Treatment of sterile panniculitis in a dog.
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Adipose Tissue↗
Biomedical subjects
K Fujiwara
Publications and source records attributed to K Fujiwara.
GIT1 mediates thrombin signaling in endothelial cells: role in turnover of RhoA-type focal adhesions.
Thrombin mediates changes in endothelial barrier function and increases endothelial permeability. A feature of thrombin-enhanced endothelial hyperpermeability is contraction of endothelial cells (ECs), accompanied by formation of focal adhesions (FAs). Recently, a G protein-coupled receptor kinase-interacting protein, GIT1, was shown to regulate FA disassembly. We hypothesized that GIT1 modulates thrombin-induced changes in FAs. In human umbilical vein ECs (HUVECs), thrombin recruited GIT1 to FAs, where GIT1 colocalized with FAK and vinculin. Recruitment of GIT1 to FAs was dependent on activation of the small GTPase RhoA, and Rho kinase, as demonstrated by adenoviral transfection of dominant-negative RhoA and treatment with Y-27632. Thrombin stimulated GIT1 tyrosine phosphorylation with a time course similar to FAK phosphorylation in a Rho kinase- and Src-dependent manner. Depletion of GIT1 with antisense GIT1 oligonucleotides had no effect on basal cell morphology, but increased cell rounding and contraction of HUVECs, increased FA formation, and increased FAK tyrosine phosphorylation in response to thrombin, concomitant with increased endothelial hyperpermeability. These data identify GIT1 as a novel mediator in agonist-dependent signaling in ECs, demonstrate that GIT1 is involved in cell shape changes, and suggest a role for GIT1 as a negative feedback regulator that augments recovery of cell contraction.
Adaptor Proteins, Signal Transducing↗
A stable prostacyclin analogue reduces high serum TNF-alpha levels in diabetic patients.
AIMS: To confirm whether a prostacyclin (prostaglandin I (2)) affects the increased TNF-alpha concentration in sera of diabetic patients, we measured serum TNF-alpha concentration and treated these patients with oral administration of the stable prostacyclin analogue (Beraprost). Twelve of 20 type II diabetic patients were investigated for follow up-study and 6 of those patients were for therapy with Beraprost for diabetic neuropathy. SUBJECTS AND METHODS: Serum TNF-alpha concentration was quantified by EASIA using monoclonal antibodies directed against distinct epitopes of TNF-alpha. RESULTS: In diabetic patients, serum TNF-alpha concentration was significantly increased compared with that of healthy subjects. The augmented TNF-alpha concentration in these patients was not decreased by diabetic control using antihyperglycemic agents for 8 weeks but was reduced with oral administration of a stable prostacyclin (prostaglandin I (2)) analogue for 5 weeks without any changes of blood glucose levels. CONCLUSIONS: Stable prostacyclin analogue administration for a short term period reduced increased TNF-alpha levels in diabetic patients, not through the improved hyperglycemic condition but another pathway, probably a cAMP system. These results imply that treatment with the prostacyclin analogue may contribute to the prevention of progression in diabetic complications.
Adult↗
Case report: internal and external jugular vein thrombosis with marked accumulation of FDG.
We report an unusual case of idiopathic internal and external jugular vein thrombosis. Positron emission tomography (PET) using (18)F-fluoro-2-deoxy-D-glucose (FDG), which was conducted to assess subclinical malignancy, revealed intense uptake of FDG, corresponding to thrombus within the left internal and external jugular veins. Although FDG-PET is widely used in differentiating between malignant and benign diseases, we should bear in mind that this benign entity can demonstrate high accumulation of FDG.
Fluorodeoxyglucose F18↗
[Multiple primary lung cancer diagnosed by thoracic computed tomography; report of 2 cases].
Two cases of bilateral multiple primary lung cancers are presented. One is synchronous, and another is metachronous. Case 1: An abnormal shadow in the left lower lobe was found on the chest radiograph of 40-year-old female during a regular check-up. Chest computed tomography (CT) film showed a micronodule in the right S2. Left lower lobectomy was performed, followed by second-staged right S2 segmentectomy 1 month after the initial operation. Case 2: A 62-year-old female underwent left lower lobectomy for lung cancer in April 1997. Follow-up CT showed a nodule in right S8. In March 2000, right basal segmentectomy was performed for second lung cancer. Moreover, follow-up CT showed a nodule in right S3. Right wedge resection was performed for third lung cancer in July 2002. It is important to carefully examine a synchronous lesion before the operation of a primary lung cancer and to perform close follow-up surveillance for early detection of a metachronous lesion.
Adenocarcinoma, Papillary↗
Genetic polymorphisms of the N-acetyltransferase genes and risk of Parkinson's disease.
