Long Non-Coding RNAs: Crucial Regulators in Alzheimer's Disease Pathogenesis and Prospects for Precision Medicine.

Long non-coding RNAs (LncRNAs) have emerged as pivotal regulators in the pathogenesis of Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. With the capacity to modulate gene expression at various levels, LncRNAs are implicated in multiple pathological mechanisms of AD, including amyloid-beta (Aβ) accumulation, tau protein phosphorylation, neuroinflammation, and neuronal apoptosis. Recent studies have highlighted the potential of LncRNAs as diagnostic biomarkers and therapeutic targets due to their differential expression patterns in AD patients.

RBM47 promotes cell proliferation and immune evasion by upregulating PDIA6: a novel mechanism of pancreatic cancer progression.

Background: Pancreatic cancer (PC) is a lethal malignancy characterized by poor prognosis and high mortality. We found the highly expressed RNA-binding motif protein 47 (RBM47) in PC progression. The RBM47 expression was negatively correlated with natural killer (NK) cell infiltrate in PC.

Updates in Alzheimer's disease: from basic research to diagnosis and therapies.

Alzheimer's disease (AD) is the most common neurodegenerative disorder, characterized pathologically by extracellular deposition of β-amyloid (Aβ) into senile plaques and intracellular accumulation of hyperphosphorylated tau (pTau) as neurofibrillary tangles. Clinically, AD patients show memory deterioration with varying cognitive dysfunctions. The exact molecular mechanisms underlying AD are still not fully understood, and there are no efficient drugs to stop or reverse the disease progression.

The expression and clinical significance of PLK1/p-PLK1 protein in NK/T cell Lymphoma.

Aims: To investigate the expression of polo-like kinase 1 protein (PLK1) and its phosphorylation level (p-PLK1) in extranodal NK/T cell lymphoma (NKTCL) and their correlation with clinical characteristics and prognosis.

Methods: We collected 40 cases of NKTCL (referred to as the experimental group), which received diagnoses at the First Affiliated Hospital of Zhengzhou University between January 2018 and October 2022. Concurrently, we assembled a control group, including 20 cases afflicted with nasopharyngeal mucosal lymphoid hyperplasia diseases during the same timeframe.

Oligomeric β-Amyloid Suppresses Hippocampal γ-Oscillations through Activation of the mTOR/S6K1 Pathway.

Neuronal synchronization at gamma frequency (30-100 Hz: γ) is impaired in early-stage Alzheimer's disease (AD) patients and AD models. Oligomeric Aβ caused a concentration-dependent reduction of γ-oscillation strength and regularity while increasing its frequency. The mTOR1 inhibitor rapamycin prevented the Aβ-induced suppression of γ-oscillations, whereas the mTOR activator leucine mimicked the Aβ-induced suppression.

Targeting a vulnerable septum-hippocampus cholinergic circuit in a critical time window ameliorates tau-impaired memory consolidation.

Background: Abnormal tau accumulation and cholinergic degeneration are hallmark pathologies in the brains of patients with Alzheimer's disease (AD). However, the sensitivity of cholinergic neurons to AD-like tau accumulation and strategies to ameliorate tau-disrupted spatial memory in terms of neural circuits still remain elusive.

Methods: To investigate the effect and mechanism of the cholinergic circuit in Alzheimer's disease-related hippocampal memory, overexpression of human wild-type Tau (hTau) in medial septum (MS)-hippocampus (HP) cholinergic was achieved by specifically injecting pAAV-EF1α-DIO-hTau-eGFP virus into the MS of ChAT-Cre mice.

encodes a protein that inhibits the activity of by JAK2-STAT3 pathway in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is an invasive malignant tumor with a high incidence rate and mortality. It is imperative to study its tumorigenesis and development for better treatment. CircRNA has been proven to play an important role in various cancers.

Clinicopathological features of CD5-positive splenic marginal zone lymphoma.

