Subarachnoid hemorrhage misdiagnosed as acute coronary syndrome leading to catastrophic neurologic injury: A case report

BACKGROUND Elevated levels of cardiac troponin and abnormal electrocardiogram changes are the primary basis for clinical diagnosis of acute coronary syndrome(ACS).Troponin levels in ACS patients can often be more than 50 times the upper reference limit.Some patients with subarachnoid hemorrhage(SAH)also show electrocardiogram abnormalities,myocardial damage,and elevated cardiac biomarkers.Unlike ACS patients,patients with SAH only have a slight increase in troponin,and the use of anticoagulants or antiplatelet drugs is prohibited.Because of the opposite treatment modalities,it is essential for clinicians to distinguish between SAH and ACS.CASE SUMMARY A 56-year-old female patient was admitted to the emergency department at night with a sudden onset of severe back pain.The final diagnosis was intraspinal hematoma in the thoracic spine.We performed an emergency thoracic spinal canal hematoma evacuation procedure with the assistance of a microscope.Intraoperatively,diffuse hematoma formation was found in the T7-T10 spinal canal,and no obvious spinal vascular malformation changes were observed.Postoperative head and spinal magnetic resonance imaging(MRI)showed a small amount of SAH in the skull,no obvious abnormalities in the cervical and thoracic spinal canals,and no abnormal signals in the lumbar spinal canal.Thoracoab-dominal aorta computed tomography angiography showed no vascular malfor-mation.Postoperative motor system examination showed Medical Research Council Scale grade 1/5 strength in both lower extremities,and the patient experienced decreased sensation below the T12 rib margin and reported a Visual Analog Scale score of 3.CONCLUSION Extremely elevated troponin levels(more than 50 times the normal range)are not unique to coronary artery disease.SAH can also result in extremely high troponin levels,and antiplatelet drugs are contraindicated in such cases.Emergency MRI can help in the early differential diagnosis,as a misdiagnosis of ACS can lead to catastrophic neurological damage in patients with spontaneous spinal SAH.

Rapid and Green Fabrication of Micro- and Nano-Structural Titanium Dioxide Coatings on Titanium and Its Alloy

Induction heat treatment(IHT)is inherently an efficient,clean,economical and easy-operated rapid thermal oxide technology,which is well appliedto surface modification of titanium and its alloys in medical field in the research.This method produces titanium dioxide coatings with a micro-and nano-

Clustering feature decision trees for semi-supervised classification from high-speed data streams

Most stream data classification algorithms apply the supervised learning strategy which requires massive labeled data.Such approaches are impractical since labeled data are usually hard to obtain in reality.In this paper,we build a clustering feature decision tree model,CFDT,from data streams having both unlabeled and a small number of labeled examples.CFDT applies a micro-clustering algorithm that scans the data only once to provide the statistical summaries of the data for incremental decision tree induction.Micro-clusters also serve as classifiers in tree leaves to improve classification accuracy and reinforce the any-time property.Our experiments on synthetic and real-world datasets show that CFDT is highly scalable for data streams while gener-ating high classification accuracy with high speed.

The membrane-associated E3 ubiquitin ligase MARCH3 downregulates the IL-6 receptor and suppresses colitis-associated carcinogenesis

The IL-6-STAT3 axis is critically involved in inflammation-associated carcinogenesis(IAC).How this axis is regulated to modulate IAC remains unknown.Here,we show that the plasma membrane-associated E3 ubiquitin ligase MARCH3 negatively regulates STAT3 activation triggered by IL-6,as well as another IL-6 subfamily member,Oncostatin M(OSM).MARCH3 is associated with the IL-6 receptorα-chain(IL-6Rα)and its coreceptor gp130.Biochemical experiments indicated that MARCH3 mediates the polyubiquitination of IL-6Rαat K401 and gp130 at K849 following IL-6 stimulation,leading to their translocation to and degradation in lysosomes.MARCH3 deficiency increases IL-6-and OSM-triggered activation of STAT3 and induction of downstream effector genes in various cell types.MARCH3 deficiency enhances dextran sulfate sodium(DSS)-induced STAT3 activation,increases the expression of inflammatory cytokines,and exacerbates colitis,as well as azoxymethane(AOM)/DSS-induced colitis-associated cancer in mice.In addition,MARCH3 is downregulated in human colorectal cancer tissues and associated with poor survival across different cancer types.Our findings suggest that MARCH3 is a pivotal negative regulator of IL-6-induced STAT3 activation,inflammation,and inflammation-associated carcinogenesis.

The zinc-finger protein ZFYVE1 modulates TLR3-mediated signaling by facilitating TLR3 ligand binding

Recognition of viral dsRNA by Toll-like receptor 3(TLR3)leads to the induction of downstream antiviral effectors and the innate antiviral immune response.Here,we identified the zinc-finger FYVE domain-containing protein ZFYVE1,a guanylate-binding protein(GBP),as a positive regulator of TLR3-mediated signaling.Overexpression of ZFYVE1 promoted the transcription of downstream antiviral genes upon stimulation with the synthetic TLR3 ligand poly(I:C).Conversely,ZFYVE1 deficiency had the opposite effect.Zfyve1^(−/−) mice were less susceptible than wild-type mice to inflammatory death induced by poly(I:C)but not LPS.ZFYVE1 was associated with TLR3,and the FYVE domain of ZFYVE1 and the ectodomain of TLR3 were shown to be responsible for their interaction.ZFYVE1 was bound to poly(I:C)and increased the binding affinity of TLR3 to poly(I:C).These findings suggest that ZFYVE1 plays an important role in the TLR3-mediated innate immune and inflammatory responses by promoting the ligand binding of TLR3.