Recently, the authors demonstrated linkage in idiopathic PD to a region on chromosome 8p that contains the N-acetyltransferase genes, NAT1 and NAT2. The authors examined NAT1 and NAT2 for association with PD using family-based association methods and single nucleotide polymorphisms (SNPs). The authors did not find evidence for association with increased risk for PD between any individual NAT1 or NAT2 SNP or acetylation haplotype (N = 397 families, 1,580 individuals).
Aged↗
Effect of peripheral lipopolysaccharide injection on dopamine content in murine anterior olfactory nucleus.
Norepinephrine turnover rate in the murine locus coeruleus (LC) is known to be enhanced by the intraperitoneal (i.p.) injection of lipopolysaccharide (LPS). Approximately 40% of LC neurons are also known to project to the olfactory bulb (OB) and the anterior olfactory nucleus (AON). Therefore, we investigated whether an i.p. injection of 500 microg LPS could modulate the catecholamine biosynthesis in these sites in 8-week-old C3H/HeN male mice. Unexpectedly, the content of norepinephrine was not elevated in both sites during 6-h-observation after LPS injection. The contents of dopamine and its metabolites in the AON were highly increased at 4 h after LPS injection, whereas those in the OB were not elevated during 6-h-observation. Although the AON has been considered not to belong to the dopaminergic neuron system, our report is the first to show an elevated dopamine content in the AON under a stressful condition such as endotoxemia.
Animals↗
Association of Fcgamma receptor IIb and IIIb polymorphisms with susceptibility to systemic lupus erythematosus in Thais.
We recently reported association of a newly identified polymorphism of Fcgamma receptor (FcgammaR) IIb, I232T, with systemic lupus erythematosus (SLE) in Japanese. To date, information on FcgammaR genotypes and their association with SLE is limited in South-east Asian populations. To gain further insight into the role of FcgammaR polymorphisms in the genetic predisposition of SLE, association of FcgammaRIIa-H131R, IIb-I232T, IIIa-F176V and IIIb-NA1/NA2 (HNA-1a/1b) polymorphisms with SLE was analyzed in the Thai population, using case-control association analysis. FcgammaRIIb-232T/T and IIIb-NA2/NA2 genotypes were associated with SLE with the odds ratio of 2.55. Genotype relative risk analysis revealed significant association of IIb-232T/T and IIIb-NA2/NA2, and a tendency of association of the IIIa-176F/F genotype. Moreover, carriers of FcgammaRIIa-131R were significantly increased in patients with lupus nephritis. Significant linkage disequilibrium was present among FcgammaRIIb, IIIa and IIIb, and two-locus analyses suggested that the tendency of association of FcgammaRIIIa could derive from linkage disequilibrium with IIb and IIIb. These results provided evidence that FcgammaR polymorphisms may be an important predisposing factor also in Thais in a complex manner.
Adolescent↗
Effect of rebamipide on prostaglandin receptors-mediated increase of inflammatory cytokine production by macrophages.
BACKGROUND: Rebamipide (Reb) is an anti-ulcer drug, and has unique properties such as anti-inflammatory action. We previously reported that prostaglandins (PGs) dramatically increased vascular endothelial growth factor (VEGF), a known angiogenic factor and a vascular permeable factor, by activated macrophages through specific PGE receptor and peroxisome proliferator-activated receptor gamma (PPARgamma, a nuclear receptor of PG) mediated process. Effects of PGs on the production of other cytokines such as interleukin (IL)-6 and IL-8 have been controversial. AIM: To clarify the anti-inflammatory roles of Reb, we examined the effect of Reb on PGE1- and 15-deoxy-Delta12, 14-PGJ2 (a potent PPARgamma ligand, 15d-PGJ2) -induced increase of VEGF production by macrophages. Additionally, effects of these PGs on the production of IL-6 and IL-8, and modulation of these actions by Reb were studied. METHODS: Phorbol 12-myristate 13-acetate-differentiated U937 cells were used as a human macrophage model (H-Mac). VEGF, IL-6, IL-8 and cAMP were measured by EIA. RESULTS: Reb suppressed PGE1-, but not 15d-PGJ2-, induced increase of VEGF production partially through decrease of cAMP formation. Reb suppressed PGE1 -, but not 15d-PGJ2-, induced increase of IL-6 and IL-8 production. CONCLUSION: Reb suppresses membrane, but not nuclear PG receptors mediated increase of inflammatory cytokine production, which may be involved in anti-ulcer action of this drug.
Alanine↗
Hepatitis A virus VP3 may activate serum response element associated transcription.
