Tuberothalamic artery infarctions following coil embolization of ruptured posterior communicating artery aneurysms with posterior communicating artery sacrifice.

BACKGROUND AND PURPOSE: Ischemic complications after coil embolization of the PcomA aneurysms are not thoroughly understood, especially in cases in which the PcomA is sacrificed. Our purpose was to examine the preoperative angiographic features and pattern of postoperative cerebral infarctions exhibited by patients who underwent embolization of ruptured PcomA aneurysms with PcomA sacrifice. MATERIALS AND METHODS: A retrospective review identified 14 patients with ruptured PcomA aneurysms who underwent embolization of the aneurysms in combination with PcomA sacrifice. Preoperative angiographic data, including the Allcock test, postoperative DWI, and neurologic status, were examined. RESULTS: Elimination of the aneurysm was complete in all cases. Postoperative DWI indicated 7 cases with infarctions (infarction group) and 7 cases without infarctions (noninfarction group). All patients in the infarction group developed infarctions in the vicinity of the tuberothalamic artery. In all 14 cases, a preoperative Allcock test demonstrated a retrograde filling of the PcomA through the P1 segment. The incidence of negative visualizations of the P1 segment on vertebral angiograms was significantly higher in the infarction group (100%) than in the noninfarction group (0%; P = .00058). The mean PcomA diameters, PcomA/P1 ratios, and aneurysm sizes observed in the infarction group were significantly greater than those in the noninfarction group (P < .05, P < .01, and P < .02, respectively). Tuberothalamic artery infarction caused hemiparesis and memory disturbance, which were associated with unfavorable outcomes. CONCLUSIONS: After the coil occlusion of ruptured PcomA aneurysms with PcomA sacrifice, tuberothalamic artery infarctions tended to occur in cases exhibiting negative visualization of the P1 segment, even when collateral flow was observed with the Allcock test.

Portal vein thrombosis treated using danaparoid sodium and antithrombin III.

A 45-year-old man under treatment for liver cirrhosis (LC) due to chronic hepatitis C and hemophilia A was seen in our emergency room because of a 10-kg weight gain in the previous week due to ascites. Portal vein thrombosis (PVT) was detected with computer tomography (CT) and ultrasonographic (US). Danaparoid sodium (DS) and antithrombin III (AT III) were administrated and doppler US images showed improvement of portal venous blood flow. DS or AT III may be safe and alternative therapies for PVT.

Effectiveness of antiplatelet drugs against experimental non-alcoholic fatty liver disease.

OBJECTIVE: No effective drugs have been developed to date to prevent or treat non-alcoholic fatty liver disease (NAFLD), although diet modification and exercise to improve obesity have been attempted. Therefore, development of a novel drug/strategy to treat NAFLD is urgently needed. In the present study, a novel concept is proposed for the treatment of NAFLD. METHODS: Fisher 344 male rats were given a choline-deficient, l-amino acid-defined (CDAA) diet or a high-fat high-calorie (HF/HC) diet with or without the antiplatelet agents, aspirin, ticlopidine or cilostazol for 16 weeks. Liver steatosis, inflammation and fibrosis, and the possible mechanisms involved were investigated. RESULTS: All three antiplatelet drugs, namely aspirin, ticlopidine and cilostazol, significantly attenuated liver steatosis, inflammation and fibrosis in the CDAA diet group. Of the three agents, cilostazol was the most effective, and the drug also suppressed HF/HC diet-induced liver steatosis. Cilostazol appeared to exert its beneficial effect against NAFLD by suppressing mitogen-activated protein kinase activation induced by oxidative stress and platelet-derived growth factor via intercepting signal transduction from Akt to c-Raf. CONCLUSION: Antiplatelet agents, especially cilostazol, offer the promise of becoming key agents for the treatment of NAFLD.

The superiority of organically cultivated vegetables to general ones regarding antimutagenic activities.

