ObjectiveTo develop a full-process data platform of renal rehabilitation, diagnosis and quality control information. MethodsA hierarchical architectural design was proposed, adhering to clinical pathway models and standardized data protocols. The platform comprehensively covered assessment, intervention, follow-up and quality control for maintenance hemodialysis (MHD) patients. By integrating multidisciplinary resources and standardizing rehabilitation workflows, it delivered standardized and intelligent rehabilitation services. ResultsThe platform achieved standardized and intelligent management of rehabilitation services, effectively improved the physiological function, psychological state and quality of life convenience for MHD patients, while significantly reduced the economic and care burden on patients' families and society. ConclusionThe rehabilitation service model based on a full-process data platform may provide scientific and systematic support for MHD patients.

Dry eye （DE） is a prevalent multifactorial disease of the ocular surface， clinically characterized by tear film homeostasis imbalance accompanied by related ocular surface symptoms. Specifically， the tear film is a thin liquid layer of tears covering the cornea and conjunctiva through blinking， while tear film homeostasis serves as the foundation for maintaining normal ocular surface structure and function. Insufficient tear secretion and excessive tear film evaporation lead to tear hyperosmolarity and the production of inflammatory mediators， disrupting tear film homeostasis and subsequently forming DE. Additionally， cascade reactions are triggered， resulting in a "vicious cycle of DE" that exacerbates the disease severity and prolongs its duration. Therefore， for DE treatment， it is crucial to restore tear film homeostasis and terminate this vicious cycle. Traditional Chinese medicine （TCM）， which differentiates and treats DE based on systemic conditions， often achieves favorable therapeutic outcomes， offering additional treatment options for DE. Studies have demonstrated that TCM can alleviate DE by regulating tear film homeostasis and terminating the vicious cycle. This review systematically summarizes recent basic experimental research in China and abroad on TCM in alleviating DE by regulating tear film homeostasis， aiming to provide a theoretical basis for clinical treatment and an insight for research design.

Intervertebral disc degeneration (IVDD) is the predominant pathological contributor to chronic low back pain, a pervasive musculoskeletal condition affecting over 630 million people globally and imposing tremendous socioeconomic and public health burdens. The etiopathogenesis of IVDD is remarkably complex and multifactorial, involving intricate crosstalk among chronic inflammatory responses, extracellular matrix (ECM) catabolism, cellular senescence, aberrant programmed cell death (including apoptosis, pyroptosis, and ferroptosis), mitochondrial dysfunction, and oxidative damage. Compelling evidence indicates that the inflammatory microenvironment acts as a decisive driving force throughout the entire degenerative course of IVDD. Among the diverse inflammatory mediators, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) serve as core pro-inflammatory cytokines that initiate and perpetuate the degenerative cascade. These two pivotal cytokines collectively activate an array of canonical intracellular signaling pathways, including nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) inflammasome, and the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) cascade. Such interconnected signaling networks trigger a self-reinforcing positive feedback loop, which exacerbates inflammatory reactions, disrupts the anabolic-catabolic homeostasis of the ECM, promotes oxidative stress and mitochondrial injury, induces multiple forms of disc cell death, and ultimately leads to progressive structural collapse and functional deterioration of the intervertebral disc. Conventional therapeutic strategies, dominated by nonsteroidal anti-inflammatory drugs and surgical interventions, are limited by systemic adverse reactions, suboptimal long-term efficacy, and the risk of adjacent segment degeneration. In contrast, traditional Chinese medicine (TCM) exhibits prominent advantages in the prevention and treatment of IVDD by virtue of its holistic regulation, syndrome differentiation, and multi-component, multi-target, multi-pathway pharmacological properties. This review systematically elucidates the molecular mechanisms by which inflammation-associated signaling pathways modulate disc cell fate and ECM metabolic homeostasis, and comprehensively summarizes the experimental progress over the past five years on TCM monomers and compound formulas for intervening in IVDD. Accumulating studies have confirmed that numerous natural active ingredients isolated from herbal medicines (ferulic acid, mangiferin, paeonol, astragaloside IV) and representative TCM compound prescriptions (Bushen Huoxue Formula, Shensuitongzhi Formula, Fuzi Decoction) exert synergistic protective effects by coordinately targeting core signaling hubs. These TCM agents demonstrate potent anti-inflammatory, antioxidant, anti-apoptotic, anti-pyroptotic, anti-ferroptotic, ECM-protective, and autophagy-regulating bioactivities, thereby effectively decelerating the pathological progression of IVDD. Despite remarkable progress, current investigations are still confronted by several critical limitations. Most studies are restricted to validating the regulatory effects of single TCM components on individual signaling pathways, leaving the systematic, dynamic, and synergistic mechanisms of TCM compound formulas within multi-pathway regulatory networks largely unexplored. Furthermore, clinical translation of TCM is severely hampered by the lack of efficient targeted drug delivery systems, unclear pharmacokinetic profiles, suboptimal local bioavailability, and incomplete long-term safety assessments. Therefore, future research should adopt an interdisciplinary paradigm integrating multi-omics technologies, artificial intelligence, organoid models, and organ-on-chip systems to systematically decipher the scientific basis of TCM against IVDD. Concurrently, the development of intelligent, site-specific delivery systems (hydrogels, nanoparticles, exosome-based carriers) is urgently needed to enhance the local accumulation and sustained release of TCM ingredients. By deepening mechanistic exploration and accelerating translational research, TCM is expected to evolve into safe, effective, and personalized precision therapeutic regimens for IVDD, offering novel and reliable solutions for the clinical management of chronic low back pain.

