MiR-18a-LncRNA NONRATG-022419 pairs targeted PRG-1 regulates diabetic induced cognitive impairment by regulating NGF\BDNF-Trkb signaling pathway.

Background: Diabetic encephalopathy (DE) is considered as one of the complications of diabetes,which is associated with cognitive impairment in the pathological process of development. Up to now, phospholipid phosphatase related 4 (Plppr4), also known as plasticity related gene 1 (PRG-1) has been revealed its important role in neuroplasticity. However, the underlying mechanisms of Plppr4 on the basis of diabetic-induced cognitive dysfunction (DCD) are still unknown.

Research progress of music intervention in nursing of premature infants in neonatal intensive care unit.

Background: With the continuous advancement of medical technology, the survival rate of preterm infants is gradually improving, However, due to the underdeveloped function of various organs and systems, preterm infants are often exposed to light, noise, medical as well as nursing operations and other stimuli during their hospitalization in neonatal intensive care unit (NICU); it is highly susceptible to a number of problems, such as pain, unstable vital signs, growth retardation, and sleep disruption.

Objective: This article reviews the research progress of music intervention in nursing of premature infants in NICU with both traditional and conventional care.

Methods: This article reviews the research background, methodology/design, and measurement/application effects of music interventions, including Chinese and Western traditional music, in the care of preterm infants in NICU.

The integrated analysis and underlying mechanisms of FNDC5 on diabetic induced cognitive deficits.

Objectives: Chronic hyperglycemia is considered as an important factor to promote the neurodegenerative process of brain, and the synaptic plasticity as well as heterogeneity of hippocampal cells are thought to be associated with cognitive dysfunction in the early process of neurodegeneration. To date, fibronectin type III domain-containing protein 5 (FNDC5) has been highlighted its protective role in multiple neurodegenerative diseases. However, the potential molecular and cellular mechanisms of FNDC5 on synaptic plasticity regulation in cognitive impairment (CI) induced by diabetics are still need to known.

A Review of Gap Junction Protein and its Potential Role in Nervous System-Related Disease.

Gap junction (GJ) is a special cell membrane structure composed of connexin. Connexin is widely distributed and expressed in all tissues except differentiated skeletal muscle, red blood cells, and mature sperm cells, which is related to the occurrence of many genetic diseases due to its mutation. Its function of regulating immune response, cell proliferation, migration, apoptosis, and carcinogenesis makes it a therapeutic target for a variety of diseases.

Heterogeneity and synaptic plasticity analysis of hippocampus based on db mice induced diabetic encephalopathy.

Chronic hyperglycemia can cause changes in synaptic plasticity of hippocampal cells, which has accelerated the pathological process of cognitive dysfunction. However, the heterogeneity of the hippocampal cell populations under long term high glucose statement remains largely unknown. To mimic chronic hyperglycemia induced cognitive function deficit in vivo, db diabetic mice was selected and Novel Object Recognition(NOR) behavior tests were performed.

What is the role of Von Willebrand factor in chronic hepatitis B virus infection to hepatocellular carcinoma: a review article.

Von Willebrand factor (VWF) is a glycoprotein synthesized and secreted by vascular endothelial cells and megakaryocytes, found on plasma surface, endothelial cells, and α-granule of platelets. VWF can be interacted with collagen and platelet membrane glycoproteins GPIb and GPIb-IIa and play an important role in platelet adhesion and aggregation. Growing research evidence suggests that VWF also mediates the prevention or protesting of hepatocellular carcinoma (HCC) in chronic hepatitis B (CHB) patients from several clinical studies.

The Molecular Mechanism of CoenzymeQ10 on Pyroptosis and its Related Diseases: A Review.

In recent years, cell pyroptosis has made it widely concerned. Pyroptosis is characterized by the activation of pathways leading to the activation of NLRP3 inflammasome and its downstream effector, such as interleukin (IL)-1β and IL-18, which has close relationship with inflammation. Recent evidence supports that CoenzymeQ10 (CoQ10) reduces related inflammatory factors (NLRP3, IL-1β and IL-18), which are associated with cell pyroptosis.

Changes in dorsal root ganglion CGRP expression in mouse pinch nerve injury model: Modulation by Somatostatin type-2 receptor.

Introduction: Our previous work has shown that somatostatin effectively inhibits neuropathic pain by activating its type 2 receptor (SSTR2) in the dorsal root ganglion (DRG) and spinal cord of mice. However, the underlying mechanism of this activation has not been elucidated.

