Effect of a Device-Free Compressed Shell Fixation Method on Hepatic Respiratory Movement: Analysis for Respiratory Amplitude of the Liver and Internal Motions of a Fiducial Marker

Purpose

Suppression of respiratory movement of the liver would be desirable for high-precision radiation therapy for liver tumors. We aimed to investigate the effect of our original device-free compressed shell fixation method and breathing instruction on suppression of respiratory movement. The characteristics of liver motion based on the movement of a fiducial marker were also analyzed.

Clinical study on the flow murmurs at the defect area of atrial septal defect by means of intracardiac phonocardiography.

In order to study flow murmurs through atrial septal defects, right heart catheterization was performed on 48 patients of secundum type, four of primum type, and five of probe-patent foramen ovale, with the double-lumen phonocatheter of Lewis, at the tip of which barium titanate was mounted. The flow murmurs at the defect area were classified into three patterns: v murmur, atriosystolic murmur, and mid-diastolic murmur. V murmur was continuous, extending from late systole to diastole, of low to medium pitch, closely related to atrial v wave and augmenting with expiration. It had no significant correlation to the ratio of left-to-right shunt. It was recorded in 32 out of 48 cases of secundum type and one of primum type, but not observed in probe-patent foramen ovale. Atriosystolic murmur was noted in 17 of 48 cases of secundum type and one of primum type. It was connected with atrial a wave. Mid-diastolic murmur was found at the defect area in four subjects of secundum type. It was thought to be an independent entity from v murmur and to be another one due to shunt flow through the septal defect, since it had no relation to v wave but it was localized between v and a waves in the pressure curve of the right atrium. It is different in localization from mid-diastolic murmur due to relative tricuspid stenosis at the inflow tract of right ventricle.     

Transesophageal cross-sectional echocardiography

A transesophageal cardiac imaging system is described. This system employs hand-held mechanical sector and linear scanners each having a flexible tube and a small ultrasonic transducer contained within a small oil bag easily swallowed by adults. In the sector scanner, a small transducer in the esophagus rotates alternately and horizontal heart images are displayed. In the linear scanner, a small transducer in the esophagus moves up and down and vertical heart images are displayed. The system was evaluated in 31 adult subjects. In all subjects, stable high quality heart images were observed continuously from base to apex as the transducer was being withdrawn or advanced in the esophagus. In horizontal scans, entire heart images were observed at the level of the atrioventricular valves. In vertical scans, the bifurcation of the pulmonary artery could be observed clearly. There was little difference in the image quality among subjects.     

Moxifloxacin resistance and genotyping of Mycobacterium avium and Mycobacterium intracellulare isolates in Japan

BackgroundAlthough fluoroquinolones are considered as alternative therapies of pulmonary Mycobacterium avium complex (MAC) disease, the association between fluoroquinolone resistance and MAC genotypes in clinical isolates from individuals not previously treated for MAC infection is not fully clear.MethodsTotals of 154 M. avium isolates and 35 Mycobacterium intracellulare isolates were obtained from treatment-naïve patients with pulmonary MAC disease at the diagnosis of MAC infection at 8 hospitals in Japan. Their susceptibilities of moxifloxacin were determined by broth microdilution methods. Moxifloxacin-resistant isolates were examined for mutations of gyrA and gyrB. Variable numbers of tandem repeats (VNTR) assay was performed using 15 M. avium VNTR loci and 16 M. intracellulare VNTR loci.ResultsMoxifloxacin susceptibility was categorized as resistant and intermediate for 6.5% and 16.9%, respectively, of M. avium isolates and 8.6% and 17.1% of M. intracellulare isolates. Although the isolates of both species had amino acid substitutions of Thr 96 and Thr 522 at the sites corresponding to Ser 95 in the M. tuberculosis GyrA and Gly 520 in the M. tuberculosis GyrB, respectively, these substitutions were observed irrespective of susceptibility and did not confer resistance. The VNTR assays showed revealed three clusters among M. avium isolates and two clusters among M. intracellulare isolates. No significant differences in moxifloxacin resistance were observed among these clusters.ConclusionsAlthough resistance or intermediate resistance to moxifloxacin was observed in approximately one-fourth of M. avium and M. intracellulare isolates, this resistance was not associated with mutations in gyrA and gyrB or with VNTR genotypes.     