Objective Magnetoreception, the remarkable ability of diverse animals to sense and utilize the geomagnetic field for orientation and navigation, remains a molecularly unresolved mystery in sensory biology. The putative magnetoreceptor (MagR, previously known as IscA1) is a highly conserved iron-sulfur protein implicated in both magnetoreception and iron metabolism; however, the functional diversity among its cross-species homologs remains poorly understood. Cellular morphology is a key genetically determined trait that can be altered through genetic or environmental modifications—a process known as cell morphology engineering. Constructing engineered cells with specific morphological features and magnetic sensitivity to achieve remote, non-invasive magnetic modulation represents a crucial goal in this field with significant application potential. Therefore, this study aims to systematically investigate the effects of MagR heterologous expression on bacterial morphology and magnetic sensing capabilities, screen for MagR-based magnetically sensitive morphology engineering pathways, and reveal the underlying molecular mechanisms. Methods We systematically screened 28 MagR homologous genes from diverse prokaryotic and animal taxa to evaluate their expression and corresponding phenotypic effects in Escherichia coli (E. coli). To compare the differential magnetic responses among bacteria expressing various recombinant MagR proteins, we utilized high-throughput automated bright-field microscopic imaging and scanning electron microscopy (SEM). Furthermore, comprehensive biochemical and biophysical characterizations of iron and iron-sulfur cluster binding were performed using Ferrozine colorimetric assays, electron paramagnetic resonance (EPR) spectroscopy, ultraviolet-visible (UV-Vis) absorption, and circular dichroism (CD) spectroscopy. Additionally, 100 mT static magnetic field (SMF) exposure experiments were conducted to assess magnetically tunable phenotypes, while the intrinsic magnetic properties of purified MagR proteins were directly measured using a superconducting quantum interference device (SQUID) magnetometer. Results Our results demonstrated that the heterologous expression of MagR homologs induced varying degrees of bacterial filamentation. From this comprehensive screen, two distinct morphological patterns were identified: hydra (Hydra vulgaris) MagR (hyMagR) promoted uniform cell elongation and filamentation, exhibiting robust magnetic sensitivity manifested as significantly enhanced filamentation under the 100 mT SMF. In contrast, pigeon (Columba livia) MagR (clMagR) induced only low-frequency, extreme filamentation (sporadically exceeding 80 μm) with a relatively weaker magnetic morphological response. Mechanistically, our data unambiguously proved that these phenotypic differences are primarily driven by distinct iron redox preferences rather than total cellular iron accumulation. Specifically, hyMagR preferentially binds ferrous iron (Fe²⁺), whereas clMagR favors ferric iron (Fe³⁺) and forms more stable iron-sulfur clusters. Intriguingly, although SQUID magnetometry showed that purified clMagR exhibited approximately five-fold higher mass magnetic susceptibility than hyMagR, its cellular magnetic response was weaker. We hypothesize that the Fe²⁺-preferred intracellular environment associated with hyMagR overexpression primes the cell for enhanced generation of reactive oxygen species (ROS) via the Fenton reaction. Exposure to an SMF synergizes with this primed redox state, triggering the bacterial SOS response and upregulating cell division inhibitors to efficiently induce uniform filamentation. Conclusion Our findings identify the Fe²⁺/Fe³⁺ redox state as a critical determinant of MagR-mediated morphological remodeling and magnetic responsiveness. This discovery suggests a potential strategy for engineering magnetically responsive cellular systems for synthetic biology applications, and provides a plausible framework, which potentially combines intrinsic protein magnetism with redox-state modulation, for further investigating the evolutionary mechanisms of MagR-mediated magnetoreception.

