Efficacy of moisture chamber goggles combined with fluorometholone eye drops on visual function and oxidative stress in patients with dry eye disease.

Objective: To evaluate the effects of Moisture Chamber Goggles combined with Fluorometholone eye drops on visual function and oxidative stress in patients with dry eye disease.

Methods: A retrospective analysis was conducted on 80 patients with dry eye disease treated at Ninghai First Hospital from January 2021 to May 2023. Patients were divided into a combination group (n=40, receiving Fluorometholone eye drops and Moisture Chamber Goggles) and a monotherapy group (n=40, receiving Fluorometholone eye drops alone) based on treatment regimens.

Mechanical characteristics and load-bearing effect of roadway anchorage composite carrier.

Bolt support improves the stress state of the surrounding rock and forms an integral bearing structure inside the anchored surrounding rock. Therefore, it is of theoretical significance and practical application value to systematically study the mechanical mechanism and bearing characteristics of the anchorage composite carrier and elucidate the interaction mechanism between the bearing effect of the anchorage composite carrier and the stability of the roadway surrounding rock. In this paper, a mechanical model for the anchorage composite carrier is meticulously constructed through a fusion of theoretical analysis and advanced numerical simulation techniques.

[Treatment of cervical ossification of posterior longitudinal ligament with titanium alloy trabecular bone three-dimensional printed artificial vertebral body].

Objective: To evaluate the effectiveness of using titanium alloy trabecular bone three-dimensional (3D) printed artificial vertebral body in treating cervical ossification of the posterior longitudinal ligament (OPLL).

Methods: A retrospective analysis was conducted on clinical data from 45 patients with cervical OPLL admitted between September 2019 and August 2021 and meeting the selection criteria. All patients underwent anterior cervical corpectomy and decompression, interbody bone graft fusion, and titanium plate internal fixation.

PARP1 Is Upregulated by Hyperglycemia Via N6-methyladenosine Modification and Promotes Diabetic Retinopathy.

Poly (ADP-ribose) polymerase 1 (PARP1) plays an irreplaceable role in the progression of diabetic retinopathy (DR). The m6A methylation in mRNA controls gene expression under various physiological and pathological conditions. However, effects of m6A methylation on PARP1 expression and DR progression at molecular level have not been documented.

Directed transforming of coke to active intermediates in methanol-to-olefins catalyst to boost light olefins selectivity.

Methanol-to-olefins (MTO), the most important catalytic process producing ethylene and propylene from non-oil feedstocks (coal, natural gas, biomass, CO, etc.), is hindered by rapid catalyst deactivation due to coke deposition. Common practice to recover catalyst activity, i.

Restoration of Hydrogen Sulfide Production in Diabetic Mice Improves Reparative Function of Bone Marrow Cells.

Background: Bone marrow cell (BMC)-based treatment for critical limb ischemia in diabetic patients yielded a modest therapeutic effect resulting from cell dysfunction. Therefore, approaches that improve diabetic stem/progenitor cell functions may provide therapeutic benefits. Here, we tested the hypothesis that restoration of hydrogen sulfide (HS) production in diabetic BMCs improves their reparative capacities.

Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy.

Rationale: Cardiac myocyte-specific deletion of either glycogen synthase kinase (GSK)-3α and GSK-3β leads to cardiac protection after myocardial infarction, suggesting that deletion of both isoforms may provide synergistic protection. This is an important consideration because of the fact that all GSK-3-targeted drugs, including the drugs already in clinical trial target both isoforms of GSK-3, and none are isoform specific.

Objective: To identify the consequences of combined deletion of cardiac myocyte GSK-3α and GSK-3β in heart function.

Cardiomyocyte-specific deletion of Gsk3α mitigates post-myocardial infarction remodeling, contractile dysfunction, and heart failure.

Background: Injury due to myocardial infarction (MI) is largely irreversible. Once an infarct has occurred, the clinical goal becomes limiting remodeling, preserving left ventricular function, and preventing heart failure. Although traditional approaches (e.

Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart.

Background: Myocardial infarction-induced remodeling includes chamber dilatation, contractile dysfunction, and fibrosis. Of these, fibrosis is the least understood. After myocardial infarction, activated cardiac fibroblasts deposit extracellular matrix.

GSK-3α is a central regulator of age-related pathologies in mice.

Aging is regulated by conserved signaling pathways. The glycogen synthase kinase-3 (GSK-3) family of serine/threonine kinases regulates several of these pathways, but the role of GSK-3 in aging is unknown. Herein, we demonstrate premature death and acceleration of age-related pathologies in the Gsk3a global KO mouse.

Glycogen synthase kinase-3α limits ischemic injury, cardiac rupture, post-myocardial infarction remodeling and death.

Background: The molecular pathways that regulate the extent of ischemic injury and post-myocardial infarction (MI) remodeling are not well understood. We recently demonstrated that glycogen synthase kinase-3α (GSK-3α) is critical to the heart's response to pressure overload. However, the role, if any, of GSK-3α in regulating ischemic injury and its consequences is not known.

