Clinical Utility of Intravascular Ultrasound (IVUS) in Carotid Artery Interventions: A Systematic Review and Meta-analysis.

BACKGROUND: Carotid plaque morphology plays an important role in determining outcome of carotid artery stenting (CAS). Intravascular ultrasound (IVUS) and its extension VH (Virtual Histology)-IVUS evaluate plaque characteristics in real time and guide decision making during stenting. To date, there is no consensus about indications of IVUS and its validated methods. This systematic review and meta-analysis aims to evaluate the clinical utility of IVUS in carotid artery interventions (CAS) and develop a future consensus for research and practice parameters. METHODS: A systematic review and meta-analysis was performed of the English literature articles published till February 2021. Studies reporting on IVUS parameters and findings and also its performance compared with other imaging modalities were included in review. Pooled prevalence with 95% confidence intervals (CI) was calculated. The statistical analysis was conducted in R version 3.6.2. RESULTS: A total of 2015 patients from 29 studies were included. Proportional meta-analysis was performed on 1566 patients from 11 studies. In 9 studies, stroke/transient ischemic attack (TIA) had a pooled prevalence of 4% (95% CI 3%-5%) while asymptomatic stroke had a pooled prevalence of 46% (95% CI 31%-62%) in 4 studies following IVUS. Two studies reported that IVUS detected more plaque protrusion compared with angiography (n=33/396 vs 11/396). IVUS led to stent type or size change in 8 of 48 cases which were missed on angiography in 3 other studies. Concordance between VH-IVUS and true histology was good at 80% to 85% reported in 2 studies. CONCLUSIONS: This systematic review and meta-analysis showed, though IVUS fared better to computed tomography (CT)/magnetic resonance (MR) angiography for better stent selection during CAS, with low to moderate risk of bias in the studies included. However, large scale, preferably randomized controlled studies are needed to predict its role in determining clinical outcome.

Expressions of isopeptide bonds and corneodesmosin in middle ear cholesteatoma.

OBJECTIVE: Isopeptide bonds form cross-links between constituent proteins in the horny layer of the epidermis. Corneodesmosin (CDSN) is a major component of corneodesmosomes, which bind corneocytes together. Both play important roles in maintaining epidermal barrier functions. In the present study, we investigated the expressions of isopeptide bonds, CDSN, and related enzymes in middle ear cholesteatoma in comparison with the skin. DESIGN: Prospective case series of patients with middle ear cholesteatoma. SETTING: Tertiary medical institute. PARTICIPANTS: Cholesteatoma and normal postauricular skin were collected from patients with acquired middle ear cholesteatoma during tympanomastoidectomy. MAIN OUTCOME MEASURES: Expression of e-(g-glutamyl)lysine isopeptide bonds was examined by immunohistochemistry; Expressions of transglutaminase (TGase)1, TGase2, TGase3, and TGase5 by immunohistochemistry and quantitative RT-PCR (qRT-PCR); expression of CDSN by immunohistochemistry, qRT-PCR, and Western blot; and expressions of tissue kallikrein-related peptidase (KLK)5, KLK7, KLK14, and serine peptidase inhibitor Kazal type 5 (SPINK5) by qRT-PCR. RESULTS: TGase2 was higher (P=0.0046) and TGase5 was lower (P=0.0008) in cholesteatoma than in the postauricular skin. Immunoreactivity for isopeptide bonds was localized in the granular and horny layers, and was not different between the two tissues. Immunoreactivity for CDSN was localized in the granular layer, and was lower in cholesteatoma than in the skin (P=0.0090). Western blot and qRT-PCR confirmed that the expression of CDSN was lower in cholesteatoma than in the skin. Expressions of KLK5, KLK7, KLK14, or SPINK5 were not different between the two tissues. CONCLUSIONS: These results indicate that the production of CDSN is likely to be suppressed in cholesteatoma, which would account, at least in part, for the mechanical fragility and increased permeability of the cholesteatoma epithelium.

Acute rapamycin treatment reveals novel mechanisms of behavioral, physiological, and functional dysfunction in a maternal inflammation mouse model of autism and sensory over-responsivity.

