT8’s inherent “double-edged sword” effect, as systemic inhibition disrupts its essential physiological functions beyond pathological roles. Long-term systemic FUT8 blockade not only impairs post-injury liver regeneration by abrogating epidermal growth factor/hepatocyte growth factor receptor signaling but also disrupts cholesterol homeostasis via the hepatocyte nuclear factor 1α-proprotein convertase subtilisin/kexin type 9-low density lipoprotein receptor axis, leading to dyslipidemia and altered bile secretion. Critically, it compromises immune surveillance by destabilizing interleukin‑2 receptor β on natural killer cells, reducing their cytotoxic activity against malignant and virally infected cells, and impairs IgG Fc-mediated effector functions, increasing susceptibility to infections. This fundamental trade-off between therapeutic efficacy and systemic toxicity necessitates a paradigm shift from non-specific global inhibition to precision modulation of pathological core fucosylation. By addressing these critical challenges, FUT8-mediated core fucosylation has the potential to transform liver disease management from late-stage intervention to early detection and precision therapy, ultimately improving patient outcomes and reducing the global burden of liver diseases.

Gastric cancer with peritoneal metastasis (GCPM) is a common and lethal manifestation of advanced gastric cancer, with a median survival of only 5-11 months. This consensus was developed by 30 experts from Asia (China, Japan, Korea, and Singapore) using the Delphi method and the GRADE evidence grading system. A total of 29 statements were formulated, covering the diagnosis and assessment of GCPM, indications for laparoscopic exploration and NIPS (normothermic intraperitoneal and systemic treatment), treatment regimens, prevention and management of complications, criteria for conversion surgery, and postoperative intraperitoneal therapy. The consensus aims to standardize clinical practice and improve the prognosis of patients with GCPM.

ObjectiveThis study aimed to investigate the effects of 4-week high-intensity interval training (HIIT) on synaptic plasticity in the prefrontal cortex (PFC) of rats exposed to chronic unpredictable mild stress (CUMS), and to explore its potential mechanisms. MethodsA total of 48 male Sprague-Dawley rats were randomly divided into 4 groups: control (C), model (M), control plus HIIT (HC), and model plus HIIT (HM). Rats in groups M and HM underwent 8 weeks of CUMS to establish depression-like behaviors, while groups HC and HM received HIIT intervention beginning from the 5th week for 4 consecutive weeks. The HIIT protocol consisted of repeated intervals of 3 min at high speed (85%-90% maximal training speed, S_max) alternated with one minute at low speed (50%-55% S_max), with 3 to 5 sets per session, conducted 5 d per week. Behavioral assessments and tail-vein blood lactate levels were measured at the end of the 4th and 8th weeks. After the intervention, rat PFC tissues were collected for Golgi staining to analyze synaptic morphology. Enzyme-linked immunosorbent assays (ELISA) were employed to detect brain-derived neurotrophic factor (BDNF), monocarboxylate transporter 1 (MCT1), lactate, and glutamate levels in the PFC, as well as serotonin (5-HT) levels in serum. Additionally, Western blot analysis was conducted to quantify the expression of synaptic plasticity-related proteins, including c-Fos, activity-regulated cytoskeleton-associated protein (Arc), and N-methyl-D-aspartate receptor 1 (NMDAR1). ResultsCompared to the control group (C), the CUMS-exposed rats (group M) exhibited significant reductions in sucrose preference rates, number of grid crossings, frequency of upright postures, and entries into and duration spent in open arms of the elevated plus maze, indicating marked depressive-like behaviors. Additionally, the group M showed significantly reduced dendritic spine density in the PFC, along with elevated levels of c-Fos, Arc, NMDAR1 protein expression, and increased concentrations of lactate and glutamate. Conversely, BDNF and MCT1 contents in the PFC and 5-HT levels in serum were significantly decreased. Following HIIT intervention, rats in the group HM displayed considerable improvement in behavioral indicators compared with the group M, accompanied by significant elevations in PFC MCT1 and lactate concentrations. Furthermore, HIIT notably normalized the expression levels of c-Fos, Arc, NMDAR1, as well as glutamate and BDNF contents in the PFC. Synaptic spine density also exhibited significant recovery. ConclusionFour weeks of HIIT intervention may alleviate depressive-like behaviors in CUMS rats by increasing lactate levels and reducing glutamate concentration in the PFC, thereby downregulating the overexpression of NMDAR, attenuating excitotoxicity, and enhancing synaptic plasticity.