We found organically cultivated (OC) vegetables, using a water-soluble chitosan as a soil improvement agent and leaf surface spray, had much longer shelf life and better taste than that of generally cultivated (GC) vegetables. The purpose of this study is to determine the relative antimutagenic activity between OC and GC vegetables. Eleven OC vegetables were harvested in March and April in 1999 and 2000, and GC ones were supplied as a control from nearby farms on the same date. The former vegetables were planted on the field where no pesticide had been used for the last 3 years. Forward mutation test with Salmonella typhimurium TM677 and 8-azaguanine as a detection agent was used to determine the antimutagenic activity of juices prepared from OC and GC vegetables against authentic mutagens, such as 4-nitroquinoline oxide (4NQO), benzo(a)pyrene (BaP), and 3-amino-1-methyl-5H-pyrido[4,3-b]indole acetate (Trp-P-2). This microbiological test is a convenient method to use for the food samples containing free histidine. Antimutagenic activity was evaluated by the difference of mutagenic activities between mutagenecity of authentic compounds and that observed upon incubation at 37 degrees C for 2h with each vegetable juice. OC Chinese cabbage, carrot, Welsh onion, and Qing-gen-cai suppressed 37-93% of the mutagenic activity of 4NQO, while the GC ones were held down to 11-65%. Against BaP, three species of OC vegetables showed 30-57% antimutagenecity, while GC ones did only 5-30%. Similarly, the OC spinach decreased the activity of Trp-P-2 to 78%, and the GC suppressed it by 49%.

Repeated administration of CGP 46381, a gamma-aminobutyric acidB antagonist, and ethosuximide suppresses seizure-associated cyclic adenosine 3'5' monophosphate response element- and activator protein-1 DNA-binding activities in lethargic (lh/lh) mice.

To characterize seizure-associated increases in cerebral cortical and thalamic cyclic AMP responsive element (CRE)- and activator protein 1 (AP-1) DNA-binding activities in lethargic (lh/lh) mice, a genetic model of absence seizures, we examined the effects of ethosuximide and CGP 46381 on these DNA-binding activities. Repeated administration (twice a day for 5 days) of ethosuximide (200 mg/kg) or CGP 46381 (60 mg/kg) attenuated both seizure behavior and the increased DNA-binding activities, and was more effective than a single administration of these drugs. These treatments did not affect either normal behavior or basal DNA-binding activities in non-epileptic control (+/+) mice. Gel supershift assays revealed that the increased CRE-binding activity was attributable to activation of the binding activity of CREB, and that the c-Fos-c-Jun complex was a component of the increased AP-1 DNA-binding activity.

Endoscopic characteristics of low-grade gastric mucosa-associated lymphoid tissue lymphoma after eradication of Helicobacter pylori.

BACKGROUND AND AIMS: It was recently reported that low-grade gastric lymphoma of mucosa-associated lymphoid tissue (MALT) was regressed by the eradication of Helicobacter pylori. The aim of this study was to confirm the effect of H. pylori eradication on low-grade gastric MALT lymphoma and to investigate the whitish mucosa that appeared with regression of the lesions. METHODS: Forty-seven H. pylori-positive patients with low-grade gastric MALT lymphoma were treated by using triple therapy. Biopsy specimens were histologically graded and B cell clonality was examined by using reverse transcription-polymerase chain reaction before and after eradication treatment. The relationship between the appearance of whitish mucosa and the degree of gastric gland loss was evaluated. RESULTS: Histologic regression was observed 2 months after eradication therapy in 42 of 47 patients. However, B cell monoclonality changed to polyclonality in only 23 patients during the follow-up period. The appearance of whitish mucosa in patients who showed histologic regression became more frequent as the degree of gastric gland loss increased (P< 0.001). CONCLUSIONS: Most low-grade gastric MALT lymphoma histologically regressed after H. pylori eradication. The appearance of whitish mucosa after histologic regression reflected the degree of gastric gland loss. Whitish mucosa is an endoscopic characteristic and may be an endoscopic marker for regression of low-grade gastric MALT lymphoma.

Molecular cloning of the crustacean DD4 cDNA encoding a Ca(2+)-binding protein.

A cDNA, named DD4, was identified in the prawn Penaeus japonicus in a search for genes that were expressed during calcification of the crustacean exoskeleton. DD4 transcripts were detected in the epidermal cells underlying the exoskeleton specifically during the postmolt stage, when the calcification takes place. In the DD4 cDNA an open reading frame of 542 amino acids was found. The deduced protein was acidic and proline-rich, and exhibited similarity to the Drosophila Ca(2+)-binding protein calphotin in the amino acid sequence and composition. The DD4 cDNA was expressed in Escherichia coli to characterize Ca(2+)-binding of the encoded protein, and Ca(2+) was found to bind to a central segment of 186 amino acids. The DD4 protein is suggested to play a role in the calcification of the crustacean exoskeleton.

