Sevoflurane anesthesia reduces the expression of inflammatory response genes and β-site amyloid precursor protein-cleaving enzyme in hippocampi of diabetic mice.

Diabetes and inhaled anesthesia are associated with an increased likelihood of developing postoperative cognitive dysfunction in humans and animal models, but the mechanisms are unclear. This study aimed to investigate the effect and mechanism of sevoflurane anesthesia on cognitive function in diabetic (DM) mice. Spontaneously diabetic db/db and control db/m mice were subject to sevoflurane anesthesia or allowed to breathe air, respectively.

Expression of prostaglandin E2 and EP receptors in human papillary thyroid carcinoma.

The objective of the present study is to determine the role of prostaglandin E2 (PGE2) and downstream EP receptors in the development of human papillary thyroid carcinoma (PTC). A total of 90 thyroid specimens excised from patients undergoing total or subtotal thyroidectomy in the Department of General Surgery, the Fifth Affiliated Hospital of Sun Yat-sen University, China, from August 2013 to September 2014, were analyzed. The quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunohistochemical analyses were employed to examine the messenger RNA (mRNA) and protein expression, respectively.

Expression and distribution of Src in the nucleus of myocytes in cardiac hypertrophy.

The Src kinase is involved in signaling events leading to cardiac hypertrophy. The exact effects of tyrosine phosphorylation and subnuclear distribution on cardiac hypertrophy and failure remain to be investigated. In this study, we examined the intranuclear expression and distribution of c-Src, Src phosphorylated at tyrosine 529 (Src[pY529]), Src phosphorylated at tyrosine 418 (Src[pY418]) and Src phosphorylated at tyrosine 215 (Src[pY215]) in the myocardial nuclei of the left ventricle (LV) from 2-, 6-, 12- and 18-month-old spontaneously hypertensive heart failure (SHHF) rats and age-matched Wistar-Kyoto (WKY) rats as normotensive controls by western blot analysis, immunofluorescent labeling and immunoprecipitation.

Expression and redistribution of β-catenin in the cardiac myocytes of left ventricle of spontaneously hypertensive rat.

Beta-catenin is not only an adhering junction protein, but also the central player of the canonical Wnt signalling pathway. In order to investigate the roles of β-catenin in the mechanism of myocardial hypertrophy, we determined the expression and distribution of β-catenin in the cardiomyocytes of spontaneously hypertensive heart failure (SHHF) rats and age-matched Wistar-Kyoto (WKY) rats. We identified the reducing of β-catenin expression in the membrane protein fraction but increasing in the nuclear protein in the 6 and 12 month-old SHHF rats as compared with the age-matched WKY rats by Western blotting.

[Correlation of early phase contrast enhancement of multi-detector row computed tomography to tumor stroma of nodular solid lung adenocarcinoma].

Background & Objective: Dynamic enhanced multi-detector row CT (MDCT) has been used in differential diagnosis of pulmonary nodules, but its mechanism was unclear yet. This study was to evaluate the correlations of early phase enhancement of MDCT to proportion and distribution of stroma in solid lung adenocarcinoma.

Methods: A total of 31 patients with lung adenocarcinoma underwent routine contrast-enhanced MDCT.

[Phosphorylation and nuclear translocation of serine 722 and serine 910 of focal adhesion kinase in hypertrophic cardiac myocytes of left ventricle of spontaneously hypertensive rats].

Objective: To investigate the role of focal adhesion kinase (FAK) in cardiac hypertrophy induced by hypertension.

Methods: Using immunofluorescent labeling, confocal microscopy and Western blot, the expression and subcellular location of FAK-pSer722 and FAK-pSer910 were determined in cardiac myocytes of the left ventricles from 2, 6, 12, and 18 month-old spontaneously hypertensive heart failure (SHHF) rats and age-matched Wistar-Kyoto (WKY) control rats, respectively.

Results: There was no obvious difference in FAK-pSer722 and FAK-pSer910 expression between 2 month-old SHHF and WKY rats.

[Expression of focal adhesion kinase in cardiac myocytes of hypertrophic ventricle].

Objectives: To investigate the role of focal adhesion kinase (FAK) in the pathogenesis of cardiac hypertrophy induced by hypertension.

Methods: Using immunofluorescent labeling, confocal microscopy and Western blotting, the expression and subcellular localization of FAK in the cardiac myocytes of left ventricle were determined in 2, 6, 12, and 18 month-old rats with spontaneously hypertensive heart failure (SHHF) along with age-matched control Wistar-Kyoto (WKY) rats.

Results: There was no significant difference of FAK expression between 2 month-old SHHF and WKY rats (50.

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.

Sonographic appearance of a testicular yolk sac tumor in a 2-year-old boy.

Yolk sac tumor (YST) of testis is the most common of all childhood testicular malignancies. We report a case of testicular YST in a 2-year-old boy. The tumor appeared sonographically as an ovoid, homogeneous, well-circumscribed, isoechoic, solid testicular mass with good sound-through transmission and increased internal vascularity on color Doppler imaging.

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.

Structural basis of ventricular remodeling: role of the myocyte.

Structural remodeling plays a major role in the progression of various heart diseases to congestive heart failure (CHF). Major contributors to this remodeling process in the heart include alterations in myocyte shape, myocyte number, and extracellular matrix. However, it is unclear as to which of these changes is most critical in the development of CHF, and this may vary by etiology.

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.

Subcellular redistribution of focal adhesion kinase and its related nonkinase in hypertrophic myocardium.

Focal adhesion kinase (FAK) and focal adhesion kinase-related nonkinase (FRNK) are likely involved in mechanical signaling during hypertension. We investigated expression, subcellular distribution, and phosphorylation of FAK, as well as FRNK in left ventricles of spontaneously hypertensive heart failure rats. Compared with normotensive controls, FAK and FRNK increased in left ventricles of hypertensive rats.

Myocyte redistribution of GRK2 and GRK5 in hypertensive, heart-failure-prone rats.

Gprotein-coupled receptor kinases (GRKs) are known to be involved in the development of cardiac hypertrophy. Their exact role and subcellular distribution during cardiac hypertrophy and failure remain to be elucidated. We examined expression and subcellular distribution of GRK2 and GRK5 in the left ventricle of female spontaneously hypertensive heart failure (SHHF) rats at 6 months of age using Western blots and fluorescent confocal microscopy.