Mechanism of chlorpromazine-induced arrhythmia arrhythmia and mitochondrial dysfunction

In this study, we investigated the mechanism of the arrhythmogenic action of chlorpromazine (CPZ). Thirty-two anesthetized mongrel dogs were used. In each, the chest was opened and a stimulating electrode was attached to the apex of the left ventricle and the ventricular multiple response threshold (VMRT) was measured. The carotid artery was cannulated to measure aortic pressure. The dogs were divided into four groups, and the time course of VMRT, blood pressure, and heart rate were determined. All groups were placed under observation for 30 min after CPZ infusion. In the control group, only saline (2ml/kg) was infused; CPZ group: CPZ (1mg/kg) was infused 10 min after saline (2ml/kg) infusion; CoQ₁₀ group: Coenzyme Q₁₀ (CoQ₁₀) (5mg/kg) was infused 10 min before CPZ (1mg/kg) infusion; FAD group: Flavin-adenine-dinucleotide (FAD) (2mg/kg) was infused 10 min before CPZ (1mg/kg) infusion. In each group, myocardial mitochondria were prepared 30 min after CPZ infusion. The mitochondrial functions, respiratory control index, ADP/0, State III rate of oxygen consumption, and activities of two segments of the electron-transport chain (NADH→CoQ→cyt.c and cyt.c→cyt.a, a₃→O₂) were measured separately. Ca⁺⁺-binding activity of the mitochondria was also determined.CPZ administration decreased VMRT and blood pressure, and caused mitochondrial dysfunction which derived from a disturbance in the first segment of the electrontransport chain. Decreased Ca⁺⁺-binding activity was observed when mitochondrial function was disturbed. CoQ₁₀ prevented significantly the decrease in VMRT and the disturbance of mitochondrial function induced by CPZ, but did not prevent the hypotensive effect of CPZ. FAD prevented not only the decrease in VMRT and the disturbance of mitochondrial function, but also the hypotensive effect of CPZ.These results suggest that the decrease in VMRT is closely related to mitochondrial dysfunction induced by CPZ. Moreover, it is suggested that the arrhythmogenic effect of CPZ is derived from the decreased mitochondrial Ca⁺⁺-binding activity.     

Ataxic mutant mice with defects in Ca2+ channel α1A subunit gene: morphological and functional abnormalities in cerebellar cortical neurons

ABSTRACT This review summarizes recent studies in the morphological and functional abnormalities of cerebella in three ataxic mutant mice, i.e. tottering mouse, leaner mouse, and rolling mouse Nagoya (RMN). These mutants carry mutations in the Ca²⁺ channel α_1A subunit gene, and become useful models for human neurological diseases such as episodic ataxia type-2, familial hemiplegic migraine, and spinocerebellar ataxia type-6. All three mutants exhibited altered morphology of the Purkinje cells, ectopic synaptic contacts between granule cell axons (parallel fibers) and Purkinje cell dendritic spines and abnormal expression of tyrosine hydroxylase in Purkinje cells. In leaner mice, Purkinje cell loss was observed in alternating sagittal compartments of the cerebellar cortex corresponding to the Zebrin II-negative zones. The mutated Ca²⁺ channel α_1A subunit was highly expressed in granule and Purkinje cells, and the P-type Ca²⁺ currents in Purkinje cells were selectively reduced in the mutant mice. Therefore, we concluded that altered Ca²⁺ currents through the mutated Ca²⁺ channel α_1A subunit might be involved in the functional and morphological abnormalities in granule and Purkinje cells, and might result in expressions of behavioral phenotypes including ataxia. Increased levels of corticotropin-releasing factor and cholecystokinin in some climbing and mossy fibers were observed in RMN. These neuropeptides modulated the excitability of granule and Purkinje cells, indicating the possible expression of ataxic symptoms.     

Recurrence after curative-intent resection of perihilar cholangiocarcinoma: analysis of a large cohort with a close postoperative follow-up approach

Background

Although several studies have been conducted on the patterns of recurrence in resected perihilar cholangiocarcinoma, they have many limitations. The aim of this study was to investigate recurrence after resection and to evaluate prognostic factors on the time to recurrence and recurrence-free survival.