Aims: To investigate the clinicopathological features, immunophenotypes and differential diagnosis of CD5-positive splenic marginal zone lymphoma (SMZL).

Methods: We retrospectively analysed 16 CD5-positive cases of SMZL. Assess their clinicopathological features and survival outcomes to evaluate their similarities and differences with a control group of 25 CD5-negative cases of SMZL.

Genetic testing and prognosis of sarcomatoid hepatocellular carcinoma patients.

Background: Sarcomatoid hepatocellular carcinoma (SHC) is a rare epithelial malignancy with high invasiveness and poor prognosis. However, the molecular characteristics and main driver genes for SHC have not been determined. The aim of this study is to explore the potentially actionable mutations of driver genes, which may provide more therapeutic options for SHC.

Intracellular accumulation of tau inhibits autophagosome formation by activating TIA1-amino acid-mTORC1 signaling.

Background: Autophagy dysfunction plays a crucial role in tau accumulation and neurodegeneration in Alzheimer's disease (AD). This study aimed to investigate whether and how the accumulating tau may in turn affect autophagy.

Methods: The primary hippocampal neurons, N2a and HEK293T cells with tau overexpression were respectively starved and treated with vinblastine to study the effects of tau on the initiating steps of autophagy, which was analysed by Student's two-tailed t-test.

Predicting cumulative effect of lifestyle risk factors for complex disease.

In medical domain, risk factors are often used to model disease predictions. In order to make the most use of the predictive models, linking the model with real patient data generates personalized disease progression and predictions. However, the risk factors are fragmented all over medical literature, certain risks can be accumulated for a disease and the aggregated probability may increase or decrease the occurrence of a disease.

Alzheimer-like tau accumulation in dentate gyrus mossy cells induces spatial cognitive deficits by disrupting multiple memory-related signaling and inhibiting local neural circuit.

Abnormal tau accumulation and spatial memory loss constitute characteristic pathology and symptoms of Alzheimer disease (AD). Yet, the intrinsic connections and the mechanism between them are not fully understood. In the current study, we observed a prominent accumulation of the AD-like hyperphosphorylated and truncated tau (hTau N368) proteins in hippocampal dentate gyrus (DG) mossy cells of 3xTg-AD mice.

Human tau accumulation promotes glycogen synthase kinase-3β acetylation and thus upregulates the kinase: A vicious cycle in Alzheimer neurodegeneration.

Background: Glycogen synthase kinase-3β (GSK-3β) is one of the most effective kinases in promoting tau hyperphosphorylation and accumulation in Alzheimer's disease (AD). However, it is not clear how GSK-3β activity is regulated during AD progression.

Methods: We firstly used mass spectrometry to identify the acetylation site of GSK-3β, and then established the cell and animal models of GSK-3β acetylation.

GNAQ T96S mutation abrogates the ability of wild-type GNAQ to induce apoptosis by phosphorylating annexin A2 in natural killer/T cell lymphoma.

Our previous study identified annexin A2 (ANXA2) as a Gaq-interacting partner in natural killer/T cell lymphoma (NKTCL) cells transfected with the GNAQ T96S mutation vector by immunoprecipitation and mass spectrometry; however, the detailed molecular mechanisms by which GNAQ T96S might regulate ANXA2 remain to be defined in NKTCL. Herein, we found that the GNAQ T96S mutation significantly promotes the phosphorylation of ANXA2 at the Y24 site, whereas phosphorylation of ANXA2 abolishes the ability of WT GNAQ to trigger cell apoptosis. Further investigation revealed that a GNAQ T96S peptide inhibitor induced apoptosis by competing with ANXA2 binding to GNAQ T96S in NKTCL cells.

Highly Stretchable and Self-Adhesive Elastomers Based on Polymer Chain Rearrangement for High-Performance Strain Sensors.

Polydimethylsiloxane (PDMS) has been widely used in many fields. However, the polymerization process of the siloxane chain is highly complex, and it is challenging to enhance the mechanical properties of PDMS elastomers significantly. We found that adding a small amount of polyoxyethylene lauryl ether (Brij-35) into siloxane polymers can result in B-PDMS elastomers with high tensile properties and strong adhesion.