Intervertebral disc degeneration (IVDD) is the predominant pathological contributor to chronic low back pain, a pervasive musculoskeletal condition affecting over 630 million people globally and imposing tremendous socioeconomic and public health burdens. The etiopathogenesis of IVDD is remarkably complex and multifactorial, involving intricate crosstalk among chronic inflammatory responses, extracellular matrix (ECM) catabolism, cellular senescence, aberrant programmed cell death (including apoptosis, pyroptosis, and ferroptosis), mitochondrial dysfunction, and oxidative damage. Compelling evidence indicates that the inflammatory microenvironment acts as a decisive driving force throughout the entire degenerative course of IVDD. Among the diverse inflammatory mediators, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) serve as core pro-inflammatory cytokines that initiate and perpetuate the degenerative cascade. These two pivotal cytokines collectively activate an array of canonical intracellular signaling pathways, including nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) inflammasome, and the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) cascade. Such interconnected signaling networks trigger a self-reinforcing positive feedback loop, which exacerbates inflammatory reactions, disrupts the anabolic-catabolic homeostasis of the ECM, promotes oxidative stress and mitochondrial injury, induces multiple forms of disc cell death, and ultimately leads to progressive structural collapse and functional deterioration of the intervertebral disc. Conventional therapeutic strategies, dominated by nonsteroidal anti-inflammatory drugs and surgical interventions, are limited by systemic adverse reactions, suboptimal long-term efficacy, and the risk of adjacent segment degeneration. In contrast, traditional Chinese medicine (TCM) exhibits prominent advantages in the prevention and treatment of IVDD by virtue of its holistic regulation, syndrome differentiation, and multi-component, multi-target, multi-pathway pharmacological properties. This review systematically elucidates the molecular mechanisms by which inflammation-associated signaling pathways modulate disc cell fate and ECM metabolic homeostasis, and comprehensively summarizes the experimental progress over the past five years on TCM monomers and compound formulas for intervening in IVDD. Accumulating studies have confirmed that numerous natural active ingredients isolated from herbal medicines (ferulic acid, mangiferin, paeonol, astragaloside IV) and representative TCM compound prescriptions (Bushen Huoxue Formula, Shensuitongzhi Formula, Fuzi Decoction) exert synergistic protective effects by coordinately targeting core signaling hubs. These TCM agents demonstrate potent anti-inflammatory, antioxidant, anti-apoptotic, anti-pyroptotic, anti-ferroptotic, ECM-protective, and autophagy-regulating bioactivities, thereby effectively decelerating the pathological progression of IVDD. Despite remarkable progress, current investigations are still confronted by several critical limitations. Most studies are restricted to validating the regulatory effects of single TCM components on individual signaling pathways, leaving the systematic, dynamic, and synergistic mechanisms of TCM compound formulas within multi-pathway regulatory networks largely unexplored. Furthermore, clinical translation of TCM is severely hampered by the lack of efficient targeted drug delivery systems, unclear pharmacokinetic profiles, suboptimal local bioavailability, and incomplete long-term safety assessments. Therefore, future research should adopt an interdisciplinary paradigm integrating multi-omics technologies, artificial intelligence, organoid models, and organ-on-chip systems to systematically decipher the scientific basis of TCM against IVDD. Concurrently, the development of intelligent, site-specific delivery systems (hydrogels, nanoparticles, exosome-based carriers) is urgently needed to enhance the local accumulation and sustained release of TCM ingredients. By deepening mechanistic exploration and accelerating translational research, TCM is expected to evolve into safe, effective, and personalized precision therapeutic regimens for IVDD, offering novel and reliable solutions for the clinical management of chronic low back pain.