Maternal inflammatory response (MIR) during early gestation in mice induces a cascade of physiological and behavioral changes that have been associated with autism spectrum disorder (ASD). In a prior study and the current one, we find that mild MIR results in chronic systemic and neuro-inflammation, mTOR pathway activation, mild brain overgrowth followed by regionally specific volumetric changes, sensory processing dysregulation, and social and repetitive behavior abnormalities. Prior studies of rapamycin treatment in autism models have focused on chronic treatments that might be expected to alter or prevent physical brain changes. Here, we have focused on the acute effects of rapamycin to uncover novel mechanisms of dysfunction and related to mTOR pathway signaling. We find that within 2 hours, rapamycin treatment could rapidly rescue neuronal hyper-excitability, seizure susceptibility, functional network connectivity and brain community structure, and repetitive behaviors and sensory over-responsivity in adult offspring with persistent brain overgrowth. These CNS-mediated effects are also associated with alteration of the expression of several ASD-,ion channel-, and epilepsy-associated genes, in the same time frame. Our findings suggest that mTOR dysregulation in MIR offspring is a key contributor to various levels of brain dysfunction, including neuronal excitability, altered gene expression in multiple cell types, sensory functional network connectivity, and modulation of information flow. However, we demonstrate that the adult MIR brain is also amenable to rapid normalization of these functional changes which results in the rescue of both core and comorbid ASD behaviors in adult animals without requiring long-term physical alterations to the brain. Thus, restoring excitatory/inhibitory imbalance and sensory functional network modularity may be important targets for therapeutically addressing both primary sensory and social behavior phenotypes, and compensatory repetitive behavior phenotypes.

Use of high-dose cisplatin with aprepitant in an outpatient setting.

Chemotherapy-induced nausea and vomiting (CINV) and nephrotoxicity are adverse events induced by cisplatin administration. These effects can be reduced by treatment regimens with low-dose cisplatin, but high-dose cisplatin is still used. In Japan, high-dose cisplatin is usually administered in an inpatient setting to permit management of CINV. However, with use of new-generation antiemetic agents such as aprepitant, CINV and nephrotoxicity are controllable in an outpatient setting. Here, we discuss issues related to the management of high-dose cisplatin administration in outpatients. Grade 2 or worse CINV induced by high-dose cisplatin occurs in more than 40% of patients without treatment with aprepitant, but is controllable by administration of a 5-HT3 receptor antagonist, steroids and aprepitant. Moreover, prevention of CINV using these drugs is cost-effective, since outpatient settings have advantages with regard to health economics and patient quality of life. These findings suggest that shifting high-dose cisplatin administration to the outpatient setting may be achieved with co-administration of aprepitant. Available facilities and the status of the patient should be considered when selecting whether an outpatient setting is suitable for administration of cisplatin, but the use of aprepitant and adequate oral hydration should allow use of cisplatin in this setting.

The incidence, treatment and prognosis of cervical carcinoma in young women: a retrospective analysis of 4,975 cases in Japan.

OBJECTIVE: To determine the clinical characteristics of patients (young women) with cervical carcinoma aged less than 35 years. METHODS: Data from patients who were treated for cervical carcinomas from 1990 to 2000 in the Kinki District were retrospectively investigated for clinical stage, histologic type, treatment procedure and prognosis. RESULTS: Of a total of 4,975 cases, 441 patients were aged less than 35 years old. The incidence of cervical carcinoma in these women was 7.9% from 1990 to 1995, 9.1% from 1996 to 2000, and 9.5% from 2001 to 2005. FIGO Stage I included 374 cases, followed by, 49 in Stage II, 11 in Stage III, and seven in Stage IV. Squamous cell carcinoma incidence was 80.7% and non-squamous cell carcinoma incidence was 19.3%. Several types of surgery were performed in patients with Stage I and II, while patients with Stage III and IV were treated with radiotherapy and/or chemotherapy without any type of surgery. In patients who underwent lymphadenectomy, 21.1% cases had nodal involvement. The 5-year survival rate was 95% for Stage I disease, 73% for Stage II, 68% for Stage III, and 19% for Stage IV. CONCLUSION: The incidence of cervical carcinoma in young women slightly increased from 1990 to 2005. The prognosis of cervical carcinoma tends to be better in young women than in older patients, especially in Stage III disease.

A randomized study of screening for ovarian cancer: a multicenter study in Japan.