Camrelizumab plus apatinib as second-line treatment for advanced oesophageal squamous cell carcinoma (CAP 02): a single-arm, open-label, phase 2 trial.

Background: Camrelizumab, an anti-PD-1 antibody, has shown moderate efficacy in oesophageal squamous cell carcinoma. Apatinib, a selective inhibitor of VEGFR2, has a synergistic effect with immunotherapy. We aimed to assess the combination of camrelizumab and apatinib as second-line treatment for advanced oesophageal squamous cell carcinoma.

Molecular characteristics and clinical outcomes of complex ALK rearrangements identified by next-generation sequencing in non-small cell lung cancers.

Background: Complex kinase rearrangement, a mutational process involving one or two chromosomes with clustered rearrangement breakpoints, interferes with the accurate detection of kinase fusions by DNA-based next-generation sequencing (NGS). We investigated the characteristics of complex ALK rearrangements in non-small cell lung cancers using multiple molecular tests.

Methods: Samples of non-small cell lung cancer patients were analyzed by targeted-capture DNA-based NGS with probes tilling the selected intronic regions of fusion partner genes, RNA-based NGS, RT-PCR, immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH).

Medial septum tau accumulation induces spatial memory deficit via disrupting medial septum-hippocampus cholinergic pathway.

Tau accumulation and cholinergic impairment are characteristic pathologies in Alzheimer's disease (AD). However, the causal role of tau accumulation in cholinergic lesion is elusive. Here, we observed an aberrant tau accumulation in the medial septum (MS) of 3xTg and 5xFAD mice, especially in their cholinergic neurons.

ZG16 regulates PD-L1 expression and promotes local immunity in colon cancer.

CRC is a heterogeneous disease due to global molecular alterations, including mismatch-repair-deficient (dMMR) and microsatellite instability-high (MSI-H). Immunotherapy has achieved durable responses in a subset of patients with dMMR-MSI-H metastatic CRC. It has been showed that Loss of ZG16 is highly associated with colorectal cancer.

Design Optimization of Resource Allocation in OFDMA-Based Cognitive Radio-Enabled Internet of Vehicles (IoVs).

Joint optimal subcarrier and transmit power allocation with QoS guarantee for enhanced packet transmission over Cognitive Radio (CR)-Internet of Vehicles (IoVs) is a challenge. This open issue is considered in this paper. A novel SNBS-based wireless radio resource scheduling scheme in OFDMA CR-IoV network systems is proposed.

Implication of Microsatellite Instability in Chinese Cohort of Human Cancers.

Background: Microsatellite instability (MSI) has been a hot topic in cancer research. Determining MSI status greatly aids tumor prognosis and treatment plans. However, MSI data for Asian cancer patients with prognostic information are scarce.

Prognostic value of a five-lncRNA signature in esophageal squamous cell carcinoma.

Background: The aim of this study was to identify prognostic long non-coding RNAs (lncRNAs) and develop a multi-lncRNA signature for suvival prediction in esophageal squamous cell carcinoma (ESCC).

Methods: The clinical and gene expression data from Gene Expression Omnibus database (GSE53624, n = 119) were obtianed as training set. A total of 98 paired ESCC tumor and normal tissues were detected by RNA sequencing and used as test set.

Tau Acetylation in Entorhinal Cortex Induces its Chronic Hippocampal Propagation and Cognitive Deficits in Mice.

Background: Increased tau acetylation at K174, K274, K280, and K281 has been observed in the brains of Alzheimer's disease (AD) patients or in transgenic mice, but the role of acetylation in tau propagation is elusive.

Objective: To study the effect of tau acetylation in entorhinal cortex on tau transmission and learning and memory.

Methods: Stereotactic brain injection, behavioral test, electrophysiological recording, immunohistochemistry, and immunofluorescence were used.