Methods: To explore further mechanisms, we examined pain behavior and the expression of neuropeptides such as calcitonin gene-related peptide (CGRP) in dorsal root ganglion neurons(DRGs) as well as the changes of the number of CGRP-IR DRGs in the mouse model of sciatic pinch nerve injury.

A Review of Phosphocreatine 3 Kinase δ Subtype (PI3Kδ) and Its Inhibitors in Malignancy.

Most cancer deaths are caused by metastasis. The phosphocreatine 3- kinase (PI3K) family includes the I-III classes, with class I divided into 4 subtypes (alpha, ß, γ, delta); and PI3K signaling participates in the regulatory processes of cell proliferation, differentiation, apoptosis, and glucose transport. Moreover, PI3Ks are modulators of cellular membrane lipids involved in signaling and trafficking events.

Inactivated AMPK-α2 promotes the progression of diabetic brain damage by Cdk5 phosphorylation at Thr485 site.

Changes in brain energy metabolism in diabetes mellitus, including increased insulin resistance and mitochondrial dysfunction, are critically involved in diabetes-related neurodegeneration, and associate with early cognitive impairment as well. The aim of this study is to detect the specific phosphorylated-Thr485- AMP-activated protein kinase (AMPK-α2), regulated by cyclin-dependent kinase 5 (Cdk5) paly the inhibitory functional role of AMPK-α2, Which is maybe the link to the accelerated diabetic brain damage progression. Here, we used GK rats, the type 2 diabetic animal model for in vivo studies and performed In vitro kinase assay, high glucose treatment, -phosphorylated mutation and protein expression in both HEK-293T and HT-22 cell lines.

Somatostatin Type 2 Receptor Antibody Enhances Mechanical Hyperalgesia in the Dorsal Root Ganglion Neurons after Sciatic Nerve-pinch Injury: Evidence of Behavioral Studies and Bax Protein Expression.

Background: Our previous study has indicated that somatostatin potently inhibits neuropathic pain through the activation of its type 2 receptor (SSTR2) in mouse dorsal root ganglion and spinal cord. However, the underlying mechanism of this activation has not been elucidated clearly.

Objective: The aim of this study is to perform the pharmacological studies on the basis of sciatic nerve-pinch mice model and explore the underlying mechanism involving SSTR2.

Resolution and evaluation of 3-chlorophenyl-3-hydroxypropionylhydroxamic acid as antivirulence agent with excellent eradication efficacy in Helicobacter pylori infected mice.

The continuing emergence of drug-resistant Helicobacter pylori (HP) drives the ongoing need for the development of new and effective anti-HP drugs. Urease inhibitor has now gained strong interest as an alternative approach for HP infections. 3-Chlorophenyl-3-hydroxypropionylhydroxamic acid (CPH), a novel urease inhibitor identified in our group, shows impressive potency, which was optically separated for a further exploration.

Alterations of synaptic plasticity in aged rats: Evidence of functional and morphological studies.

Background: The aging-related disease and associated neurodegenerative complications, such as cognitive impairment, has received increasing attention.

Objective: The aim of this study was to show changes in cognitive behavior and molecular related the synaptic plasticity in aged-induced cognitive deficits rats.

Methods: We used novel object recognition testing and morphological staining as well as western blot to detect changes in cognitive behavior and molecular related the synaptic plasticity.

Allicin attenuates tunicamycin-induced cognitive deficits in rats via its synaptic plasticity regulatory activity.

Objectives: To illuminate the functional effects of allicin on rats with cognitive deficits induced by tunicamycin (TM) and the molecular mechanism of this process.

Materials And Methods: 200-250 g male SD rats were divided into three groups at random: control group (n=12), TM group (5 μl, 50 μM, ICV, n=12), and allicin treatment group (180 mg/kg/d with chow diet, n=12). After 16 weeks of allicin treatment, the learning ability and memory were tested using novel object recognition (NOR) testing on rats with 72 hr TM treatment (5 μl, 50 μM, ICV); meanwhile, the variation of field excitatory postsynaptic potential (fEPSP) in the Schaffer Collateral (SC)-CA1 synapse was detected by extracellular electrophysiological recordings and the morphology of dendritic spine was observed by Golgi staining as well as detecting several synaptic plasticity-related proteins by Western blot.

Nuclear factor erythroid 2-related factor 2 antibody attenuates thermal hyperalgesia in the dorsal root ganglion: Neurochemical changes and behavioral studies after sciatic nerve-pinch injury.

Oxidative stress is generated in several peripheral nerve injury models.Nuclear factor erythroid 2-related factor 2 (Nrf2) is activated to have a role in antioxidant effect. After nerve injury, the severely painful behavior is also performed.

