ObjectiveTo explore the possible mechanisms by which ligustilide （LIG） exerts neuroprotective effects on ischemic stroke （IS） by inhibiting the release of neutrophil extracellular traps （NETs）， promoting blood-brain barrier repair， and alleviating post-ischemic neuroinflammation， thereby providing a new direction for IS treatment. MethodsA middle cerebral artery occlusion （MCAO） model was established in rats. The rats were divided into the sham operation （Sham） group， model （Model） group， low- and high-dose LIG groups （20， 40 mg·kg^-1）， and the NET inhibitor CI-amidine group （CI-amidine， 10 mg·kg^-1）. Drug treatments were administered for 3 days. Neurological injury after ischemia was evaluated by 2，3，5-triphenyltetrazolium chloride （TTC） staining， neurological deficit scoring， and brain index measurement. Flow cytometry and Western blot were used to analyze changes in neutrophil expression. Immunofluorescence was used to observe the fluorescence intensity of the NET marker citrullinated histone H3 （H3Cit）. Western blot was performed to detect the expression of blood-brain barrier tight junction-related proteins and inflammatory factors， including interleukin-18 （IL-18） and interleukin-1β （IL-1β）. ResultsCompared with the Sham group， the Model group exhibited significant brain tissue injury （P<0.05）， significantly increased neutrophil numbers and NET expression （P<0.05）， significantly impaired blood-brain barrier permeability （P<0.05）， and significantly increased expression of inflammatory factors （P<0.05）. Compared with the Model group， both low- and high-dose LIG significantly alleviated brain tissue injury in rats （P<0.01）， inhibited neutrophil numbers and NET expression （P<0.01）， reduced blood-brain barrier damage （P<0.01）， and suppressed the expression of inflammatory factors IL-18 and IL-1β （P<0.01）， thereby ultimately exerting a neuroprotective effect. ConclusionThe neuroprotective effect of LIG in rats with cerebral ischemia-reperfusion injury may be related to inhibition of neutrophils and the NETs induced by them.

ObjectiveTo explore the possible mechanisms by which ligustilide （LIG） exerts neuroprotective effects on ischemic stroke （IS） by inhibiting the release of neutrophil extracellular traps （NETs）， promoting blood-brain barrier repair， and alleviating post-ischemic neuroinflammation， thereby providing a new direction for IS treatment. MethodsA middle cerebral artery occlusion （MCAO） model was established in rats. The rats were divided into the sham operation （Sham） group， model （Model） group， low- and high-dose LIG groups （20， 40 mg·kg^-1）， and the NET inhibitor CI-amidine group （CI-amidine， 10 mg·kg^-1）. Drug treatments were administered for 3 days. Neurological injury after ischemia was evaluated by 2，3，5-triphenyltetrazolium chloride （TTC） staining， neurological deficit scoring， and brain index measurement. Flow cytometry and Western blot were used to analyze changes in neutrophil expression. Immunofluorescence was used to observe the fluorescence intensity of the NET marker citrullinated histone H3 （H3Cit）. Western blot was performed to detect the expression of blood-brain barrier tight junction-related proteins and inflammatory factors， including interleukin-18 （IL-18） and interleukin-1β （IL-1β）. ResultsCompared with the Sham group， the Model group exhibited significant brain tissue injury （P<0.05）， significantly increased neutrophil numbers and NET expression （P<0.05）， significantly impaired blood-brain barrier permeability （P<0.05）， and significantly increased expression of inflammatory factors （P<0.05）. Compared with the Model group， both low- and high-dose LIG significantly alleviated brain tissue injury in rats （P<0.01）， inhibited neutrophil numbers and NET expression （P<0.01）， reduced blood-brain barrier damage （P<0.01）， and suppressed the expression of inflammatory factors IL-18 and IL-1β （P<0.01）， thereby ultimately exerting a neuroprotective effect. ConclusionThe neuroprotective effect of LIG in rats with cerebral ischemia-reperfusion injury may be related to inhibition of neutrophils and the NETs induced by them.