Objective Magnetoreception, the remarkable ability of diverse animals to sense and utilize the geomagnetic field for orientation and navigation, remains a molecularly unresolved mystery in sensory biology. The putative magnetoreceptor (MagR, previously known as IscA1) is a highly conserved iron-sulfur protein implicated in both magnetoreception and iron metabolism; however, the functional diversity among its cross-species homologs remains poorly understood. Cellular morphology is a key genetically determined trait that can be altered through genetic or environmental modifications—a process known as cell morphology engineering. Constructing engineered cells with specific morphological features and magnetic sensitivity to achieve remote, non-invasive magnetic modulation represents a crucial goal in this field with significant application potential. Therefore, this study aims to systematically investigate the effects of MagR heterologous expression on bacterial morphology and magnetic sensing capabilities, screen for MagR-based magnetically sensitive morphology engineering pathways, and reveal the underlying molecular mechanisms. Methods We systematically screened 28 MagR homologous genes from diverse prokaryotic and animal taxa to evaluate their expression and corresponding phenotypic effects in Escherichia coli (E. coli). To compare the differential magnetic responses among bacteria expressing various recombinant MagR proteins, we utilized high-throughput automated bright-field microscopic imaging and scanning electron microscopy (SEM). Furthermore, comprehensive biochemical and biophysical characterizations of iron and iron-sulfur cluster binding were performed using Ferrozine colorimetric assays, electron paramagnetic resonance (EPR) spectroscopy, ultraviolet-visible (UV-Vis) absorption, and circular dichroism (CD) spectroscopy. Additionally, 100 mT static magnetic field (SMF) exposure experiments were conducted to assess magnetically tunable phenotypes, while the intrinsic magnetic properties of purified MagR proteins were directly measured using a superconducting quantum interference device (SQUID) magnetometer. Results Our results demonstrated that the heterologous expression of MagR homologs induced varying degrees of bacterial filamentation. From this comprehensive screen, two distinct morphological patterns were identified: hydra (Hydra vulgaris) MagR (hyMagR) promoted uniform cell elongation and filamentation, exhibiting robust magnetic sensitivity manifested as significantly enhanced filamentation under the 100 mT SMF. In contrast, pigeon (Columba livia) MagR (clMagR) induced only low-frequency, extreme filamentation (sporadically exceeding 80 μm) with a relatively weaker magnetic morphological response. Mechanistically, our data unambiguously proved that these phenotypic differences are primarily driven by distinct iron redox preferences rather than total cellular iron accumulation. Specifically, hyMagR preferentially binds ferrous iron (Fe²⁺), whereas clMagR favors ferric iron (Fe³⁺) and forms more stable iron-sulfur clusters. Intriguingly, although SQUID magnetometry showed that purified clMagR exhibited approximately five-fold higher mass magnetic susceptibility than hyMagR, its cellular magnetic response was weaker. We hypothesize that the Fe²⁺-preferred intracellular environment associated with hyMagR overexpression primes the cell for enhanced generation of reactive oxygen species (ROS) via the Fenton reaction. Exposure to an SMF synergizes with this primed redox state, triggering the bacterial SOS response and upregulating cell division inhibitors to efficiently induce uniform filamentation. Conclusion Our findings identify the Fe²⁺/Fe³⁺ redox state as a critical determinant of MagR-mediated morphological remodeling and magnetic responsiveness. This discovery suggests a potential strategy for engineering magnetically responsive cellular systems for synthetic biology applications, and provides a plausible framework, which potentially combines intrinsic protein magnetism with redox-state modulation, for further investigating the evolutionary mechanisms of MagR-mediated magnetoreception.

