Electroencephalogram abnormalities in panic disorder patients: a study of symptom characteristics and pathology

Background  

Since the 1980s, a high EEG abnormality rate has been reported for patients with panic disorder. However, how the EEG abnormalities of panic disorder patients are related to the clinical features and pathology of these patients has yet to be clarified. In this study we investigated whether or not EEG abnormalities are related to the 13 symptoms in the DSM-IV criteria for a diagnosis of panic attacks.     

Mid-successional stand dynamics in a cool-temperate conifer-hardwood forest in northern Japan

Stand dynamics was studied over 13 years in a cool-temperate conifer-hardwood forest, northern Japan. A total 30 hardwood species and one conifer, Abies sachalinensis, larger than 1.5 cm DBH were recorded. The total stand density was 1677 trees ha⁻¹ at the beginning, decreasing to 1184 trees ha⁻¹ (30% reduction) over the study period, but the total stand basal area was almost unchanged (about 49 m² ha⁻¹). This large reduction in total density was mainly due to the death of saplings and infrequent recruitment. Number of recruits gradually decreased with time, while that of dead trees was constant. Cause of death of small trees was mainly due to suppression by tall trees. Skewness of the DBH frequency distribution varied among the species. A less skewed frequency distribution (i.e., few number of saplings) was shown by shade-intolerant species such as Populus maximowiczii and Betula maximowicziana, and a more skewed frequency distribution (i.e., large number of saplings) by shade-tolerant species such as Acer mono and Tilia japonica. DBH frequency distribution changed to less skewed patterns with reduction of density in most species during the census period. Rank of shade tolerance positively correlated with tree density and skewness, and negatively correlated with mean DBH. Skewness also positively correlated with recruitment rates. Furthermore, rank of shade tolerance positively correlated with seed size. These results suggest that shade-intolerant species regenerated immediately after disturbances by wide dispersal of small seeds, but their recruitment was interrupted after that. By contrast, shade-tolerant species were able to recruit even after the ceasation of recruitment of shade-intolerant species, but suffered severe mortality due to the increasing shading with the progress of stand development. This study suggests that the stand is still developing, with changes in species composition and size structure, and that species differences in shade tolerance and seed size are important for the stand structural changes.     

High Cadmium Accumulation Among Humans and Primates: Comparison Across Various Mammalian Species—A Study from Japan

The majority of existing literature reports that cadmium (Cd) is toxic to humans and most living organisms. This paper reports the results of our study that measured Cd levels in the livers and kidneys of humans and other 50 mammalian species under normal conditions in Japan. The study tests the differences in the Cd concentrations across different mammalian species and sexes. Our results revealed that (1) there is a strong correlation between the Cd levels in the livers and kidneys across all examined species, (2) humans exhibit the highest Cd accumulation level in both organs, (3) primates also show a high Cd concentration at a level close to humans, (4) mice and rats show low Cd levels in both organs, indicating that humans accumulate about a few thousand times more Cd than mice and rats, and (5) the Cd concentration of female mammals is more than double of males for both organs. Our results indicate that these cross-sex as well as cross-species discrepancies cannot be explained by the difference in daily Cd intake. While further research is necessary to determine any potential role of Cd accumulation, we speculate that Cd plays some physiological function in the renal cortex of humans and primates.     

Prostaglandin E receptor type 4-associated protein interacts directly with NF-kappaB1 and attenuates macrophage activation

Macrophage activation participates pivotally in the pathophysiology of chronic inflammatory diseases, including atherosclerosis. Through the receptor EP4, prostaglandin E(2) (PGE(2)) exerts an anti-inflammatory action in macrophages, suppressing stimulus-induced expression of certain proinflammatory genes, including chemokines. We recently identified a novel EP4 receptor-associated protein (EPRAP), whose function in PGE(2)-mediated anti-inflammation remains undefined. Here we demonstrate that PGE(2) pretreatment selectively inhibits lipopolysaccharide (LPS)-induced nuclear factor kappaB1 (NF-kappaB1) p105 phosphorylation and degradation in mouse bone marrow-derived macrophages through EP4-dependent mechanisms. Similarly, directed EPRAP expression in RAW264.7 cells suppresses LPS-induced p105 phosphorylation and degradation, and subsequent activation of mitogen-activated protein kinase kinase 1/2. Forced expression of EPRAP also inhibits NF-kappaB activation induced by various proinflammatory stimuli in a concentration-dependent manner. In co-transfected cells, EPRAP, which contains multiple ankyrin repeat motifs, directly interacts with NF-kappaB1 p105/p50 and forms a complex with EP4. In EP4-overexpressing cells, PGE(2) enhances the protective action of EPRAP against stimulus-induced p105 phosphorylation, whereas EPRAP silencing in RAW264.7 cells impairs the inhibitory effect of PGE(2)-EP4 signaling on LPS-induced p105 phosphorylation. Additionally, EPRAP knockdown as well as deficiency of NF-kappaB1 in macrophages attenuates the inhibitory effect of PGE(2) on LPS-induced MIP-1beta production. Thus, PGE(2)-EP4 signaling augments NF-kappaB1 p105 protein stability through EPRAP after proinflammatory stimulation, limiting macrophage activation.     