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 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 investigate the diagnostic value of computed tomography (CT) grading in evaluating sacroiliac joint lesions and the extent of joint injury in patients with ankylosing spondylitis (AS) so as to provide evidence-based evidence for CT imaging diagnosis and severity evaluation of AS. Methods A total of 107 patients with AS admitted to the hospital between December 2020 and December 2024 were selected. All patients underwent X-ray and CT examinations, and were graded based on the examination results. The diagnostic value of X-ray and CT in sacroiliac joint lesions and the severity of joint injury in patients with AS was compared. Results The detection rates of osteosclerosis, bone erosion, subchondral bone cystic changes, ankylosis, and soft tissue swelling using CT (90.65%、100.00%、87.85%、41.12%、56.07%、22.43%、33.64%) were higher than those using X-ray (75.70%、84.11%、58.88%、32.71%、48.60%、10.28%、7.48%) (P<0.05). The detection rates of osteosclerosis, bone erosion, subchondral bone cystic changes, joint space narrowing, joint space widening, ankylosis, and soft tissue swelling using CT combined with X-ray (97.20%、10.00%、95.33%、57.94%、73.83%、34.58%、39.25%) were higher than those using CT or X-ray alone (P<0.05). The comparison of the detection of grade I, grade II and grade III joint injury degrees by CT, X-ray and combined examination showed statistically significant differences (P<0.05). The detection rates of grades I and II joint injuries using CT (26.17%、35.51%) were higher than those using X-ray (14.95%、22.43%) (P<0.05). The detection rates of grades 0, I, II, and III joint injury by the combined examination of X-ray and CT were higher than those using X-ray alone (P<0.05). Conclusion CT has greater diagnostic value for sacroiliac joint lesions and severity of joint injury in patients with AS, and allowing for more accurate in AS grading, and combined it with X-ray further improves diagnostic efficacy.

Objective To investigate the diagnostic value of computed tomography (CT) grading in evaluating sacroiliac joint lesions and the extent of joint injury in patients with ankylosing spondylitis (AS) so as to provide evidence-based evidence for CT imaging diagnosis and severity evaluation of AS. Methods A total of 107 patients with AS admitted to the hospital between December 2020 and December 2024 were selected. All patients underwent X-ray and CT examinations, and were graded based on the examination results. The diagnostic value of X-ray and CT in sacroiliac joint lesions and the severity of joint injury in patients with AS was compared. Results The detection rates of osteosclerosis, bone erosion, subchondral bone cystic changes, ankylosis, and soft tissue swelling using CT (90.65%、100.00%、87.85%、41.12%、56.07%、22.43%、33.64%) were higher than those using X-ray (75.70%、84.11%、58.88%、32.71%、48.60%、10.28%、7.48%) (P<0.05). The detection rates of osteosclerosis, bone erosion, subchondral bone cystic changes, joint space narrowing, joint space widening, ankylosis, and soft tissue swelling using CT combined with X-ray (97.20%、10.00%、95.33%、57.94%、73.83%、34.58%、39.25%) were higher than those using CT or X-ray alone (P<0.05). The comparison of the detection of grade I, grade II and grade III joint injury degrees by CT, X-ray and combined examination showed statistically significant differences (P<0.05). The detection rates of grades I and II joint injuries using CT (26.17%、35.51%) were higher than those using X-ray (14.95%、22.43%) (P<0.05). The detection rates of grades 0, I, II, and III joint injury by the combined examination of X-ray and CT were higher than those using X-ray alone (P<0.05). Conclusion CT has greater diagnostic value for sacroiliac joint lesions and severity of joint injury in patients with AS, and allowing for more accurate in AS grading, and combined it with X-ray further improves diagnostic efficacy.

Objective To investigate the diagnostic value of computed tomography (CT) grading in evaluating sacroiliac joint lesions and the extent of joint injury in patients with ankylosing spondylitis (AS) so as to provide evidence-based evidence for CT imaging diagnosis and severity evaluation of AS. Methods A total of 107 patients with AS admitted to the hospital between December 2020 and December 2024 were selected. All patients underwent X-ray and CT examinations, and were graded based on the examination results. The diagnostic value of X-ray and CT in sacroiliac joint lesions and the severity of joint injury in patients with AS was compared. Results The detection rates of osteosclerosis, bone erosion, subchondral bone cystic changes, ankylosis, and soft tissue swelling using CT (90.65%、100.00%、87.85%、41.12%、56.07%、22.43%、33.64%) were higher than those using X-ray (75.70%、84.11%、58.88%、32.71%、48.60%、10.28%、7.48%) (P<0.05). The detection rates of osteosclerosis, bone erosion, subchondral bone cystic changes, joint space narrowing, joint space widening, ankylosis, and soft tissue swelling using CT combined with X-ray (97.20%、10.00%、95.33%、57.94%、73.83%、34.58%、39.25%) were higher than those using CT or X-ray alone (P<0.05). The comparison of the detection of grade I, grade II and grade III joint injury degrees by CT, X-ray and combined examination showed statistically significant differences (P<0.05). The detection rates of grades I and II joint injuries using CT (26.17%、35.51%) were higher than those using X-ray (14.95%、22.43%) (P<0.05). The detection rates of grades 0, I, II, and III joint injury by the combined examination of X-ray and CT were higher than those using X-ray alone (P<0.05). Conclusion CT has greater diagnostic value for sacroiliac joint lesions and severity of joint injury in patients with AS, and allowing for more accurate in AS grading, and combined it with X-ray further improves diagnostic efficacy.