Objective To prepare the recombinant Echinococcus granulosus Polo-like kinase 2 (rEgPLK2) protein and evaluate its immunoprotective efficacy against cystic echinococcosis, so as to provide insights into research and development of novel vaccines against echinococcosis. Methods The Polo-like kinase (PLK) protein sequences were retrieved from 12 species in the NCBI protein database, including E. granulosus and E. multilocularis. Multiple sequence alignment was performed using the Clustal Omega program, and structural visualization and homology analysis were conducted using the ESPript 3.2 program. The recombinant plasmid pET-30a-EgPLK2 was transformed into BL21(DE3) competent cells. Protein expression was induced with isopropyl-β-D-thiogalactoside (IPTG), and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) was performed to characterize the expression and molecular weight of the rEgPLK2 protein. The purified rEgPLK2 protein was thoroughly emulsified with Freund’s complete adjuvant at a 1 : 1 volume ratio. Two New Zealand white rabbits were immunized with multipoint subcutaneous injection on the back at a dose of 300 μg per rabbit for primary immunization. For booster immunizations, the protein was emulsified with Freund’s incomplete adjuvant at a 1 : 1 volume ratio and administered on days 14, 28, and 42 after the primary immunization at a dose of 150 μg per rabbit. Serum was sampled from the rabbit ear vein on day 7 after the final immunization to yield anti-rEgPLK2 polyclonal antibodies. Antibody titer was determined by indirect enzyme-linked immunosorbent assay (ELISA), and antibody specificity was verified by Western blotting. The tissue localization of the EgPLK2 protein was detected in E. granulosus protoscoleces and adult worms using immunofluorescence assay (IFA). Eighteen 6- to 8-week-old female SPF-grade BALB/c mice were randomly divided into three groups, including the blank control group, rEgPLK2-ISA immunization group, and PBS-ISA adjuvant control group, of 6 mice each group. Mice in the rEgPLK2-ISA immunization group and PBSISA group received three primary immunizations via intramuscular injection, and animals in the rEgPLK2-ISA immunization group was inoculated with immunogens prepared by emulsifying rEgPLK2 protein with ISA 201 adjuvant at a 1 : 1 volume ratio (6 μg per mouse), while mice in the PBS-ISA adjuvant control group received an equal volume of PBS emulsified with ISA adjuvant at a 1 : 1 volume ratio. A fourth booster immunization was administered via intraperitoneal injection. Mice in the rEgPLK2-ISA immunization group received a booster immunization with 8 μg of rEgPLK2 protein per mouse, and animals in the PBS-ISA group received an equal volume of PBS, with immunizations given at 2-week intervals. Mice in the blank control group were given no treatment, and housed under standard conditions. Tail vein blood was collected from all mice 7 days after the final immunization, and levels of specific anti-rEgPLK2 IgG antibody and its subclasses (IgG1, IgG2a, IgG2b, IgG3) were measured by indirect ELISA. E. granulosus infection was modelled in mice through injection with 1 000 E. granulosus protoscoleces via intrahepatic portal vein in the rEgPLK2-ISA immunization group and PBS-ISA adjuvant control group 2 weeks after the last immunization. All mice were sacrificed and dissected. The number of cysts was counted in mouse livers, and the cyst reduction rate was calculated. Liver tissues were processed for paraffin sectioning and stained with hematoxylin and eosin (HE), and histopathological changes were examined under a light microscope. Results Sequence analysis revealed that EgPLK2 shared a high amino acid sequence homology with E. multilocularis PLK2 (EmPLK2) and contained the typical domains of the Polo-like kinase family, including the serine/threonine protein kinase catalytic domain (STKc) and Polo-box. The IPTG-induced rEgPLK2 protein was mainly expressed in the form of inclusion bodies, and the purified rEgPLK2 protein showed a relative molecular mass of approximately 70 kDa. The prepared rabbit anti-rEgPLK2 polyclonal antibody had a titer of 1 : 256 000, and Western blotting assay showed that this anti-body specifically recognized the rEgPLK2 protein with a relative molecular mass of approximately 70 kDa. Immunofluorescence assay showed that the EgPLK2 protein was localized in the excretory bladder and rostellum of E. granulosus protoscoleces, as well as the tegument, suckers, and inter-proglottid junctions of adult worms. Immunoprotective assay showed that the serum levels of specific anti-rEgPLK2 IgG, IgG1, IgG2a, and IgG2b antibodies were 2.92 ± 0.49, 0.33 ± 0.10, 0.31 (0.36), and 3.12 (1.73) in mice in the rEgPLK2-ISA immunization group, which were all significantly higher than those in the PBS-ISA adjuvant control group (0.14 ± 0.04, 0.07 ± 0.01, 0.12 ± 0.04, and 0.11 ± 0.04, respectively) (t = 19.28 and 8.46, Z = 3.75 and 4.15; all P values < 0.001); however, there was no significant