ObjectiveTo clarify the relationship of clinical factors with isolated vertigo or dizziness of cerebrovascular origin.MethodsClinical data of patients admitted in East Hospital from Jan. 2015 to Apr. 2016, whose complaint were acute vertigo or dizziness were retrospectively collected. All patients arrived at the emergency department within 24 hr of symptom onset, had no acute ischemic lesion first CT and NIHSS score of 0. Patients were divided into cerebral infarction group and noncerebral infarction group according to subsequent cerebral imaging results and clinical and laboratory factors related to cerebral infarction were analyzed.Result51.6% of patients were female (n = 141). 46 patients (16.8%) were diagnosed with acute cerebral infarction. Baseline demographic data of the two groups was not significantly different. Univariate analysis found that history of smoking (p = 0.009), headache (p = 0.028), unsteadiness (p = 0.009), neuron specific enolase (p = 0.001), and vertebral artery abnormalities found on imaging (p = 0.009) were the significant difference between two groups. Increased neuron specific enolase (p = 0.005) and an abnormal vertebral artery (p = 0.044) were significant on multivariate analysis.Conclusions16.8% of acute isolated vertigo or dizziness presentations were diagnosed with acute cerebral infarction. Increased serum neuron specific enolase and vertebral artery abnormalities were the strongest indicators of acute cerebral infarction.

We aimed to investigate the clinicoradiologic determinants of negative diffusion-weighted image (DWI) results in patients with acute cerebral infarction (ACI). The medical records were reviewed of ACI patients. Patients were divided to the DWI positive and negative group. Positive DWI was used as independent variable and patients' clinicoradiologic factors were used as co-variables for multivariate logistic regression analysis. 349 patients received initial cerebral MRI within 72 hours of admission. Lacunar infarction was most common (42.1%) followed by posterior circulation infarction (30.1%) and partial anterior circulation infarction (18.1%). The majority of the patients (72.2%) had an NIHSS score of less than 5 at admission. 316 patients (90.54%) were positive on initial DWI. Patients with smoking, initial SBP ≥ 140 or DBP ≥ 90 mmHg, initial fasting plasma glucose (FPG) ≥7.0 mmol/L, initial MRI from onset of disease >1 d and anterior circulation infarction were liable to show positive DWI. Furthermore, DWI negative patients had significantly lower NIHSS scores (IQR 0,1,2) than DWI positive patients (IQR 1,2,4) (P = 0.000) at two weeks post onset of acute cerebral infarction. In conclusion, multiple clinicoradiologic factors are associated with negative and positive DWI and further delineation of these factors is required in future prospective studies.

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The purpose of this study is to explore the neuroprotection mechanism of levetiracetam (LEV) with acute focal cerebral ischemia-reperfusion (I/P) mouse. The cerebral artery I/P animal model was prepared with a middle artery cerebral occlusion method. For drug intervention, mice were intraperitoneally injected with LEV with a dose of either 15 or 150 mg/kg. Neuronal injury was evaluated by measuring the infarct area, apoptosis ratio, and observation of blood-brain barrier ultrastructure with transmission electron microscope. CD8(+) antibody and perforin antibody were used to make cross-reference screen through flow cytometry to determine a perforin-positive rate in CD8(+) T lymphocytes (PFN + %). Injection of LEV can reduce infarct area, apoptosis ratio, and blood-brain barrier damage 24 h later after acute I/P in WT mice. In vitro, perforin can lower hippocampal neuron viability. In vivo, removing perforin can relieve neuronal injury. High dose injection of LEV (150 mg/kg) can inhibit perforin secreting from CD8(+)T lymphocytes. In addition, LEV can still protect neurons with perforin knockout mice. Therefore, our results suggested that LEV may contribute to neuron protection after cerebral ischemia reperfusion. The possible mechanism may be related with perforin release. However, we cannot roll out other mechanisms.

Abstract. Resistance to chemotherapeutic agents is the main reason for treatment failure in patients with cancer. The primary mechanism of multidrug resistance (MDR) is the overexpression of drug efflux transporters, including ATP-binding cassette transporter G2 (ABCG2). To the best of our knowledge, the MDR mechanisms of esophageal cancer have not been described. An adriamycin (ADM)-resistant subline, Eca109/ADM, was generated from the Eca109 esophageal cancer cell line by a stepwise selection in ADM from 0.002 to 0.02 ng/µl. The resulting subline, designated Eca109/ADM, revealed a 3.29-fold resistance against ADM compared with the Eca109 cell line. The ABCG2 gene expression in the Eca109/ADM cells was increased compared with that of the Eca109 cells. The cellular properties of the Eca109/ADM cells were detected by reverse transcription polymerase chain reaction (RT-PCR), flow cytometry and western blotting. The ABCG2 expression levels were detected by RT-PCR and flow cytometry, and the drug efflux effect was detected by flow cytometry. The present study detected the correlation between ABCG2 and the multidrug resistance of esophageal cancer. ABCG2 gene expression and the drug efflux effect of the Eca109/ADM cells were increased compared with those of the Eca109 cells. Collectively, the results of this study indicated that the overexpression of ABCG2 in the Eca109/ADM cells resulted in drug efflux, which may be responsible for the development of esophageal cancer MDR.

The overexpression of ATP-binding cassette (ABC) transporters confers multidrug resistance (MDR) to tumor cells. ABCG2 is a member of the ABC superfamily. The present study aimed to investigate the correlation between ABCG2 expression and the MDR of esophageal cancer and to estimate the therapeutic benefit of downregulating ABCG2 expression and reversing chemoresistance in esophageal cells using artesunate (Art). The Eca109/ABCG2 cell line was established by transfecting the ABCG2 gene into Eca109 cells. The Eca109/ABCG2 esophageal cancer cells with ABCG2 gene overexpression were resistant to adriamycin (ADM), daunorubicin (DNR) and mitoxantrone (MIT), which indicated that ABCG2 may be associated with drug resistance in esophageal cancer. Art is a noteworthy antimalarial agent, particularly in severe and drug-resistant cancer cases, as Art is able to reverse drug resistance. In the present study, Art also exerted profound anticancer activity. The mechanism for the reversal of multidrug resistance by Art in esophageal carcinoma was analyzed using cellular experiments, but still remains largely unknown.

Background: Therapeutic applications of stem cells, especially mesenchymal stem cells, were once regarded as a promising therapy for mitigating acute cerebral infarction. Unfortunately, all the stem cell clinical trials have been futile. A new stroke therapeutic strategy of combining stem cells with nanotechnology has recently gained significant attention. The objective of this study was to evaluate the application of cerium oxide nanoparticle (nanoceria)-labeled human umbilical cord mesenchymal stem cells (HucMSCs) for stroke therapy. Methods: In our study, cerium oxide nanoparticles were precovered with hyaluronic acid before labeling HucMSCs and the synergistic effects from both HucMSCs and cerium oxide nanoparticles were analyzed in in vivo and in vitro experiments Results: The nanoceria-labeled HucMSCs combined advantages from both sides, including the capacity for inflammatory modulation of HucMSCs and the antioxidant effects of nanoceria. Compared with either HucMSCs or nanoceria individually, nanoceria-labeled HucMSCs exerted significantly enhanced capacities after gaining combined antioxidant and anti-inflammatory effects. Conclusion: Our findings suggest a novel strategy with effective and well-tolerated applications of stem cells for acute cerebral infarction therapy after modification of cells with nanomaterials.

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