Spatio-temporal analysis of cortical activity evoked by gustatory stimulation in humans.

Gustatory activated regions in the cerebral cortex have not been identified precisely in humans. In this study we recorded the magnetic fields from the brain in response to two tastants, 1 M NaCl and 3 mM saccharin. We estimated the location of areas activated sequentially after the onset of stimulation with magnetic source imaging. We investigated the primary gustatory area (area G) precisely, and found it at the transition between the parietal operculum and the insular cortex. The central sulcus was activated less frequently than area G but with almost the same latency in cases of NaCl stimulation. Following area G, we found activation in several cortical regions, e.g. both the frontal operculum and the anterior part of the insula, the hippocampus, the parahippocampal gyrus and the superior temporal sulcus.

Temporal structure of implicit motor imagery in visual hand-shape discrimination as revealed by MEG.

We investigated the spatio-temporal brain activity on the time scale of several milliseconds related to the mental rotation task requiring judgements of hand orientation, using a whole-cortex MEG (magnetoencephalography) system. Neuronal activity in the visual cortex was observed approximately 100-200 ms from stimulus onset, and that in inferior parietal lobe followed (after 200 ms). Both of these activities showed a contralateral dominance to visual stimulus hemifield. Premotor activity started later than the inferior parietal lobe activity, and these activities partially overlapped. Activity in primary motor and/or motosensory areas was observed in some subjects. The whole-cortex neuromagnetic measurements provided the time course of activity in the human brain associated with the implicit motor imagery: visual cortex-->inferior parietal lobe<-->premotor cortex. This process is considered to be the transformation process of retinotopic locations into a body-centered reference frame necessary for the mental rotation task.

A gamma Gly-268 to Glu substitution is responsible for impaired fibrin assembly in a homozygous dysfibrinogen Kurashiki I.

A new type of gamma Gly-268 (GGA) to Glu (GAA) substitution has been identified in a homozygous dysfibrinogen by analyses of the affected polypeptide and its encoding gene derived from a 58 year-old man manifesting no major bleeding or thrombosis. The functional abnormality was characterized by impaired fibrin assembly most likely due to failure to construct properly aligned double-stranded fibrin protofibrils. This presumption was deduced from the following findings: (1) Factor XIIIa-catalyzed cross-linking of the fibrin gamma-chains progressed in a normal fashion, indicating that the contact between the central E domain of one fibrin monomer and the D domain of another took place normally; (2) Nevertheless, factor XIIIa-catalyzed cross-linking of the fibrinogen gamma-chains was obviously delayed, suggesting that longitudinal association of D domains of different fibrin monomers, ie, D:D association was perturbed; (3) Plasminogen activation catalyzed by tissue-type plasminogen activator was not as efficiently facilitated by polymerizing fibrin monomer derived from the patient as by the normal counterpart. Therefore, gamma Gly-268 would not be involved in the 'a' site residing in the D domain, which functions as a complementary binding site with the thrombin-activated 'A' site in the central E domain, but would be rather involved in the D:D self association sites recently proposed for human fibrinogen. Thus, the gamma Glu-268 substitution newly identified in this homozygous dysfibrinogen seems to impair proper alignment of adjacent D domains of neighboring fibrin molecules in the double-stranded fibrin protofibril, resulting in delayed fibrin gel formation.

Microgravity generated by space flight has little effect on the growth and development of chick embryonic bone.

Seven days' space flight of fertilized chicken eggs pre- incubated for 7 and 10 days on earth caused no differences in the morphology of osteoblasts, osteoclasts, and osteocytes of humerus and tibia from those of control embryos. Bone-resorbing and -forming activities of the femur were not different between control and flight groups. As a consequence, calcium and phosphorus contents of the femora between control and flight groups were not changed. Alkaline phosphatase activity of 3 different regions (resting cartilage, growth cartilage, and cortical bone) of tibia showed no significant difference between control and flight groups. No significant difference of gene expressions of hepatocyte growth factor and receptors of fibroblast growth factor was observed in perichondrium, trabecula, and skeletal muscles and tendons of hind limbs between control and flight groups. Unlike the results of previous space flight experiments in which young growing mammals were used, these morphological and biochemical results indicate that microgravity has little effect on bone metabolism of the chick embryo.