Metabolism of urea in Chlorella ellipsoidea

The effect of cyanide on ammonia and urea metabolism was studiedwith intact cells of Chlorella ellipsoidea Gerneck, a greenalga which apparently lacks urease. Ammonia uptake was inhibited more readily by cyanide than wasurea uptake. Urea uptake was stimulated by lower concentrationsof cyanide. The addition of cyanide caused the formation ofammonia from some cellular nitrogenous compounds. In the presenceof exogenously added urea, the molar ratio of ammonia accumulatedin the medium to urea taken up exceeded 2.0 as the cyanide concentrationincreased. However, the molar ratio of ammonia actually producedfrom urea nitrogen to urea taken up was less than 1.35 at anyconcentration of cyanide tested. In the presence of higher concentrationsof cyanide, the rate of incorporation of ¹⁵N into amino acidsfrom ¹⁵N-urea was higher than that from ¹⁵N-ammonium sulfate. The results suggest that Chlorella ellipsoidea possesses a pathwaythrough which urea nitrogen is assimilated directly withouta preliminary breakdown to ammonia. (Received October 18, 1976; )     

Domain architecture of the atypical Arf-family GTPase Arl13b involved in cilia formation

Arl13b is an atypical Arf/Arl-family GTPase consisting of an extending large C-terminal region (C domain) and Arf-homologous GTP-binding motifs in the N terminus (N domain). Although Arl13b appears to be involved in cilia formation, its precise function and roles of the domains remain unknown. Here, we show the unique domain architecture of Arl13b by analyzing the relationship between its biochemical properties and cilia formation. Arl13b binds guanine nucleotides and specifically localizes to cilia. The ciliary localization of Arl13b requires both N and C domains but is independent of its guanine nucleotide-binding ability. Arl13b is capable of self-associating via N domain, and overexpression of N domain inhibits not only cilia formation but also the maintenance of pre-generated cilia. These findings suggest that N and C domains of Arl13b cooperatively regulate its ciliary localization and that N domain-dependent self-association of Arl13b may be important for its function in cilia biogenesis.     

Changes in nucleic acid metabolism in barley seedlings during vernalization

Changes in nucleic acid metabolism of barley seedlings duringvernalization were investigated using thymidine-³H and uridine-³H. DNA content increased in the early germination stage from the1st to 3rd week in vernalized seedlings. In unvernalized seedlings,the most rapid increase was found in the late germination stage.RNA content in the vernalized seedlings increased after 1 weekand reached maximum level after 3 weeks of vernalization treatment.The unvernalized seedlings had a comparatively high contentat 2 days' germination which then gradually increased. Much thymidine-³H was incorporated into DNA and uridine-³H intoRNA fractions in the seedlings during early vernalization. Onthe contrary, without vernalization, heavy incorporation ofthymidine-³H was delayed during the late germination stage.Incorporation of uridine-³H showed a linear increase. A more detailed distribution of thymidine-³H and uridine-³Hin the nucleic acids was examined by methylated albumin-coatedkieselguhr column chromatography. A considerable amount of theincorporated uridine-³H was found in the tenaciouslybound ribonucleicacid (TB-RNA) in the vernalized seedlings. (Received January 18, 1973; )     

Disruption of GM2/GD2 synthase gene resulted in overt expression of 9-O-acetyl GD3 irrespective of Tis21

GM2/GD2 synthase gene knockout mice lack all complex gangliosides, which are abundantly expressed in the nervous systems of vertebrates. In turn, they have increased precursor structures GM3 and GD3, probably replacing the roles of the depleted complex gangliosides. In this study, we found that 9-O-acetyl GD3 is also highly expressed as one of the major glycosphingolipids accumulating in the nervous tissues of the mutant mice. The identity of the novel component was confirmed by neuraminidase treatment, thin layer chromatography-immunostaining, two-dimensional thin layer chromatography with base treatment, and mass spectrometry. All candidate factors reported to be possible inducer of 9-O- acetylation, such as bitamine D binding protein, acetyl CoA transporter, or O-acetyl ganglioside synthase were not up-regulated. Tis21 which had been reported to be a 9-O-acetylation inducer was partially down-regulated in the null mutants, suggesting that Tis21 is not involved in the induction of 9-O-acetyl-GD3 and that accumulated high amount of GD3 might be the main factor for the dramatic increase of 9-O-acetyl GD3. The ability to acetylate exogenously added GD3 in the normal mouse astrocytes was examined, showing that the wild-type brain might be able to synthesize very low levels of 9-O-acetyl GD3. Increased 9-O-acetyl GD3, in addition to GM3 and GD3, may play an important role in the compensation for deleted complex gangliosides in the mutant mice.