Ovarian cancer is common in women from developed countries. We designed a prospective randomized controlled trial of ovarian cancer screening to establish an improved strategy for the early detection of cancers. Asymptomatic postmenopausal women were randomly assigned between 1985 and 1999 to either an intervention group (n = 41,688) or a control group (n = 40,799) in a ratio of 1:1, with follow-up of mean 9.2 years, in Shizuoka district, Japan. The original intention was to offer women in the intervention group annual screens by gynecological examination (sequential pelvic ultrasound [US] and serum CA125 test). Women with abnormal US findings and/or raised CA125 values were referred for surgical investigation by a gynecological oncologist. In December 2002, the code was broken and the Shizuoka Cohort Study of Ovarian Cancer Screening and Shizuoka Cancer Registry were searched to determine both malignant and nonmalignant diagnoses. Twenty-seven cancers were detected in the 41,688-screened women. Eight more cancers were diagnosed outside the screening program. Detection rates of ovarian cancer were 0.31 per 1000 at the prevalent screen and 0.38-0.74 per 1000 at subsequent screens; they increased with successive screening rounds. Among the 40,779 control women, 32 women developed ovarian cancer. The proportion of stage I ovarian cancer was higher in the screened group (63%) than in the control group (38%), which did not reach statistical significance (P = 0.2285). This is to our knowledge the first prospective randomized report of the ovarian cancer screening. The rise in the detection of early-stage ovarian cancer in asymptomatic postmenopausal women is not significant, but future decisions on screening policy should be informed by further follow-up from this trial.

CREB controls cortical circuit plasticity and functional recovery after stroke.

Treatments that stimulate neuronal excitability enhance motor performance after stroke. cAMP-response-element binding protein (CREB) is a transcription factor that plays a key role in neuronal excitability. Increasing the levels of CREB with a viral vector in a small pool of motor neurons enhances motor recovery after stroke, while blocking CREB signaling prevents stroke recovery. Silencing CREB-transfected neurons in the peri-infarct region with the hM4Di-DREADD blocks motor recovery. Reversing this inhibition allows recovery to continue, demonstrating that by manipulating the activity of CREB-transfected neurons it is possible to turn off and on stroke recovery. CREB transfection enhances remapping of injured somatosensory and motor circuits, and induces the formation of new connections within these circuits. CREB is a central molecular node in the circuit responses after stroke that lead to recovery from motor deficits.

Serum CA125 level before the development of ovarian cancer.

BACKGROUND: Little is known about the natural history of ovarian cancer with respect to the change of serum CA125 level. METHODS: The Shizuoka Cohort Study on Ovarian Cancer Screening (SCSOCS) Trial contains approximately 100,000 data on serum tumor marker CA125 prospectively obtained from more than 70,000 women. We reviewed the clinical charts and collected serum samples 2 months to 9.4 years prior to the surgery were available. RESULTS: In 396 (95%) of the 419 patients with ovarian cancer, one serum sample was present before the diagnosis (mean, 4.1 years). The change of CA125 level before the diagnosis of ovarian cancer could be clearly separated into two groups according to the length of the following intervals: 47% (107/228) of patients with non-serous-type ovarian cancers develop secondarily from slightly elevated CA125 level (35

Stent thrombosis in the era of drug eluting stents.

Despite a marked reduction in restenosis and the need for repeat revascularization procedures with the use of drug-eluting stents (DES), the risk for stent thrombosis remains of serious concern. Although the safety profiles of DES dose not seem to differ from those of bare metal stent (BMS) in the acute and subacute phases following coronary intervention, recent data suggest a potential increase of thrombotic events late after DES deployment. The main factors associated with late stent thrombosis remain elusive. Delayed re-endothelialization, hypersensitivity reaction, technical and mechanical factors and hypercoagulability have all been proposed as contributing factors. It is unlikely that any of these variables alone can cause stent thrombosis, as the incidence of each factor is much higher than the currently known rates of DES thrombosis. Further, temporal appearances of the thrombotic events represent a challenge to our understanding of re-endothelialization, as one would expect that endothelial coverage would be higher in the later phases after treatment. New expanded definitions of stent thrombosis, which also include events secondary to repeat revascularization, have been proposed to provide a better comparative endpoint between BMS and DES. Such clinical attempt to characterize stent thrombosis is valuable, but does not provide much insight into the pathophysiology and intrinsic thrombotic risk of each device. A true progress in this field will only be possible after we improve our understanding of the patho-physiology of very late stent thromboses, which may differ from events occurring earlier after treatment. The incidence of stent thrombosis remains rare, but its potential catastrophic consequences should remind clinicians and scientists to make every effort to develop strategies and technologies for its prevention. The topic of stent thrombosis in the era of DES will be reviewed in this article.

Percutaneous coronary intervention of bifurcation coronary disease.