BACKGROUND: Hepatitis A virus (HAV) infection is a major public health problem worldwide. The infection does not induce any visible cytopathic effects or interfere with macromolecular synthesis in host cells. However, the hepatitis B and C viruses have recently been reported to activate intracellular signals. To clarify the effects of HAV infection on intracellular signalling, we examined the influence of 9 FLAG-tagged HAV proteins (VP2, VP3, VP1-2A, 2B, 2C, 3A, 3BC, 3C and 3D) on signal transduction pathways. METHODS: Viral protein expression vectors were co-transfected into HeLa cells with reporter plasmids controlled by a synthetic promoter containing direct repeats of the cyclic AMP response element (CRE), serum response factor (SRF), activator protein 1 (AP-1), nuclear factor kappaB (NF-kappaB) or serum response element (SRE). Cells were harvested 42 h after transfection and luciferase assays were performed. Viral protein activation twice that of the control was defined as significant. RESULTS: VP3 induced an SRE-associated signal 2.2 +/- 0.3 times higher than that of control. VP3 did not activate CRE-, SRF-, AP-1- or NF-kappaB- associated signalling. The other HAV proteins tested also failed to induce these pathways. CONCLUSIONS: HAV interacts with the host signalling mechanism, and HAV VP3, different from HBX and hepatitis C core protein, may activate only SRE-associated intracellular signalling, a pathway associated with cell proliferation and differentiation.
Blotting, Western↗
[Needle tract implantation of thymoma after transthoracic needle biopsy].
A 53-year-old man was admitted to hospital because of an anterior mediastinal mass. For definite diagnosis, needle biopsy was performed under ultrasonic examination. The histopathological diagnosis was thymoma and thymo-thymectomy was performed. The tumor recurred in the right anterior chest wall 10 years later. It is suggested that the thymoma tissue had been implanted in the needle tract. To our knowledge, this is the 2nd reported case of thymoma which has been implanted in the needle tract.
Biopsy, Needle↗
[The surgical technique of heart displacement during off-pump coronary artery bypass grafting in the exposure of the anastomotic site of posterior descending artery].
Heart displacement during off-pump coronary artery bypass grafting (OPCAB) is necessary to expose the anastomotic site. However, such displacement causes hemodynamic deterioration especially in the exposure of the circumflex branches and posterior descending artery (PDA). In this study we present two different cardiac positioning for the exposure of the anastomotic site of PDA. To expose the mid-portion of PDA the heart is vertically displaced by fixing the suction cup of the heart positioner on apex. To expose the proximal portion of PDA the suction cup is attached on the acute margin of the right ventricle (off apex). By using these 2 different techniques properly, hemodynamic deterioration can be avoided during OPCAB for PDA.
Anastomosis, Surgical↗
Expression of cyclooxygenase-2 in human hyperplastic gastric polyps.
Cyclooxygenase (COX)-2, an inducible isoform of prostaglandin synthetase, has been reported to be a key molecular target of colon cancer prevention by nonsteroidal anti-inflammatory drugs. Recently, it has been shown that Helicobacter pylori (H. pylori) could induce COX-2 together with inflammatory cytokines. Although human hyperplastic gastric polyps disappeared or decreased in number and size after eradication of H. pylori, the mechanisms in this step, especially the roles of COX-2, have not been yet elucidated. The aims of the present study were to examine the expression and localization of COX-2 in human hyperplastic gastric polyps immunohistochemically. Twelve specimens of human hyperplastic gastric polyps were obtained from endoscopic polypectomy. The expression of the COX-2 protein was immunohistochemically examined on formalin-fixed and paraffin-embedded tissue sections using an anti-COX-2 antibody and an avidin-biotin complex method. Cells expressing COX-2 were further immunohistochemically identified using a specific antibody against macrophages (CD68), and myofibroblasts (alpha-smooth muscle actin). Immunoreactive COX-2 was predominantly and strongly expressed in interstitial cells in the sub-epithelial layer of 10 hyperplastic polyps. Semi-quantitative analysis revealed a significant increase in COX-2 expression in interstitial cells. The staining pattern of macrophages and myofibroblasts partly corresponded to that observed for COX-2 in hyperplastic gastric polyps. These results suggest that COX-2 in mesenchymal cells induced by H. pylori may play an important role in the tumorigenesis of human hyperplastic gastric polyps.
Aged↗
[Lung cancer with both sarcoid reaction and metastasis in the mediastinal lymph nodes; report of a case].
A 66-year-old man was admitted to our hospital for detailed investigation of an abnormal shadow on his chest X-ray. Chest radiography and computed tomography(CT) of the chest showed mediastinal lymphadenopathy and a tumor shadow in the left upper lobe. Biopsy of the mediastinal lymph nodes by mediastinoscopy showed that sarcoid nodules existed in all the biopsies nodes. Therefore, the lymphadenopathy was thought to be sarcoidosis or sarcoid reaction accompanied with lung cancer. Left upper lobectomy and dissection of hilar and mediastinal lymph nodes were performed. Although sarcoid nodules were seen in all the dissected lymph nodes, the cancer involved #5 and #14 lymph nodes. He died of brain metastasis 10 months after surgery.
