Association of insomnia symptoms and non-restorative sleep with Typus melancholicus: a Japanese general population survey

Sleep and Biological Rhythms - This study aimed to investigate the association between insomnia symptoms and non-restorative sleep (NRS) in individuals with Typus melancholicus, a personality trait...     

Enzyme Kinetics of an Alternative Splicing Isoform of Mitochondrial 8‐Oxoguanine DNA Glycosylase,OGG1‐1b,and Compared with the Nuclear OGG1‐1a

Eight alternatively spliced isoforms of human 8‐oxoguanine DNA glycosylase (OGG1) (OGG1‐1a to ‐1c and ‐2a to ‐2e) are registered in the National Center for Biotechnology Information. OGG1(s) in mitochondria have not yet been fully characterized biochemically. In this study, we purified mitochondrial recombinant OGG1‐1b protein and compared its activity with nuclear OGG1‐1a protein. The reaction rate constant (k_g) of the 7,8‐dihydro‐8‐oxoguanine (8‐oxoG) glycosylase activity of OGG1‐1b was 8‐oxoG:C >> 8‐oxoG:T >> 8‐oxoG:G > 8‐oxoG:A (7.96, 0.805, 0.070, and 0.015 min^?1, respectively) and that of the N‐glycosylase/DNA lyase activity (k_gl) of OGG1‐1b was 8‐oxoG:C > 8‐oxoG:T ?8‐oxoG:G >> 8‐oxoG:A (0.286, 0.079, 0.040, and negligible min^?1, respectively). These reaction rate constants were similar to those of OGG1‐1a except for k_gl against 8‐oxoG:A. APEX nuclease 1 was required to promote DNA strand breakage by OGG1‐1b. These results suggest that OGG1‐1b is associated with 8‐oxoG cleavage in human mitochondria and that the mechanism of this repair is similar to that of nuclear OGG1‐1a.     

Purification,molecular cloning,and functional expression of inducible liver acylcarnitine hydrolase in C57BL/6 mouse,belonging to the carboxylesterase multigene family

To identify the peroxisome proliferator-inducible acylcarnitine hydrolase in C57BL/6 mice, acylcarnitine hydrolase was purified to homogeneity using column chromatography. The purified enzyme, named ACH M1, had a subunit molecular weight of 60kDa. ACH M1 could hydrolyze classical carboxylesterase (CES) substrates as well as palmitoyl-dl-carnitine and these activities were inhibited by anti-rat CES antibodies. The peptide fragments of ACH M1 were identical to those of the deduced amino acid sequence of mouse CES2 isozyme. These findings suggested that ACH M1 was a member of the CES2 family. The mouse CES2 cDNA, designated mCES2, was cloned from mouse liver. The recombinant mCES2 expressing in Sf9 cells showed high level of catalytic activity toward acylcarnitines. Furthermore, the biological characteristics of the expressed protein were identical with those of ACH M1 in many cases, suggesting that mCES2 encodes mouse liver ACH M1.     

Premature induction of amylase in pancreas and parotid gland of growing rats by dexamethasone.

Studies were made on changes in the contents of alpha-amylase (EC 3.2.1.1) in the pancreas and parotid gland of rats during postnatal development, on the premature induction of this enzyme by hormones and on the existence of specific glucocorticoid receptors in these tissues. The amylase content in the pancreas increased from the 9th day after birth and reached the adult level on the 28th day, its content in the parotid gland increased rapidly from the 16th to the 28th day after birth and then rose more gradually to the adult level. Injection of dexamethasone into rats 6--8 days after birth induced increase in the amylase of the pancreas but not the parotid gland. However, injection of dexamethasone into weanling rats 21--23 days after birth resulted in precocious induction of amylase in both tissues. Specific glucocorticoid receptors were detectable in the parotid gland of rats from 6 days after birth but were almost undetectable in the pancreas until adolescence.     

Influence of oral Helicobacter pylori on the success of eradication therapy against gastric Helicobacter pylori

Background. The goal of this study was to see whether Helicobacter pylori ( H. pylori ) in the oral cavity might adversely affect the outcome of eradication therapy for gastric H. pylori.
Materials and Methods. Forty-seven patients (36 males, 11 females) with gastric H. pylori infection were enrolled in this study. Gastric H. pylori infection was confirmed by both immunohistological staining with anti- H. pylori antibody and bacterial culture of biopsy specimens. The therapeutic regimen consisted of 30 mg/day lansoprazole, 750 mg/day metronidazole, and 400 mg/day clarithromycin administered for 2 weeks. A fragment of the H. pylori urease gene was amplified by nested PCR for DNA extracted from saliva and dental plaque from the same patients. We examined the correlation between the gastric eradication success rate and the prevalence of H. pylori in the oral cavity as determined by PCR before and after the eradication therapy.
Results. The eradication success rate was significantly lower in the oral H. pylori -positive cases (12/23, 52.1%) than in the negative cases (22/24, 91.6%) at 4 weeks after the therapy (p = .0028). Two years later, only 16 of the 23 (69.5%) oral H. pylori -positive cases were disease-free, as compared to 23 of the 24 (95.8%) oral H. pylori -negative cases (p = .018).
Conclusions. H. pylori in the oral cavity affected the outcome of eradication therapy and was associated with a recurrence of gastric infection. We recommend that oral H. pylori should be examined by nested PCR and, if positive, should be considered a causal factor in refractory or recurrent cases.     

Characterization of a novel synGAP isoform, synGAP-beta

We cloned a cDNA encoding a novel synGAP, synGAP-d (GenBank(TM) accession number ), from a rat brain cDNA library. The clone consisted of 4801 nucleotides with a coding sequence of 3501 nucleotides, encoded a protein consisting of 1166 amino acids with >99% homology with 1092 amino acid overlaps to synGAP, and contained a 13-nucleotide insertion to the previously reported synGAP mRNAs, which suggested that the clone was a splice variant of synGAP. We also found that there are at least seven variants in the 3' portion of the synGAP mRNA and that they encoded five different protein isoforms. The coding sequence of these C-terminal variants were classified into alpha1, alpha2, beta1, beta2, beta3, beta4, and gamma, and synGAP-d was classified as the beta1 form. The previously reported synGAPs (synGAP-a, -b, and -c and p135synGAP) can be classified as the alpha1 isoform. All isoforms were expressed specifically in the brain. Unexpectedly, the beta isoform, which lacks a C-terminal PSD-95-binding motif ((S/T)XV), was more restricted to the postsynaptic density fraction than the motif-containing alpha1 isoform. The beta isoform did not interact with PSD-95 but specifically interacted with a nonphosphorylated alpha subunit of Ca(2+)/calmodulin-dependent protein kinase II through its unique C-terminal tail.     

Microbial transformation of 18β-glycyrrhetinic acid by Sphingomonas paucimobilis strain G5

The effects of the oxygenase inhibitors, 1-aminobenzotriazole (ABT), ketoconazole, metyrapone and proadifen, on the metabolism of 18-glycyrrhetinic acid (18-GRA) in Sphingomonas paucimobilis strain G5 were investigated. Strain G5 transformed 18-GRA into a major new metabolite (M-D) in the presence of 1 mM ABT or metyrapone. M-D was purified and identified as 3-hydroxy-11-oxo-olean-12-en-24,30-dioic acid by NMR and MS. Based on the structure of M-D, we propose the metabolic pathway of 18-GRA in strain G5.