Effect of KCA-098, a new benzofuroquinoline derivative, on bone mineral metabolism.

The effect of 3,9-bis(N,N-dimethylcarbamoyloxy)-5H-benzofuro[3,2-c]quinoli ne-6-one designated as KCA-098) on the bone mineral metabolism of chick embryonic bone was examined. KCA-098 dose-dependently inhibited bone resorption of cultured chick embryonic femora and calvariae. It increased the length, dry weight, and calcium and phosphorus contents of 9-d-old chick embryonic femurs cultivated for 6 d, indicating that it stimulated bone formation. These results show that KCA-098 has the unique effects of inhibiting bone resorption and stimulating bone formation of chick embryo. In addition, in an in vivo experiment, oral administration of KCA-098 (3.0 mg/kg/d) for 16 weeks led to an increase in calcium and phosphorus content as well as an increase in the amount of force required to break the femur from ovariectomized rats, suggesting that it may be useful for the treatment of bone diseases.

In vitro effect of KCA-098, a derivative of coumestrol, on bone resorption of fetal rat femurs.

The effects of 3,9-bis(N,N-dimethylcarbamoyloxy)-5H-benzofuro[3,2-c]quinoli ne-6-one (KCA-098), a derivative of coumestrol, on bone resorption was studied in organ cultures of 20-day fetal rat femora. KCA-098 increased the length, dry weight, and calcium and phosphorus contents of parathyroid hormone (PTH)-treated fetal rat femur. As PTH significantly reduced the calcium and phosphorus contents of the femora, probably by stimulating bone resorption, KCA-098 seems to inhibit bone resorption. In fact, KCA-098 inhibited the PTH-induced release of 45Ca from pre-labeled fetal rat femora into the medium in organ culture. Coumestrol also inhibited the release of 45Ca from bone into the medium. However, KCA-098 did not increase the uterine weight of ovariectomized rats, whereas coumestrol did so. Thus KCA-098 is a unique, new inhibitor of bone resorption that has no estrogenic activity.

Growth hormone-releasing hormone peptide and mRNA are overexpressed in GH-deficient Ames dwarf mice.

Hypothalamic expression of growth hormone-releasing hormone (GHRH) was quantified morphologically in dwarf mice which exhibit spontaneous genetic GH absence. Mouse GHRH mRNA was assessed by in situ hybridization; densitometric evaluation of total mRNA in dwarfs showed levels 2.3-fold higher than in phenotypically normal siblings (p < 0.01); assessment of mRNA per neuron by autoradiographic grain counting indicated a 2.5-fold increase per cell in dwarfs (p < 0.005). GHRH peptide was evaluated immunocytochemically using a new mouse-specific antiserum; numbers of neurons containing detectable levels were 3-fold higher in dwarfs (p < 0.005). The increase in GHRH mRNA corroborates that reported previously in the GH-deficient little mouse, and after hypophysectomy in rats; GHRH peptide increase contrasts with previous reports of the effect of acute GH removal by hypophysectomy, in which GHRH levels fell. The results suggest that chronic GH deficiency is accompanied by increased translation as well as transcription of GHRH.

[Comparative toxicity study of rokitamycin and josamycin in rats].

A comparative toxicity study on macrolide antibiotics, rokitamycin (TMS-19-Q) and josamycin, was performed in male rats. These drugs were given orally for 1 month at daily doses of 250, 500, 1,000, and 2,000 mg/kg. No animals died in the study. No abnormal symptoms or changes in body weights and food consumption were observed. Results of urinalysis, hematological analysis and biochemical analysis of serum and organ weights were normal except that a dose-dependent hypertrophy of caecum was observed in all dosage groups. Necropsy revealed no notable drug related abnormalities except in caecum of all test groups. Pathological examination found no significant drug-related abnormalities in the test groups. No toxicological signs were detected in the group administered with 2,000 mg/kg of either drug and no difference was found between the 2 drugs.