Adenocarcinoma↗
Review article: COX-2, prostanoids and colon cancer.
Epidemiological, experimental, and clinical studies have demonstrated that colon carcinogenesis may be prevented by nonsteroidal anti-inflammatory drugs (NSAIDs). Although controversy remains, recent studies, including ours, have revealed that NSAIDs suppress colon carcinogenesis at the adenoma stage where cyclooxygenase-2 (COX-2), a major molecular target in this action, is mainly expressed in interstitial cells but not in tumour cells. Therefore, it is unlikely that NSAIDs prevent colon cancer formation through modulating the functions of tumour cells. A more possible assumption is that NSAIDs suppress colon carcinogenesis through the inhibition of prostaglandin formation. However, the mechanisms by which prostanoids promote colon carcinogenesis have not been elucidated to date. A prostanoids act through both membrane receptors and nuclear receptors such as peroxisome proliferator receptor (PPAR) gamma or delta, one focus in this area is to investigate their roles in colon carcinogenesis, including the induction of growth factors.
Animals↗
The effects of CD40- and interleukin (IL-4)-activated CD23+ cells on the production of IL-10 by mononuclear cells in Graves' disease: the role of CD8+ cells.
The possible roles of CD8+ cells in the abnormal T cell-dependent B-cell activation in Graves' disease were investigated by analysing lymphocyte subsets in peripheral blood mononuclear cells (PBMC) and their production of soluble factors and cytokines such as IL-10 in patients with Graves' disease, Hashimoto's thyroiditis and normal controls. The PBMC were separated into CD8+ and CD8-depleted cells by magnetic separation columns, and cultured for 7 days with or without anti-CD40 monoclonal antibodies and IL-4. The culture supernatant was assayed for sCD23 and IL-10 using EIA, and the remaining cells were analysed by flow cytometry. Stimulation with anti-CD40 antibody together with IL-4 increased sCD23 levels and the number of CD23+ cells. The latter was further augmented by depletion of CD8+ cells. This combination of B cell stimulants increased production of IL-10 by PBMC from patients with Graves' disease. The CD40- and IL-4-activated production of IL-10 was decreased by CD8+ cell depletion. In contrast, constitutive production of IL-10 was increased after CD8+ cell depletion in a group of patients with low basal secretion levels (<35 ng/ml). It was, however, decreased in a group with higher basal production levels, but such a relationship was not found in the normal control group. Thus, T cell-dependent B-cell activation via a CD40 pathway activates CD23+ cells, leading to over-production of IL-10 and a shift of the Th1/Th2 balance to Th2 dominance, while CD8+ cells may suppress this activation to counteract the Th2 deviation in Graves' disease.
Adult↗
Isolation of Fusarium solani from a dog: identification by molecular analysis.
A strain of Fusarium solani was isolated from a dog showing many cutaneous and submucosal nodules and pyogranulomatous kidney lesions. Clinical isolates from this systemic infection were identified using microscopic examination and confirmed by molecular analysis.
Animals↗
Association between severity of type A hepatitis and nucleotide variations in the 5' non-translated region of hepatitis A virus RNA: strains from fulminant hepatitis have fewer nucleotide substitutions.
BACKGROUND: Type A hepatitis is still a considerable problem in both underdeveloped and developed countries. Why some patients progress to fulminant type A hepatitis and others do not is unclear. AIMS: To determine if nucleotide differences in the genome of hepatitis A virus (HAV) are responsible for the range of clinical severities, we analysed the 5' non-translated region (5'NTR) of the HAV genome, which has an internal ribosomal entry site and is important for cap independent translation of the viral message. METHODS: Serum samples from 84 Japanese patients with sporadic type A hepatitis from five distant regions of Japan, comprising 12 patients with fulminant hepatitis (FH), 13 with severe acute hepatitis (AHs), and 59 with acute hepatitis (AH), were examined for HAV RNA. The fragment between nucleotides 75 and 638 of the 5'NTR was amplified by reverse transcription-polymerase chain reaction, and the nucleotide sequence was determined by direct sequencing. RESULTS: Comparison of sequences of the 5'NTR revealed relatively fewer nucleotide substitutions in FH and AHs patients compared with the considerable sequence variations found in strains of AH. This tendency was most prominent between nucleotides 200 and 500. Strains from FH and AHs cases had fewer nucleotide substitutions (p<0.001) in this region. CONCLUSIONS: Nucleotide variations in the central portion of the 5'NTR of HAV may influence the severity of type A hepatitis.
5' Untranslated Regions↗