Objective To explore the relationship between miR-409-3p and miR-325-3p with the efficacy of inter-ventional therapy in patients with primary liver cancer.Methods Ninety-six patients with primary liver cancer who visited Nanyang Central Hospital from October 2021 to January 2024 were regarded as the liver cancer group.All patients underwent transcatheter arterial chemoembolization(TACE)treatment and were separated into an effective group(complete remission,partial remission)and an ineffective group(disease stability,disease progression)based on the treatment effect.Totally 91 patients with liver cirrhosis who underwent treatment in our hospital during the same period were selected as liver cancer group and 98 healthy individuals who received physical examinations during the same period were selected as the healthy group.Serum miR-409-3p,miR-325-3p levels were detected and analyzed for their correlation.Logistic regression was applied to analyze the relevant factors affecting the effi-cacy of TACE treatment.Receiver operating characteristic(ROC)curve was applied to evaluate their predictive value for TACE treatment efficacy of serum miR-409-3p,miR-325-3p levels.Results Compared with the healthy group,the serum level of miR-409-3p and miR-325-3p in the liver cirrhosis group and liver cancer group were re-duced(P＜0.05).Compared with the liver cirrhosis group,the serum level of miR-409-3p and miR-325-3p in the liver cancer group were also reduced(P＜0.05).Compared with the effective group,the serum level of miR-409-3p and miR-325-3p in the ineffective group significantly decreased(P＜0.05).There was a positive correlation between serum level of miR-409-3p and of miR-325-3p in patients with primary liver cancer(r=0.472,P＜0.001).The elevated level of miR-409-3p and miR-325-3p were protective factors for ineffective TACE treat-ment in primary liver cancer patients(P＜0.05).The combination of serum miR-409-3p and miR-325-3p was su-perior to single prediction in predicting efficacy after TACE treatment in primary liver cancer patients(Zcombination-miR-409-3p=4.556,P＜0.001,Zcombination-miR-325-3p=2.613,P＜0.01).Conclusions The serum level of miR-409-3p as well as miR-325-3p is both reduced in patients with primary liver cancer,and is related to the effi-cacy of interventional therapy.

Good endometrial receptivity is an essential factor for embryo implantation,and gene expression in endometrial tissue during the window of implantation(WOI)is closely related to receptivity.Transcriptome sequencing technology enables the identification of gene expression profiles of endometrium during different menstrual phases,as well as microRNAs and long-chain non-coding RNA sequences involved in regulating gene expression.Combining this technology with bioinformatics analysis provides a better understanding of specific gene expression during the receptive period and offers technical support for studying its regulatory mechanism.Moreover,gene expression profiles of the endometrium during different menstrual phases hold significant clinical application value for accurately assessing endometrium receptivity in infertility patients and those with repeated implantation failure,thereby guiding individualized embryo transfer strategies.This review summarizes the progress of transcriptome sequencing in evaluating human endometrial receptivity and discusses future research directions.This review aims to understand the complex molecular mechanisms of endometrial receptivity formation and regulation from the transcriptional level,in order to improve the implantation rate of embryos in assisted reproductive technology and reduce the abortion rate.

Objective To explore the behavioral patterns and hippocampal neurogenesis of CHD8+mice,and to provide behavioral and morphological basis for improving autism like behavior and neurogenesis.Methods Genotype of wild type(WT)and CHD8+/-mice was identified.Weight measurement was conducted on both male and female mice of the WT and CHD8+/-strains.Subsequently,a battery of behavioral tests was administered,which included three-chamber test,self-grooming test,nesting test,Y-maze spontaneous alternation test,food burial test,open-field test and light-dark transition test.Afterwards,the mice were administered 2％pentobarbital sodium(2 ml/kg)to induce anesthesia.Their brains were frozen with 4％paraformaldehyde,removed for photography and analysis to identify any alterations in brain size.Western blotting and immunofluorescent labeling were used to detect changes in the process of hippocampus neurogenesis.Results Western blotting analysis demonstrated a decrease in the amounts of chromodomain helicase DNA binding protein 8(CHD8)protein in both male and female mice with CHD8+genotype,as compared to WT mice.There were no notable disparities in body weight between male and female WT and CHD8+mice,as well as in brain size.The three-chamber social behavior test revealed that both male and female CHD8+/-mice had social deficiencies(P＜0.05).During the open field test,there was no significant difference in the total distance moved by male and female WT and CHD8+/-mice.However,the amount of time spent in the central region was considerably lower in CHD8+/-mice compared to the WT mice(P＜0.01).Furthermore,the light-dark transition test revealed that both male and female CHD8+/-mice spent considerably less time investigating the white box compared to the WT mice(P＜0.05).Nevertheless,there were no notable alterations found in self-grooming,nesting,spontaneous alternation of Y-maze,and food burial experiments.In addition,Western blotting result demonstrated a significant drop in doublecortin(DCX)expression(P＜0.001),and immunofluorescent staining revealed a notable reduction in the number of DCX+cells(P＜0.01)in the hippocampus of CHD8+/-mice.Conclusion CHD8+/-mice exhibit social disorders and anxiety-like behaviors,with a decrease in the number of newly generated neurons in the hippocampus and neurogenesis disorders.