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.

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 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 mechanism of Wenyang Yiqi Huoxue Prescription(WYYQHXP)in the treatment of chronic heart failure(CHF)by regulating miR-126-3p and PI3K/Akt signaling pathway based on network pharmacology and experimental studies.Methods Active components and targets of WYYQHXP were obtained through TCMSP,SwissTargetPrediction,SwissADME and PubChem.Four miRNA databases were used to obtain miR-126-3p targets,and four disease databases were used to obtain CHF related targets.The intersection of the three was taken as the potential target of action;the protein-protein interaction network relationships of potential targets were explored using STRING and Cytoscape 3.9.1 software,and the main active components and core targets were screened;GO and KEGG pathway enrichment analysis was performed using R 4.2.1 software;Molecular docking was performed on the main active components with the core targets.Isoproterenol was used to induce a rat model of CHF with qi deficiency and blood stasis syndrome,and intervened with WYYQHXP.MiR-126-3p and core target expression in coronary endothelial cells were detected by immunohistochemistry,RT-qPCR,and Western blot.Results Network pharmacology screened main active components of WYYQHXP,including β-sitosterol,doustanol,kaempferol,quercetin,baicalein and luteolin,and the core targets of EGFR,VEGFA and AKT1;KEGG was enriched to the signaling pathways such as PI3K/Akt,and the 3 core targets were distributed to the PI3K/Akt signaling pathway;molecular docking showed good binding ability of β-sitosterol and stigmasterol to three core targets.Animal experiments showed that WYYQHXP could increase left ventricular ejection fraction and left ventricular fractional shortening in model rats(P<0.01),reduce serum brain natriuretic peptide content(P<0.01),increase expression of miR-126-3p(P<0.05,P<0.01,P<0.001),the medium-dosage of WYYQHXP could increase mRNA and protein expressions of EGFR,PI3K,AKT1 and VEGFA in coronary endothelial cells(P<0.01).Conclusion WYYQHXP may activate PI3K/Akt signaling pathway by acting on miR-126-3p,thereby restoring endothelial dependent vasodilation of coronary arteries,repairing endothelial dysfunction of coronary arteries,and treating CHF.

AIM To investigate the effects of rice wine type and wine processing method on chemical constituents and anti-coagulation effect of Angelicae sinensis Radix.METHODS Wine-washed products and wine-stir-fried products were prepared by different types and ages of rice wine,respectively,after which HPLC was adopted in the content determination of tryptophan,chlorogenic acid,vanillic acid,phthalic acid,ferulic acid,senkyunolide I,senkyunolide H,coniferyl ferulate and ligustilide,and PT,APTT,TT were detected in rabbit plasma.RESULTS Phenolic acids and volatile constituents demonstrated lower contents in the wine-stir-fried products than those in the raw product(P＜0.05),while those in the wine-washed products displayed no obvious changes(except for senkyunolide I)(P＞0.05).The contents of volatile constituents in the wine-washed products were higher than those in the wine-stir-fried products(P＜0.05).After being processed with dry rice wine,various constituents exhibited increased contents as compared with those after being processed with sweet rice wine(P＜0.05).Compared with the raw product,prolonged PT,APTT and TT were observable in the processed products prepared by 3-year semi-dry rice wine(P＜0.05).CONCLUSION The optimal rice wine type is determined to be 3-year semi-dry.Wine-washed Angelicae sinensis Radix shows high contents of ferulic acid and volatile constituents,whose activating blood and resolving stasis effect may be stronger.

By summarizing the mass spectrometric fragmentation patterns of oxyphenisatin substances,an analytical method was established for screening of illegally added oxyphenisatin compounds in weight-loss health foods using high performance liquid chromatography-in-source-fragmentation-quadrupole time-of-flight mass spectrometry(HPLC-ISF-QTOF-MS),along with a quantitative method for 11 kinds of oxyphenisatin compounds.Based on the developed screening method,an oxyphenisatin derivative was discovered in the reference standards,which was tentatively identified as 4-(3-(4-hydroxyphenyl)-2-oxoindolin-3-yl)phenyl acetate and confirmed by MS/MS analysis.The results showed that all 11 kinds of oxyphenisatin compounds had correlation coefficients greater than 0.9971,with limits of detection(LODs)ranging from 0.12 to 0.68 μg/L and limits of quantification(LOQ)from 0.21 to 2.29 μg/L.The LODs for 11 kinds of characteristic ions ranged from 0.45 to 9.11 μg/kg.At spiking levels of 25,50 and 100 μg/kg,the recoveries ranged from 78.9%to 117.3%.The instrumental precision,intra-day method precision and inter-day method precision were 0.23%?1.70%,0.7%?2.4%,and 1.1%?3.3%,respectively.The developed targeted and non-targeted detection method demonstrated high sensitivity,strong stability,rapid analysis,and an expanded screening range for oxyphenisatin substances,and provided robust technical support for regulatory authorities in combating illegal adulteration.