Powellabrahamsen2119

In addition, tumor tissue KIF2A protein and mRNA expressions were positively associated with lymph node metastasis (P = 0.025 and P = 0.010, respectively) and FIGO stage (P = 0.022 and P = 0.015, respectively) in cervical cancer patients. Moreover, patients with tumor tissue KIF2A high expression (mRNA and protein) displayed worse DFS (P = 0.010 and P = 0.046, respectively) and OS (P = 0.042 and P = 0.030, respectively) compared to patients with tumor tissue KIF2A low expression (mRNA and protein).

Tumor tissue KIF2A expression could serve as a biomarker enhancing the disease surveillance and prognostication in cervical cancer management.

Tumor tissue KIF2A expression could serve as a biomarker enhancing the disease surveillance and prognostication in cervical cancer management.Alzheimer's disease (AD) is the most common cause of dementia among elderly people. Majority of AD cases are sporadic (SAD) with unknown cause. Transgenic animal models closely reflect the familial (genetic) aspect of the disease but not the sporadic type. However, most new drug candidates which are tested positive in transgenic animal models failed in clinical studies so far. Herein, we aim to develop an AD animal model that combines most of the neuropathological features seen in sporadic AD in humans with amyloid plaques observed in transgenic mice. Four-month-old wild-type and APP/PS1 AD mice were given a single intracerebroventricular (ICV) injection of 3 mg/kg streptozotocin (STZ), a diabetogenic agent. Three weeks later, their cognitive behavior was assessed, and their brain tissues were collected for biochemical and histological analysis. STZ produced cognitive deficits in both non-transgenic mice and AD mice. Biochemical analysis showed a severe decline in synaptic proteins, increase in tau phosphorylation, oxidative stress, disturbed brain insulin signaling with extensive neuroinflammation, and cell death. Significant increase was also observed in the level of the soluble beta amyloid precursor protein (APP) fragments and robust accumulation of amyloid plaques in AD mice compared to the control. These results suggest that STZ ICV treatment causes disturbance in multiple metabolic and cell signaling pathways in the brain that facilitated amyloid plaque accumulation and tau phosphorylation. Therefore, this animal model can be used to evaluate new AD therapeutic agents for clinical translation.

Acute type A aortic dissection complicated with brain ischemia is associated with significantly higher mortality risks. Even if rescued with central aortic repair, some patients develop permanent postoperative neurological deficiency postoperatively. We recently introduced direct common carotid artery perfusion for acute type A aortic dissection involving the common carotid artery. This study introduced this technique to prevent postoperative neurological deficiency by comparing brain protection strategies.

Among 91 acute type A aortic dissection patients treated at our hospital during August 2015-October 2020, the common carotid artery was involved in 19 (21%), which had > 90% stenosis in either of the carotid arteries on preoperative contrast-enhanced computed tomography. see more Twelve patients underwent conventional selective cerebral perfusion during August 2015-December 2018 and seven patients underwent direct carotid artery perfusion during January 2019-October 2020. We assessed patient characteristics,ociated with intraoperative cerebral infarction. However, it may be ineffective when cerebral infarction has already developed.

Follicular lymphoma is a common indolent non-Hodgkin lymphoma with survival improving in the modern era. Despite favorable responses and improving remission duration, FL remains largely incurable with patterns of relapsing and remitting disease with many patients requiring multiple lines of therapy. As our understanding of the malignant B-cell biology evolves, more targeted therapies have emerged for the treatment of follicular lymphoma.

Targeted therapies entering the treatment landscape of follicular lymphoma include lenalidomide in combination with rituximab based on the randomized AUGMENT. Tazemetostat, an EZH2 inhibitor, joins the list of targeted therapies approved based on single-arm phase 2 studies in the relapsed setting. There are three PI3K inhibitors currently approved and more under development. Herein, I will review the available evidence that supports the use of targeted therapy across the disease course of follicular lymphoma.

Targeted therapies entering the treatment landscape of follicular lymphoma include lenalidomide in combination with rituximab based on the randomized AUGMENT. Tazemetostat, an EZH2 inhibitor, joins the list of targeted therapies approved based on single-arm phase 2 studies in the relapsed setting. There are three PI3K inhibitors currently approved and more under development. Herein, I will review the available evidence that supports the use of targeted therapy across the disease course of follicular lymphoma.Cholangiocarcinoma (CCA) is a malignant tumour with high recurrence and mortality rates and poor prognosis. However, the pathogenic mechanism remains unclear. In the present study, we aimed to investigate the roles and regulatory mechanism of SNHG16 in the occurrence and development of CCA. Gene Expression Profiling Interactive Analysis (GEPIA) was used to predict the expressions of SNHG16 and GATA6 in CCA samples from TCGA database. The levels of SNHG16, miR-146a-5p and GATA6 were evaluated using qRT-PCR. CCK-8 and flow cytometry assays were conducted to evaluate cell proliferation and apoptosis, respectively. Western blotting was applied to analyse the protein levels of GATA6 and apoptosis-related proteins. SNHG16 was significantly elevated in CCA tissues from TCGA database and CCA cell lines. Moreover, downregulation of SNHG16 restricted cell proliferation and increased apoptotic rate of RBE and HuCCT1 cells. miR-146a-5p, a downstream target of SNHG16, was shown to be an intermediate mediator of GATA6 expression regulated by SNHG16. In addition, either the miR-146a-5p inhibitor or overexpression of GATA6 obviously impaired the regulatory effects of SNHG16 downregulation in RBE and HuCCT1 cells. These data demonstrated that SNHG16 promoted cell proliferation and repressed apoptosis by regulating the miR-146a-5p/GATA6 axis, which provides some helpful insights for the diagnosis and treatment of CCA.