LncRNA LINC01857 promotes cell growth and diminishes apoptosis via PI3K/mTOR pathway and EMT process by regulating miR-141-3p/MAP4K4 axis in diffuse large B-cell lymphoma.

LINC01857 has been proven to be involved in glioma and breast cancer. However, the biological function of LINC01857 in diffuse large B-cell lymphoma (DLBCL) is poorly investigated. By accessing to the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTE), LINC01857 expression was found upregulated in both DLBCL tissues and cells.

D-dimer >2.785 μg/ml and multiple infarcts ≥3 vascular territories are two characteristics of identifying cancer-associated ischemic stroke patients.

Background: The patterns and mechanisms underlying stroke in cancer patients differ from those of the conventional etiology. In this study, we further investigated the characteristics distinguishing cancer-associated ischemic stroke (CAIS) and the relationship of D-dimer value with CAIS.

Methods: Sixty-one acute ischemic stroke patients with cancer (cancer group) and 76 stroke patients without cancer (control group) were recruited.

Inhibition of receptor-interacting protein 3 upregulation and nuclear translocation involved in Necrostatin-1 protection against hippocampal neuronal programmed necrosis induced by ischemia/reperfusion injury.

Receptor-interacting protein 3 (RIP3) is a key molecular switch in tumor necrosis factor-induced necroptosis requiring the formation of an RIP3-RIP1 complex. We have recently shown that hippocampal cornu ammonis 1 (CA1) neuronal death induced by 20-min global cerebral ischemia/reperfusion (I/R) injury is a form of programmed necrosis. However, the mechanism behind this process is still unclear and was studied here.

Temporal coincidence of myasthenia gravis and Guillain Barré syndrome associated with Hashimoto thyroiditis.

Both myasthenia gravis (MG) and Guillain Barré syndrome (GBS) are autoimmune diseases leading to muscle weakness, while the temporal coincidence of MG and GBS is rare. Here, we report a case of MG and GBS, as well as Hashimoto's thyroiditis, for the first time. All these diseases were relieved by immunomodulatory therapy, which suggested abnormal regulation of the autoimmune system might be the cause in our case.

[The properties and research methods of pannexins].

The gene encoding pannexin is a new gap junction family member discovered in 2000. Recent studies indicated that pannexin protein can form hemichannel on the membrane or intercellular gap junction channel, which is involved in many physiological and pathological activities. Here, we make a review of the latest research progress on the expression and cellular localization, the channel properties and the research methods of pannexins in an attempt to provide some evidences and methodological references to further investigation on the physiological and pathological functions of pannexin.

Effect of enoxaparin and aspirin on hemodynamic disturbances after global cerebral ischemia in rats.

Study Aim: Whether patients benefit from anticoagulation or anti-platelet agents when subjected to global ischemia is controversial. In this study we assessed the effect of enoxaparin and aspirin on hemodynamic disturbances following global ischemia in rats.

Methods: Twenty-minute global ischemia was induced by four-vessel occlusion in Sprague-Dawley rats.

Antioxidant action of a Chrysanthemum morifolium extract protects rat brain against ischemia and reperfusion injury.

The present study evaluated the potential neuroprotective effect and underlying mechanism of the total flavones extracted from Chrysanthemum morifolium (TFCM) against ischemia/reperfusion (I/R) injury. An animal model of cerebral ischemia was established by occluding the right middle cerebral artery for 90 minutes followed by reperfusion for 22 hours. The neurobehavioral scores, infarct area, and hemispheric edema were evaluated.

Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus.

Oxidative stress is believed to contribute to neuronal damage induced by cerebral ischemia/reperfusion (I/R) injury. The present study was undertaken to evaluate the possible antioxidant neuroprotective effect of genistein against neuronal death in hippocampal CA1 neurons following transient global cerebral ischemia in the rat. Transient global cerebral ischemia was induced in male Sprague-Dawley rats by four-vessel-occlusion for 10min.

Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats.

Background And Purpose: Ischemic postconditioning has been found to decrease brain infarct area and spinal cord ischemic injury. In this study, we tested the hypothesis that ischemic postconditioning reduces global cerebral ischemia/reperfusion-induced structural and functional injury in rats.

Methods: Ten-minute global ischemia was induced by 4-vessel occlusion in male Sprague-Dawley rats.