difference in the serum anti-IgG3 antibody level between the rEgPLK2-ISA immunization group and the PBS-ISA adjuvant control group [0.07 (0.01) vs. 0.073 (0.07); Z = 0.69, P > 0.05)]. In the mouse model of E. granulosus infections, the area of hepatic lesions was reduced and the inflammatory infiltration was alleviated in the rEgPLK2-ISA immunization group than in the PBS-ISA adjuvant control group, and the number of hepatic cysts was higher in the PBS-ISA adjuvant control group than in the rEgPLK2-ISA immunization group [8.00 (2.00) vs. 1.00 (0.75); Z = −2.93, P < 0.01], with a cyst reduction rate of 80.40%. Indirect ELISA assay measured higher serum levels of specific anti-rEgPLK2 IgG (3.28 ± 0.48 vs. 0.11 ± 0.04; t = 15.86, P < 0.01), IgG1 (0.29 ± 0.02 vs. 0.09 ± 0.01; t = 15.67, P < 0.01), IgG2a [3.71 (1.09) vs. 0.08 (0.03); Z = 2.88, P < 0.01], and IgG2b antibodies [3.34 (1.01) vs. 0.08 (0.03); Z = 2.88, P < 0.01] in the rEgPLK2-ISA immunization group than in the PBS-ISA adjuvant control group, and there was no significant difference in the serum level of the specific anti-rEgPLK2 IgG3 antibody between the rEgPLK2-ISA immunization group and the PBS-ISA adjuvant control group (0.07 ± 0.01 vs. 0.07 ± 0.01; t = 1.29, P > 0.05). Conclusions The prokaryotic expression system has been successfully constructed for the EgPLK2 gene and the anti-rEgPLK2 polyclonal antibody has been obtained. The rEgPLK2 protein exhibits a high immunogenicity, and is effective to protect against E. granulosus infection, and inhibits cyst development, which is a promising candidate vaccine target against cystic echinococcosis.

Objective:To investigate the completion rate of tumor evaluation at initial assessment and after neoadjuvant therapy for mid and low rectal cancer patients in the national multicenter real-world database.Methods:The prospective real-world study was conducted. The clinicopathological data of 1 074 patients who underwent surgical treatment for mid and low rectal cancer in 47 national medical institutions, including Peking Union Medical College Hospital et al, from May 12,2023 to May 11,2024 were collected. Observation indicators: (1) clinical characteristics of patients with mid and low rectal cancer; (2) initial colonoscopy and pathologic evaluation of tumors in patients with mid and low rectal cancer; (3) initial imaging evaluation of patients with mid and low rectal cancer; (4) imaging evaluation after neoadjuvant therapy for patients with mid and low rectal cancer. Measurement data with normal distribution were represented as Mean± SD, and measurement data with skewed distribution were represented as M( Q1, Q3). Count data were described as absoluter numbers and/or percentages. Results:(1) Clinical characteristics of patients with mid and low rectal cancer. Of the 1 074 patients, there were 713 males and 361 females, aged 63(56,70)years. The body mass index of 1 074 patients was 24(21,26)kg/m 2.For American Society of Anesthesiologists classification, there were 147 cases of stage Ⅰ, 641 cases of stage Ⅱ, 157 cases of stage Ⅲ, 2 cases of stage Ⅳ, and there were 127 cases missing data. (2) Initial colonoscopy and pathologic evaluation of tumors in patients with mid and low rectal cancer. Of the 1 074 patients, there were 787 cases (73.28%) undergoing complete colonoscopy, and there were only 197 cases (18.34%) undergoing immunohistochemical evaluation of all four mismatch repair proteins. (3) Initial imaging evaluation of patients with mid and low rectal cancer. Of the 1 074 patients, there were 842(78.40%) patients completing magnetic resonance imaging (MRI) or ultrasound evaluation, and there were 914(85.10%) patients completing chest, abdomen, and pelvis enhanced computed tomography (CT) evaluation. In the 149 patients completing rectal ultrasound evaluation, there were 122 cases (81.88%) comple-ting T staging evaluation, and there were 81 cases (54.36%) completing N staging evaluation. In the 808 patients completing rectal MRI evaluation, there were 708 cases (87.62%) completing T staging evaluation, and there were 590 cases (73.02%) completing N staging evaluation. (4) Imaging evalua-tion after neoadjuvant therapy for patients with mid and low rectal cancer. Of the 388 patients with neoadjuvant therapy, there were 332 patients (85.57%) completing MRI or ultrasound evaluation, and there were 327 patients (84.28%) completing chest, abdomen, and pelvis enhanced CT evalua-tion. In the 70 patients completing rectal ultrasound evaluation, there were 65 cases (92.86%) com-pleting T staging evaluation, and there were 49 cases (70.00%) completing N staging evaluation. In the 327 patients completing rectal MRI evaluation, there were 246 cases (75.23%) completing T staging, and there were 228 cases (69.72%) completing N staging evaluation. Conclusion:The com-pletion rate of tumor imaging evaluation at initial assessment and after neoadjuvant therapy for mid and low rectal cancer patients on a national scale is relatively good.