Bifurcation coronary artery disease is a frequent problem faced by interventional cardiologists and it affects approximately 15-20% of patients undergoing percutaneous coronary intervention (PCI). The application of drug-eluting stents (DES) technology to prevent restenosis after PCI represents one of the success stories in cardiology, but DES have not resolved the bifurcation PCI challenge. Bifurcation PCI remains associated with higher procedural failure and worse outcomes compared with PCI of non-bifurcated lesions even in DES era. A dependable strategy for PCI of bifurcation lesions has yet to be established, which is likely due to the paucity of studies evaluating the anatomical intricacies of the bifurcation as well as the lack of large scale randomized therapeutic trials. Further, bifurcation has many anatomical variants and it is unlike that one technique will fit all. Currently, we are left with the option of a tailor-made strategy for each patient and bifurcation anatomy and make the most of the limited evidence available to support our therapeutic decisions. In this review, we attempted to describe the current understanding of bifurcation anatomy and corresponding PCI strategies.

Usefulness of cardiac magnetic resonance imaging for coronary artery disease detection.

Cardiac magnetic resonance imaging (cMRI) is a promising non-invasive technique to assess the presence of coronary artery disease (CAD), which is free of ionizing radiation and iodine contrast. cMRI can detect CAD by angiographic methods or indirectly by perfusion stress techniques. While coronary angiography by cMRI remains limited to research protocols, stress perfusion cMRI is currently being applied worldwide in the clinical setting. Studies have shown good correlation between adenosine-induced stress myocardial perfusion cMRI and single-photon-emission computed tomography or positron emission tomography to detect CAD. Quantitative methods to analyze cMRI perfusion data have been developed in an attempt to provide a more objective imaging interpretation. Standardization of such quantitative methods, with minimal operator dependency, would be useful for clinical and research applications. Myocardial perfusion reserve (MPR), calculated using Fermi deconvolution technique, has been compared with well established anatomical and physiological CAD detection techniques. MPR appears to be the most accurate quantitative index to detect anatomical and hemodynamically significant CAD. Beyond physiological assessment of CAD, cMRI provides information regarding regional and global left ventricular function and morphology, myocardial infarction size, transmurality and viability. Such comprehensive information would require the performance of multiple tests if other modalities were used. This article describes current applications of cMRI for evaluation of patients with CAD.

Cloning and characterization of four types of cDNA encoding myeloperoxidase from human monocytic leukemia cell line, SKM-1.

Four cDNA clones encoding myeloperoxidase were isolated from a cDNA library of monocytic leukemia SKM-1 cells. The sequences of two of them were identical to those of cDNA clones previously isolated from a HL-60 cell cDNA library. The sequences of the other two cDNA clones, MP-S34 and MP-S29, differed from those previously described. There was a deletion of 57 bp in the MP-S34 sequence, which was generated by partially skipping exon 9. MP-S29 had a 171 bp deletion, which was generated by completely skipping exon 10. Thus MP-S34 and MP-S29 encoded polypeptides lacking 19 and 57 amino acids, respectively. Both deletions were located on the sequence encoding the heavy subunit. These results indicate that the heterogeneity of the heavy subunit of MPO observed in leukocytes or leukemia could be in part produced by partial or complete skipping of an exon.

The monocytic cell line SKM-1 strongly expresses the myeloperoxidase gene.

A newly established human monocytic cell line, SKM-1, showed strong expression of myeloperoxidase mRNA, to the same extent as in HL-60 cells. We studied the cell morphology and myeloperoxidase expression of this cell line, which was established from a patient with myelodysplastic syndrome who had an abnormal chromosome on the upstream region of 17p13. Electron micrographs showed the cells to have a fragile and irregular cell surface. SKM-1 cells were peroxidase-positive. About 60% of myeloperoxidase (MPO) was released to the culture fluid from SKM-1 cells but only a few percent of MPO was released from HL-60 cells into the culture fluid. The predominant mRNA size of SKM-1 myeloperoxidase was 3.3 kb although there was a smaller size as well. Fluorescent in situ hybridization of MPO mRNA showed strong staining in 5% to 10% of SKM-1 cells and of bone marrow cells from patients with myelogenous leukemia, while all cells from HL-60 were positive.

Mitochondrial aldehyde dehydrogenase in diabetes associated with mitochondrial tRNA(Leu(UUR)) mutation at position 3243.