Adenosine analogs as inhibitors of tyrosyl-tRNA synthetase: Design, synthesis and antibacterial evaluation.

Herein we describe the synthesis and evaluation of a series of adenosine analogs for in vitro antibacterial activity against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa. Out of these compounds, compound c6 has much stronger antibacterial potency against Pseudomonas aeruginosa than ciprofloxacin, and was determined to target tyrosyl-tRNA synthetase with IC50 of 0.8±0.

Insulin resistance-induced hyperglycemia decreased the activation of Akt/CREB in hippocampus neurons: Molecular evidence for mechanism of diabetes-induced cognitive dysfunction.

Several previous studies have indicated that diabetic have higher risk of suffering from Alzheimer's disease, which severely induced cognitive dysfunction. However, the underlying molecular mechanism and more details on the cognitive deficits induced by hyperglycemia have not been elucidated. Here in our present study, on the basis of Goto-Kakizaki (GK) rats and streptozotocin (STZ)-induced diabetic model, we detected the variation of dendritic spine density in hippocampus as well as the differential expression of some important signal transduction molecules that were of relevance in learning and memory function.

Synthesis and evaluation of new tyrosyl-tRNA synthetase inhibitors as antibacterial agents based on a N2-(arylacetyl)glycinanilide scaffold.

Tyrosyl-tRNA synthetase (TyrRS), an essential enzyme in bacterial protein biosynthesis, is an attractive therapeutic target for finding novel antibacterial agents, and a series of N2-(arylacetyl)glycinanilides has been herein synthesized and identified as TyrRS inhibitors. These efforts yielded several compounds, with IC50 in the low micromolar range against TyrRS from Staphylococcus aureus. Out of the obtained compounds, 3ap is the most active and exhibits excellent activity against both Gram-positive (S.

Allicin improves endoplasmic reticulum stress-related cognitive deficits via PERK/Nrf2 antioxidative signaling pathway.

Endoplasmic reticulum (ER) stress is involved in neurodegenerative diseases including Alzheimer's disease (AD), in which dysregulation of double-stranded RNA-dependent protein kinase (PKR)-like ER-resident kinase (PERK) is considered to play a critical role. Allicin, a garlic extract, has been demonstrated a protective role in AD model. The present study was designed to investigate the possible protective effect of allicin on ER stress-induced cognitive deficits and underlying mechanisms in rats.

Synthesis, molecular docking and biological evaluation of 3-arylfuran-2(5H)-ones as anti-gastric ulcer agent.

3-Arylfuran-2(5H)-one derivatives show good antibacterial activity and were determined as tyrosyl-tRNA synthetase (TyrRS) inhibitors. In a systematic medicinal chemistry exploration, we demonstrated chemical opportunities to treat infections caused by Helicobacter pylori. Twenty 3-arylfuran-2(5H)-ones were synthesized and evaluated for anti-H.

Pentamethylquercetin ameliorates fibrosis in diabetic Goto-Kakizaki rat kidneys and mesangial cells with suppression of TGF-β/Smads signaling.

Pentamethylquercetin (PMQ) has been shown to possess glucose-lowering properties, but its effect on renal fibrosis in diabetes is still unclear. This study was designed to investigate the effect of PMQ on renal fibrosis and the underlying mechanisms in spontaneous type II diabetic Goto-Kakizaki rats and mesangial cells in high glucose. We found that in Goto-Kakizaki rats, PMQ treatment attenuated glomerular volume, glycogen deposition, renal collagen and fibronectin accumulation, in addition to amelioration of diabetic symptoms, including reduction of urine volume and urine glucose levels.

Pentamethylquercetin protects against diabetes-related cognitive deficits in diabetic Goto-Kakizaki rats.

Diabetic patients have a signifiantly higher risk of developing all forms of dementia. Pentamethylquercetin (PMQ) has been proven to have potential as an anti-diabetic agent. Nevertheless, whether PMQ can improve diabetes-induced cognitive dysfunction has not been investigated.

Allicin ameliorates cardiac hypertrophy and fibrosis through enhancing of Nrf2 antioxidant signaling pathways.

Aim: To evaluate the protective effects of allicin on Ang II-induced cardiac hypertrophy.

Methods: Sprague-Dawley male rats were randomized into 3 groups:1)sham group (saline)(n = 12), 2) Ang II group(n = 9), 3) allicin group (Ang II + allicin)(n = 9). They received infusions of either saline or Ang II (250 ng/kg body weight per min) through mini-osmotic pumps implanted subcutaneously for 2 weeks and given a diet containing 180 mg/kg/day of allicin for 8 consecutive weeks.