Objective:To investigate the neurorestorative effect of basic fibroblast growth factor (bFGF) on neurological function recovery in rats with spinal cord injury and its potential mechanisms.Methods:Ninety adult SD rats were selected and randomly divided into 6 groups using a random number table: sham-operated group ( n=24), spinal cord injury group ( n=24), bFGF group ( n=24), bFGF autophagy pathway validation group ( n=6), bFGF+rapamycin group ( n=6), and bFGF+MHY1485 group ( n=6). A spinal cord injury model was established by impacting the T 10 spinal cord segment using a self-made Allen′s weight-drop impactor. The sham-operated group underwent a 3 cm midline dorsal incision without spinal cord injury; the bFGF group received immediate intrathecal injection of 100 μl bFGF solution (20 μg/L) after injury; the sham surgery group and spinal cord injury group received an equal volume of saline after injury; the bFGF autophagy pathway validation group received the identical treatment as the bFGF group; the bFGF+rapamycin group received the same treatment as the bFGF group with additional intraperitoneal injection of rapamycin (4 mg·kg -1·d -1); the bFGF+MHY1485 group received the identical bFGF treatment plus intraperitoneal injection of MHY1485 (10 mg·kg -1·d -1). At 28 days after injury, the rats were sacrificed and the spinal cord tissue was collected at 5 mm from the injury epicenter for HE staining and pathological observation. At 7, 14, 21, and 28 days after injury, BBB scoring was used to assess hindlimb motor function; P wave latency and P1-N1 wave amplitude were recorded to evaluate neuroelectrophysiological changes; Western blot analysis was performed to detect the expression levels of phosphorylated mammalian target of rapamycin (p-mTOR)/mammalian target of rapamycin (mTOR) and microtubule-associated protein light chain 3-II (LC3-II) and evaluate changes in mTOR signaling pathway and autophagy activity. At 28 days after injury, behavioral alterations, neuroelectrophysiological changes, and auctophagy-related protein expression levels were assessed in the bFGF autophagy pathyway validation group, bFGF+rapamycin group and bFGF+MHY1485 group. Results:At 28 days after injury, the sham-operated group exhibited regular nuclear morphology, while the spinal cord injury group showed disordered cell structures and the bFGF group displayed relatively normal nuclear morphology. At 7, 14, 21, and 28 days after injury, the BBB scores in both the spinal cord injury group and bFGF group were lower than those in the sham-operated group ( P<0.01), with higher scores in the bFGF group than those in the spinal cord injury group ( P<0.01). At 7, 14, 21, and 28 days after injury, P-wave latency was longer and P1-N1 wave amplitude was lower in both the spinal cord injury group and bFGF group compared to those in the sham-operated group ( P<0.01), with shorter P-wave latency and higher P1-N1 wave amplitude in the bFGF group compared to those in the spinal cord injury group ( P<0.01). Western blot results indicated that at 7, 14, 21, and 28 days after injury, in the spinal cord injury group, p-mTOR/mTOR levels were lower than those in both the sham-operated group and bFGF group ( P<0.01), while LC3-II expression levels were higher ( P<0.01); in the bFGF group, p-mTOR/mTOR levels were higher than those in the spinal cord injury group but lower than those in the sham-operated group ( P<0.01), and LC3-II expression levels were lower than those in the spinal cord injury group but higher than those in the sham-operated group ( P<0.01). At 28 days after injury, the BBB scores were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher scores in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). P-wave latency was shorter in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with shorter P-wave latency in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). P1-N1 wave amplitude was lower in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than that in the bFGF+rapamycin group ( P<0.01), with lower P1-N1 wave amplitude in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). The p-mTOR/mTOR levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher p-mTOR/mTOR levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). The LC3-II expression levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher LC3-II expression levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). Conclusion:bFGF can improve the pathological state, motor behavior, and neuroelectrophysiological function in rats with spinal cord injury, for which the mechanism of action may involve downregulating cellular autophagy function by activating the mTOR pathway, thereby inhibiting excessive autophagy to promote neuronal regeneration and repair.