OBJECTIVE: To ascertain why alcohol is prone to manifest unpleasant effects in diabetes associated with mitochondrial tRNA(Leu(UUR) mutation at position 3243 (DM-Mt3243), we investigated the genotype of aldehyde dehydrogenase (ALDH) 2 and alcohol dehydrogenase 2 (ADH2) in DM-Mt3243. RESEARCH DESIGN AND METHODS: Nineteen unrelated patients with DM-Mt3243 were included in the study (12 men and 7 women). They were recruited from approximately 700 diabetic patients at three different institutes, without prior information of alcohol habit. ALDH2, ADH2, and 3243 mutation were genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) methods. There were 461 unrelated Japanese individuals and 170 non-3243 mutant NIDDM patients enrolled as control subjects. RESULTS: In the DM-Mt3243 group, 15 (79%) patients had inactive ALDH2 and 18 (95%) had atypical ADH2. The frequency of the inactive ALDH2 genotype was higher than that in the normal control subjects (P < 0.002) and that in the NIDDM control subjects (P < 0.003). However, the frequencies of ADH2 genotype in the DM-Mt3243 group, the normal control subjects, and the NIDDM control subjects were not different. CONCLUSIONS: Inactive ALDH2 genotype was frequently observed in DM-Mt3243. It suggests that DM-Mt3243 is associated with ALDH2 inactivity. We speculate the trait of acetaldehyde accumulation on ALDH2 inactivity may favor mitochondrial DNA abnormalities, thereby worsening ATP production and impairing insulin secretion. In addition, the interaction of ALDH1 and ALDH2 may alter the retinoid metabolism in the pancreas, thereby influencing insulin secretion and precipitating diabetes. Thus, this association of ALDH2 genotype with DM-Mt3243 provides insight into the etiology of diabetes in the mitochondrial diseases.

Prenatal diagnosis of oculocutaneous albinism by analysis of the fetal tyrosinase gene.

Tyrosinase-negative oculocutaneous albinism, the most severe subtype of a heterogeneous group of albinism, is an autosomal recessive trait caused by mutations in the tyrosinase gene. Prenatal diagnosis had been made previously only by evaluating fetal skin obtained by biopsy, an invasive procedure that cannot be performed earlier than 19 weeks of gestation. A pregnant mother of a 9-year-old Japanese boy with tyrosinase-negative oculocutaneous albinism wanted a prenatal diagnosis. Polymerase chain reaction amplification and allele-specific oligonucleotide hybridization revealed that the child is homozygous and the parents heterozygous for the pathologic mutation of the tyrosinase gene in exon 2 (single base insertion) but not for the one in exon 1. Prenatal diagnosis was made by analyzing the tyrosinase gene in fetal cells obtained by amniocentesis at 14 weeks of gestation, which demonstrated that the fetus was heterozygous for mutant tyrosinase gene. Pregnancy was therefore continued and a normal male infant was born. This procedure, the analysis of the fetal genomic tyrosinase DNA, is a rapid and reliable approach to the prenatal diagnosis of oculocutaneous albinism at a relatively early stage of pregnancy and is safer and less invasive than previous methods using fetal skin biopsy.

In situ demonstration of the HTLV-I genome in the spinal cord of a patient with HTLV-I-associated myelopathy.

Using polymerase chain reaction (PCR) and in situ hybridization, we investigated the HTLV-I genome in the CNS of an HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patient with a 20-year disease duration. Neuropathologically, there was severe white matter degeneration throughout the spinal cord, but lymphocytic infiltrates were not evident in any lesion. PCR amplification of the pX region of HTLV-I DNA detected its sequence in the spinal cord and all extra-CNS tissue samples. In situ hybridization using probes complementary to the pX and gag regions detected the HTLV-I genome in the cytoplasm and nucleus of cells in the thoracic cord. The findings indicate a direct involvement of HTLV-I in the neurodegeneration of HAM/TSP.

High-yield, in vitro protein expression using a continuous-exchange, coupled transcription/ translation system.

The Rapid Translation System (RTS 500) (Roche Molecular Biochemicals) is a high-yield protein expression system that utilizes an enhanced E. coli lysate for an in vitro transcription/translation reaction. In contrast to conventional transcription/translation, this system allows protein expression to continue for more than 24 h. We demonstrated the utility of the RTS 500 by expressing different soluble and active proteins that generally pose problems in cell-based expression systems. We first expressed GFP-lunasin, a fusion protein that, because of its toxicity, has been impossible to produce in whole cells. The second protein we expressed, human interleukin-2 (IL-2), is generally difficult to produce, either as the native molecule or as a GSTfusion protein, in a soluble form in bacteria. Finally, we demonstrated the capacity of the RTS 500 to co-express proteins, by the simultaneous production of GFP and CAT in a single reaction. This new technology appears to be particularly usefulfor the convenient production of preparative amounts (100-900 microg) of proteins that are toxic or insoluble in cell-based systems.

