Hemodialysis as a Risk Factor for Ceftriaxone-Associated Pseudolithiasis in Adults.

Ceftriaxone-associated biliary pseudolithiasis is common among children; however, there are only a few reports of pseudolithiasis in adult patients on HD. This retrospective cohort study included 278 adult patients on ceftriaxone therapy from 1 February 2016 to 1 September 2018. Pseudolithiasis was defined as a new development of sludge or stones in the gallbladder within 60 days of ceftriaxone therapy.

A protective role of Nox1/NADPH oxidase in a mouse model with hypoxia-induced bradycardia.

Although it has been reported that endotoxin-induced expression of Nox1 in the heart contributes to apoptosis in cardiomyocytes, functional role of Nox1 at the physiological expression level has not been elucidated. The aim of this study was to clarify the role of Nox1 under a hypoxic condition using wild-type (WT, Nox1(+/Y)) and Nox1-deficient (Nox1(-/Y)) mice. ECG recordings from anesthetized mice revealed that Nox1(-/Y) mice were more sensitive to hypoxia, resulting in bradycardia, compared to WT mice.

Termination of aconitine-induced atrial fibrillation by the KACh-channel blocker tertiapin: underlying electrophysiological mechanism.

The acetylcholine receptor-operated K(+) (KACh) channel may be a novel target for atrial-specific antiarrhythmic therapy. Recently it has been demonstrated that tertiapin, a selective blocker of KACh channel, suppressed aconitine-induced atrial fibrillation (AF) in dogs. However, the precise mechanism by which the KACh-channel blocker inhibits the aconitine-induced AF remains unknown.

Biochemistry and physiology of mitochondrial ion channels involved in cardioprotection.

Over the past decades there has been considerable progress in understanding the multifunctional roles of mitochondrial ion channels in metabolism, energy transduction, ion transport, signaling, and cell death. Recent data have suggested that some of these channels function under physiological condition, and others may be activated in response to pathological insults and play a key role in cytoprotection. This review outlines our current understanding of the molecular identity and pathophysiological roles of the mitochondrial ion channels in the heart with particular emphasis on cardioprotection against ischemia/reperfusion injury, and future research on mitochondrial ion channels.

New aspects for the treatment of cardiac diseases based on the diversity of functional controls on cardiac muscles: mitochondrial ion channels and cardioprotection.

Mitochondrial ATP-sensitive K(+) (mitoK(ATP)) and Ca(2+)-activated K(+) (mitoK(Ca)) channels exist in cardiac myocytes, and they play key roles in cardioprotection. We have recently reported that K(+) influx through mitoK(ATP) or mitoK(Ca) channels occurs independently of each other and confers cardioprotection in a similar manner. Activation of mitoK(ATP) channel is augmented by protein kinase C (PKC), whereas mitoK(Ca) channel is activated by protein kinase A (PKA).

Glimepiride treatment upon reperfusion limits infarct size via the phosphatidylinositol 3-kinase/Akt pathway in rabbit hearts.

The phenomenon termed postconditioning, that is, brief episodes of ischemia/reperfusion at the onset of reperfusion reduce infarct size, is thought to involve the activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Treatment with a drug activating PI3K at the onset of reperfusion may confer a similar cardioprotection. The sulfonylurea glimepiride has been shown to activate PI3K in human endothelial cells.

[Inactivation mechanism of microorganisms by the synergy of silver and light irradiation, and the application in household electrical appliances].

The inactivation efficiencies of microorganisms were found to be enhanced by using silver solution together with ultraviolet light (UV-A, 395 nm) irradiation. The inactivation efficiencies were improved remarkably especially in eukaryotic microorganism. To make clear the inactivation mechanism of microorganisms by the combination effect of silver and ultraviolet light irradiation, the resultant solution was characterized by ESR (Electron spin resonance, ESR).

Physicochemical, morphological and therapeutic evaluation of agarose hydrogel particles as a reservoir for basic fibroblast growth factor.

Micron-sized agarose hydrogel particles were prepared using an emulsification/gelation method as a controlled release reservoir for basic fibroblast growth factor (bFGF). Mean particle size of agarose hydrogel particles decreased with an increase in stirring speed and also with an increasing temperature of the oil phase, as measured before cooling. Morphologies of agarose particles before and after dispersing into water were investigated by scanning electron microscopy (SEM) and cryogenic SEM, respectively.

6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2-(1H)quinolinone (cilostazol), a phosphodiesterase type 3 inhibitor, reduces infarct size via activation of mitochondrial Ca2+-activated K+ channels in rabbit hearts.

6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2-(1H)quinolinone (cilostazol), a phosphodiesterase type 3 (PDE III) inhibitor, activates cAMP-dependent protein kinase A (PKA). The cAMP/PKA pathway potentiates the opening of mitochondrial Ca(2+)-activated K(+) (mitoK(Ca)) channels and confers cardioprotection. Although cilostazol has been reported to directly activate sarcolemmal large-conductance Ca(2+)-activated K(+) channels, it remains unclear whether cilostazol modulates the opening of mitoK(Ca) channels.

Infarct size limitation by adrenomedullin: protein kinase A but not PI3-kinase is linked to mitochondrial KCa channels.

Aim: Adrenomedullin (ADM) has been shown to protect the heart against ischaemic injury, but little is known of the underlying mechanism. Mitochondrial Ca(2+)-activated K(+) (mitoK(Ca)) channels play a key role in cardioprotection. This study examined whether mitoK(Ca) channel is involved in the protection afforded by ADM.

Late-term regression of stenosis at the kink site in the internal thoracic artery in two cases.

A kink in the internal thoracic artery (ITA) is a rare postoperative complication after coronary artery bypass surgery. The kink can be accompanied by significant stenosis and has been observed after the ITAs are harvested by the skeletonization method. In this report, we present two cases in which early postoperative angiography showed the kink accompanied by significant stenosis, and late angiography revealed regression of stenosis at the kink site.

Effects of sulfonylureas on mitochondrial ATP-sensitive K+ channels in cardiac myocytes: implications for sulfonylurea controversy.

Background: Mitochondrial ATP-sensitive K(+) (mitoK(ATP)) channel plays a key role in cardioprotection. Hence, a sulfonylurea that does not block mitoK(ATP) channels would be desirable to avoid damage to the heart. Accordingly, we examined the effects of sulfonylureas on the mitoK(ATP) channel and mitochondrial Ca(2+) overload.

Long-term evaluation of bovine pericardial bioprostheses in young women: influence of pregnancy.

Objectives: To avoid the fetal and maternal risks associated with anticoagulant therapy during pregnancy, the use of bioprostheses has been advocated for young women with cardiac valve disease during the childbearing years. Several reports have suggested the probability of pregnancy-related accelerated structural valve deterioration (SVD). The aim of this study was to assess the effect of pregnancy and delivery on bovine pericardial bioprostheses.

Mitral stenosis after mitral valve repair using the duran flexible annuloplasty ring for degenerative mitral regurgitation.

The case is presented of a 47-year-old woman who had undergone mitral valve repair using the Duran annuloplasty ring four years earlier, and who was diagnosed with mitral stenosis owing to fibrous tissue overgrowth. In this patient, dense whitish fibrous tissue covered the annuloplasty ring and extended onto both leaflets of the mitral valve, narrowing its orifice and rendering the leaflets stiff and immobile. The pannus covering the mitral valve could not be stripped off without damaging the leaflets, making mitral valve replacement necessary.