Objective:To investigate the neurorestorative effect of basic fibroblast growth factor (bFGF) on neurological function recovery in rats with spinal cord injury and its potential mechanisms.Methods:Ninety adult SD rats were selected and randomly divided into 6 groups using a random number table: sham-operated group ( n=24), spinal cord injury group ( n=24), bFGF group ( n=24), bFGF autophagy pathway validation group ( n=6), bFGF+rapamycin group ( n=6), and bFGF+MHY1485 group ( n=6). A spinal cord injury model was established by impacting the T 10 spinal cord segment using a self-made Allen′s weight-drop impactor. The sham-operated group underwent a 3 cm midline dorsal incision without spinal cord injury; the bFGF group received immediate intrathecal injection of 100 μl bFGF solution (20 μg/L) after injury; the sham surgery group and spinal cord injury group received an equal volume of saline after injury; the bFGF autophagy pathway validation group received the identical treatment as the bFGF group; the bFGF+rapamycin group received the same treatment as the bFGF group with additional intraperitoneal injection of rapamycin (4 mg·kg -1·d -1); the bFGF+MHY1485 group received the identical bFGF treatment plus intraperitoneal injection of MHY1485 (10 mg·kg -1·d -1). At 28 days after injury, the rats were sacrificed and the spinal cord tissue was collected at 5 mm from the injury epicenter for HE staining and pathological observation. At 7, 14, 21, and 28 days after injury, BBB scoring was used to assess hindlimb motor function; P wave latency and P1-N1 wave amplitude were recorded to evaluate neuroelectrophysiological changes; Western blot analysis was performed to detect the expression levels of phosphorylated mammalian target of rapamycin (p-mTOR)/mammalian target of rapamycin (mTOR) and microtubule-associated protein light chain 3-II (LC3-II) and evaluate changes in mTOR signaling pathway and autophagy activity. At 28 days after injury, behavioral alterations, neuroelectrophysiological changes, and auctophagy-related protein expression levels were assessed in the bFGF autophagy pathyway validation group, bFGF+rapamycin group and bFGF+MHY1485 group. Results:At 28 days after injury, the sham-operated group exhibited regular nuclear morphology, while the spinal cord injury group showed disordered cell structures and the bFGF group displayed relatively normal nuclear morphology. At 7, 14, 21, and 28 days after injury, the BBB scores in both the spinal cord injury group and bFGF group were lower than those in the sham-operated group ( P<0.01), with higher scores in the bFGF group than those in the spinal cord injury group ( P<0.01). At 7, 14, 21, and 28 days after injury, P-wave latency was longer and P1-N1 wave amplitude was lower in both the spinal cord injury group and bFGF group compared to those in the sham-operated group ( P<0.01), with shorter P-wave latency and higher P1-N1 wave amplitude in the bFGF group compared to those in the spinal cord injury group ( P<0.01). Western blot results indicated that at 7, 14, 21, and 28 days after injury, in the spinal cord injury group, p-mTOR/mTOR levels were lower than those in both the sham-operated group and bFGF group ( P<0.01), while LC3-II expression levels were higher ( P<0.01); in the bFGF group, p-mTOR/mTOR levels were higher than those in the spinal cord injury group but lower than those in the sham-operated group ( P<0.01), and LC3-II expression levels were lower than those in the spinal cord injury group but higher than those in the sham-operated group ( P<0.01). At 28 days after injury, the BBB scores were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher scores in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). P-wave latency was shorter in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with shorter P-wave latency in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). P1-N1 wave amplitude was lower in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than that in the bFGF+rapamycin group ( P<0.01), with lower P1-N1 wave amplitude in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). The p-mTOR/mTOR levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher p-mTOR/mTOR levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). The LC3-II expression levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher LC3-II expression levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). Conclusion:bFGF can improve the pathological state, motor behavior, and neuroelectrophysiological function in rats with spinal cord injury, for which the mechanism of action may involve downregulating cellular autophagy function by activating the mTOR pathway, thereby inhibiting excessive autophagy to promote neuronal regeneration and repair.