Establishment of permanent cell lines exhibiting vitamin D-dependent expression of beta-galactosidase activity.

The active hormonal form of vitamin D3, 1alpha,25-dihydroxyvitamin D3 (1alpha,25(OH)2D3), has been described as a principal mediator of skeletal homeostasis. Treatment of rat osteosarcoma (ROS)17/2.8, an osteoblast-like cell line, with 1alpha,25(OH)2D3 results in a ligand-dependent increase in transcription of the bone-specific osteocalcin gene. We isolated permanent cell lines that were established by transfecting ROS 17/2.8 cells with plasmids consisting of the human osteocalcin gene promoter containing the vitamin D responsive element linked to a bacterial beta-galactosidase gene. In one of many cell lines, especially in clone NK-31, 1alpha,25(OH)2D3 strongly stimulated beta-galactosidase activity. Reverse transcription-polymerase chain reaction analysis also showed endogenous osteocalcin gene expression and beta-galactosidase gene expression in clone NK-31 cells, which paralleled the increase in beta-galactosidase activity. Using a synthetic analogue of 1alpha,25(OH)2D3, 24,24-difluoro-1alpha,25-dihydroxyvitamin D3, we found that the levels of this activity and these gene expressions were nearly parallel to those of 1alpha,25(OH)2D3. 24R,25-dihydroxyvitamin D3 and 25-hydroxyvitamin D3 at high doses (concentration: 10(-7) M) also induced beta-galactosidase activity in clone NK-31. These cell lines, harboring the plasmid-carrying beta-galactosidase gene under the control of the osteocalcin gene promoter, may contribute to studies on the regulation by 1alpha,25(OH)2D3 or to the development of synthetic analogues of 1alpha,25(OH)2D3.

Autonomic nervous activity before and after eradication of Helicobacter pylori in patients with chronic duodenal ulcer.

BACKGROUND: Helicobacter pylori infection is involved in the formation of chronic peptic ulcer. However, a previously reported hypothesis concerning the involvement of central autonomic nervous disorder in this condition cannot be ruled out. AIM: To use spectrum analysis of heart rate viability to examine autonomic nervous activity before and after H. pylori eradication. METHODS: Twenty patients with chronic duodenal ulcer (duodenal ulcer group) and 20 age-matched normal adults (N group). In both groups, 24-h Holter electrocardiograms (ECGs) were recorded and spectrum analysis of heartrate variability was performed. In the duodenal ulcer group, Holter ECG was recorded before and after H. pylori eradication. RESULTS: In the N group, analysis of heart rate variability showed that high frequency (HF) power, an index of parasympathetic activity, was high at night, while the low frequency (LF)/HF ratio, an index of sympathetic function, was high during the daytime. In the duodenal ulcer group, HF power was higher at night than during the daytime, showing a similar pattern to the N group, but the power value was higher than in the N group (P < 0.05). In the duodenal ulcer group, LF/HF at night was significantly higher than that of the N group. In addition, in the duodenal ulcer group, autonomic activity after H. pylori eradication did not differ significantly from that before H. pylori eradication. CONCLUSIONS: In patients with chronic peptic ulcer, both sympatheticotonia and parasympatheticotonia may occur at night, and this abnormality in autonomic nervous activity may cause increased gastric acid secretion and gastric mucosal vasoconstriction. Abnormalities in autonomic activity persist even after H. pylori eradication, suggesting that they may be an independent risk factor in the formation of chronic peptic ulcer in addition to H. pylori infection.

Phylogenetic analysis of a novel sulfate-reducing magnetic bacterium, RS-1, demonstrates its membership of the delta-Proteobacteria.

Most of the 16S ribosomal RNA gene of a sulfate-reducing magnetic bacterium, RS-1, was sequenced, and phylogenetic analysis was carried out. The results suggest that RS-1 is a member of the delta-Proteobacteria, and it appears to represent a new genus. RS-1 is the first bacterium reported outside the alpha-Proteobacteria that contains magnetite inclusions. RS-1 therefore disrupts the correlation between the alpha-Proteobacteria and possession of magnetite inclusions, and that between the delta-Proteobacteria and possession of greigite inclusions. The existence of RS-1 also suggests that intracellular magnetite biomineralization is of multiple evolutionary origins.