GSK-3alpha directly regulates beta-adrenergic signaling and the response of the heart to hemodynamic stress in mice.

The glycogen synthase kinase-3 (GSK-3) family of serine/threonine kinases consists of 2 highly related isoforms, alpha and beta. Although GSK-3beta has an important role in cardiac development, much remains unknown about the function of either GSK-3 isoform in the postnatal heart. Herein, we present what we believe to be the first studies defining the role of GSK-3alpha in the mouse heart using gene targeting.

Glycogen synthase kinase-3beta regulates post-myocardial infarction remodeling and stress-induced cardiomyocyte proliferation in vivo.

Rationale: Numerous studies have proposed that glycogen synthase kinase (GSK)-3beta is a central regulator of the hypertrophic response of cardiomyocytes. However, all of this work has relied on overexpression of GSK-3beta, expression of constitutively active mutants, or small molecule inhibitors with documented off-target effects. Genetic loss of function approaches have not been used in the adult mouse because germ-line deletion of GSK-3beta is embryonic-lethal.

Serine 58 of 14-3-3zeta is a molecular switch regulating ASK1 and oxidant stress-induced cell death.

Oxidant stress is a ubiquitous stressor with negative impacts on multiple cell types. ASK1 is a central mediator of oxidant injury, but while mechanisms of its inhibition, such as sequestration by 14-3-3 proteins and thioredoxin, have been identified, mechanisms of activation have remained obscure and the signaling pathways regulating this are not clear. Here, we report that phosphorylation of 14-3-3zeta at serine 58 (S58) is dynamically regulated in the cell and that the phosphorylation status of S58 is a critical factor regulating oxidant stress-induced cell death.

Deletion of GSK-3beta in mice leads to hypertrophic cardiomyopathy secondary to cardiomyoblast hyperproliferation.

Based on extensive preclinical data, glycogen synthase kinase-3 (GSK-3) has been proposed to be a viable drug target for a wide variety of disease states, ranging from diabetes to bipolar disorder. Since these new drugs, which will be more powerful GSK-3 inhibitors than lithium, may potentially be given to women of childbearing potential, and since it has controversially been suggested that lithium therapy might be linked to congenital cardiac defects, we asked whether GSK-3 family members are required for normal heart development in mice. We report that terminal cardiomyocyte differentiation was substantially blunted in Gsk3b(-/-) embryoid bodies.

Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction.

In addition to its role in cell adhesion, beta-catenin is an important signaling molecule in the Wnt/Wingless signaling pathway. Recent studies have indicated that beta-catenin is stabilized by hypertrophic stimuli and may regulate cardiac hypertrophic responses. To explore the role and requirement of beta-catenin in cardiac development and hypertrophy, we deleted the beta-catenin gene specifically in cardiac myocytes by crossing loxP-floxed beta-catenin mice with transgenic mice expressing a Cre recombinase under the control of the alpha-myosin heavy chain promoter.

[The research advances of biomechanics of human knee joint ligaments].

Ligaments are the main parts which stabilize the knee joint. How to analog the ligaments in biomechanical model will affect the characteristics of the human knee dynamics and in the computation of the stress in ligaments between two bones. This symposium is aimed at the survey of the simplified method of the ligaments via mechanical parameters, and providing an exact method of constructing model.

Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes.

Recent progresses in signal transduction have revealed that beta-catenin signaling controls embryonic development, tumorigenesis, cell shape, and polarity. The role of this pathway in myocyte shape regulation during cardiac hypertrophy and failure is, however, not clearly defined. Since homozygous knockout of beta-catenin is embryonically lethal, we have deleted beta-catenin genes specifically in the heart of adult mice by crossing loxP-flanked beta-catenin mice with transgenic mice expressing tamoxifen-activated MerCreMer protein (MCM) driven by the alpha-myosin heavy chain promoter.

Nuclear compartmentalization of FAK and FRNK in cardiac myocytes.

Focal adhesion kinase (FAK) and FAK-related non-kinase (FRNK) accumulate in the nucleus of cardiac myocytes during hypertensive hypertrophy. Nuclear FAK and FRNK are phosphorylated on different serines and form distinct bright spots. The subnuclear distribution of serine-phosphorylated FAK and FRNK was examined in this study by double labeling with fibrillarin, a component of nucleoli, and Sam68, a constituent of Sam68 nuclear bodies.

Myocardial expression and redistribution of GRKs in hypertensive hypertrophy and failure.

G-protein-coupled receptor kinases (GRKs) are involved in cardiac hypertrophy and failure. But their temporal expression and cellular localization during the development of hypertrophy and its transition to failure remains to be investigated. In this study, we determined the expression and subcellular distribution of GRK2, GRK3, GRK5, and GRK6 in cardiac myocytes of 2- to 24-month-old spontaneously hypertensive heart failure (SHHF) rats.