OBJECTIVE: To evaluate the clinical efficacy and safety of Yangxue Qingnao Pills (YXQNP) combined with amlodipine in treating patients with grade 1 hypertension. METHODS: This is a multicenter, randomized, double-blind, and placebo-controlled study. Adult patients with grade 1 hypertension of blood deficiency and Gan (Liver)-yang hyperactivity syndrome were randomly divided into the treatment or the control groups at a 1:1 ratio. The treatment group received YXQNP and amlodipine besylate, while the control group received YXQNP's placebo and amlodipine besylate. The treatment duration lasted for 180 days. Outcomes assessed included changes in blood pressure, Chinese medicine (CM) syndrome scores, symptoms and target organ functions before and after treatment in both groups. Additionally, adverse events, such as nausea, vomiting, rash, itching, and diarrhea, were recorded in both groups. RESULTS: A total of 662 subjects were enrolled, of whom 608 (91.8%) completed the trial (306 in the treatment and 302 in the control groups). After 180 days of treatment, the standard deviations and coefficients of variation of systolic and diastolic blood pressure levels were lower in the treatment group compared with the control group. The improvement rates of dizziness, headache, insomnia, and waist soreness were significantly higher in the treatment group compared with the control group (P<0.05). After 30 days of treatment, the overall therapeutic effects on CM clinical syndromes were significantly increased in the treatment group as compared with the control group (P<0.05). After 180 days of treatment, brachial-ankle pulse wave velocity, ankle brachial index and albumin-to-creatinine ratio were improved in both groups, with no statistically significant differences (P>0.05). No serious treatment-related adverse events occurred during the study period. CONCLUSIONS Combination therapy of YXQNP with amlodipine significantly improved symptoms such as dizziness and headache, reduced blood pressure variability, and showed a trend toward lowering urinary microalbumin in hypertensive patients. These findings suggest that this regimen has good clinical efficacy and safety. (Registration No. ChiCTR1900022470).
Humans ; Amlodipine/adverse effects* ; Drugs, Chinese Herbal/adverse effects* ; Male ; Female ; Hypertension/complications* ; Middle Aged ; Treatment Outcome ; Drug Therapy, Combination ; Adult ; Blood Pressure/drug effects* ; Double-Blind Method ; Aged ; Antihypertensive Agents/adverse effects*

This study investigated the molecular mechanism of phenotypic switching of vascular smooth muscle cells (VSMCs), which play a crucial role in vascular remodeling using 9H-Carbazol-3-yl 4-aminobenzoate (CAB). CAB significantly attenuated platelet-derived growth factor (PDGF)-induced VSMC proliferation and migration. CAB suppressed PDGF-induced STAT3 activation by directly binding to the SH2 domain of STAT3. Downregulation of STAT3 phosphorylation by CAB attenuated CIAPIN1/JAK2/STAT3 axis through a decrease in CIAPIN1 transcription. Furthermore, abrogated CIAPIN1 decreased KLF4-mediated VSMC dedifferentiation and increased CDKN1B-induced cell cycle arrest and MMP9 suppression. CAB inhibited intimal hyperplasia in injury-induced neointima animal models by inhibition of the CIAPIN1/JAK2/STAT3 axis. However, CIAPIN1 overexpression attenuated CAB-mediated suppression of VSMC proliferation, migration, phenotypic switching, and intimal hyperplasia. Our study clarified the molecular mechanism underlying STAT3 inhibition of VSMC phenotypic switching and vascular remodeling and identified novel active CAB. These findings demonstrated that STAT3 can be a major regulator to control CIAPIN1/JAK2/STAT3 axis that may be a therapeutic target for treating vascular proliferative diseases.

Postoperative infection of internal fixation of closed fractures the lower limbs in adults represents a devastating complication, characterized by diagnostic challenges, prolonged treatment duration and high disability rates. Current management of these infections faces multiple challenges, such as difficulties in early accurate diagnosis, and various controversies about the treatment plan, leading to poor overall diagnosis and treatment results. To address these issues, based on evidence-based medicine and principles with emphasis on scientific rigor, clinical applicability and innovation, the Trauma Branch of the Chinese Medical Association, Orthopedic Branch of the Chinese Medical Doctor Association, Orthopedics Branch of the Chinese Medical Association, and Trauma Orthopedics and Polytrauma Group of the Resuscitation and Emergency Committee of the Chinese Medical Doctor Association have collaboratively organized a panel of relevant experts to develop the Guideline for diagnosis and treatment of infection after internal fixation of closed lower limb fractures in adults ( version 2025). The guideline proposed 10 recommendations, aiming to provide a foundation for standardized diagnosis and treatment of postoperative infection in adults with closed lower limb fractures.

Microplastics are widely present in various environments such as water bodies,land,and atmosphere,which pose threats to the ecological environment and human health through transmission and accumulation in the food chain.The existing detection techniques for microplastics face challenges such as complex preparation procedure of samples,low efficiency in processing large batches of samples,and difficulties in handling complex samples.Therefore,there is an urgent need for rapid and efficient detection techniques suitable for complex microplastics samples in the field of environmental monitoring.Raman spectroscopy,known for its advantages such as rapidity,accuracy,high sensitivity,non-destructiveness,and non-contact,demonstrates great application potential in detection of microplastics.Deep learning,an artificial intelligence method known for its large-scale data processing,nonlinear modeling and automatic feature extraction capabilities,is receiving increasing attention in the analysis of Raman spectroscopy signals.The application of deep learning-based Raman spectroscopy has significantly improved performance indicators such as detection efficiency and accuracy.This article introduced the existing Raman enhancement techniques,summarized the deep learning methods applied in Raman spectroscopy signal analysis,reviewed the recent research and application progress of deep learning-based Raman spectroscopy in detection of microplastics,and finally discussed the challenges and future prospects of deep learning-based Raman spectroscopy in detection of microplastics.