Resolution of sigma-fields for multiparticle finite-state action evolutions with infinite past

For multiparticle finite-state action evolutions, we prove that the observation $\sigma$-field admits a resolution involving a third noise which is generated by a random variable with uniform law. The Rees decomposition from the semigroup theory and the theory of infinite convolutions are utilized in our proofs

Adiponectin and AMP kinase activator stimulate proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells

<p>Abstract</p> <p>Background</p> <p>Adiponectin is a key mediator of the metabolic syndrome that is caused by visceral fat accumulation. Adiponectin and its receptors are known to be expressed in osteoblasts, but their actions with regard to bone metabolism are still unclear. In this study, we investigated the effects of adiponectin on the proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells.</p> <p>Results</p> <p>Adiponectin receptor type 1 (AdipoR1) mRNA was detected in the cells by RT-PCR. The adenosine monophosphate-activated protein kinase (AMP kinase) was phosphorylated by both adiponectin and a pharmacological AMP kinase activator, 5-amino-imidazole-4-carboxamide-riboside (AICAR), in the cells. AdipoR1 small interfering RNA (siRNA) transfection potently knocked down the receptor mRNA, and the effect of this knockdown persisted for as long as 10 days after the transfection. The transfected cells showed decreased expressions of type I collagen and osteocalcin mRNA, as determined by real-time PCR, and reduced ALP activity and mineralization, as determined by von Kossa and Alizarin red stainings. In contrast, AMP kinase activation by AICAR (0.01–0.5 mM) in wild-type MC3T3-E1 cells augmented their proliferation, differentiation, and mineralization. BrdU assay showed that the addition of adiponectin (0.01–1.0 μg/ml) also promoted their proliferation. Osterix, but not Runx-2, appeared to be involved in these processes because AdipoR1 siRNA transfection and AICAR treatments suppressed and enhanced osterix mRNA expression, respectively.</p> <p>Conclusion</p> <p>Taken together, this study suggests that adiponectin stimulates the proliferation, differentiation, and mineralization of osteoblasts via the AdipoR1 and AMP kinase signaling pathways in autocrine and/or paracrine fashions.</p

Baseline tumour necrosis factor alpha levels predict the necessity for dose escalation of infliximab therapy in patients with rheumatoid arthritis

Objectives: To investigate the possible role of baseline plasma tumour necrosis factor alpha levels (baseline-TNF) on the clinical response to infliximab in patients with rheumatoid arthritis (RA). Methods: Patients with RA refractory to methotrexate received 3, 6, or 10 mg/kg of infliximab every 8 weeks, in a randomised, double-blind manner: the RISING study. Clinical response (disease activity score in 28 joints based on C-reactive protein or American College of Rheumatology core set) at week 54 and serum infliximab levels were compared in three patient groups with low, intermediate, or high baseline-TNF (TNF-low, TNF-int, or TNF-high). Results: In TNF-low patients, the clinical response to different doses of infliximab was comparable, whereas TNF-int patients exhibited a dose-dependent trend. In contrast, TNF-high patients (approximately 13% of the total patients) had a clinical response to 10 mg/kg significantly better than the response to 3 and 6 mg/kg of infliximab. In TNF-high patients, the median trough serum levels of infliximab were below the detection limit (<0.1 μg/ml) at 3 and 6 mg/kg but were greater than 2 μg/ml at 10 mg/kg, whereas the levels were approximately 1 μg/ml for each dosage group in TNF-low patients. Conclusion: In patients with RA, baseline-TNF is significantly associated with the clinical response to infliximab in patients with a high baseline-TNF. A higher dose of infliximab may be necessary in these patients, whereas lower doses of infliximab are sufficient for those with a low baseline-TNF. Baseline-TNF may be a useful measure for personalising the treatment of RA using infliximab

ショウエネルギー ニジュウ ハンテンケイ コガタ ジクリュウ ファン ノ ナイブ ナガレ ト コウセイノウ セッケイ ニ カンスル ケンキュウ

Small-sized axial fans are used as air cooler for electric equipments. But there is a strong demand for higher power of fan according to the increase of quantity of heat from electric devices. Therefore, higher rotational speed design is conducted although, it causes the deterioration of efficiency and the increase of noise. Then the adoption of contra-rotating rotors for small-sized fan was proposed for the improvement of performance. In the present paper, the performance and internal flow condition of a small-sized axial fan with 100mm diameter are shown as a first step of the research for the contra-rotating small-sized axial fan and the similarity law of this small-sized axial fan is discussed. Furthermore, the numerical flow simulation was conducted to investigate the performance of the contra-rotating small-sized axial fan and internal flow field and pressure distributions were clarified and the effect of contra-rotating rotors would be considered

Acinar Cell Carcinoma of the Pancreas with Colon Involvement

We report a case of acinar cell carcinoma of the pancreas with colon involvement that was difficult to distinguish from primary colon cancer. A 60-year-old man was admitted with a 1-month history of diarrhea. Contrast-enhanced computed tomography (CT) revealed a large tumor (10.6×11.6 cm) at the splenic flexure of the colon. Colonoscopy showed completely round ulcerative lesions, and biopsy revealed poorly differentiated adenocarcinoma. Left hemicolectomy, resection of the jejunum and pancreas body and tail, and splenectomy were performed based on a diagnosis of descending colon cancer (cT4N0M0, stage IIB), and surgery was considered to be curative. Diagnosis was subsequently confirmed as moderately differentiated acinar cell carcinoma of the pancreas by immunohistochemical staining (pT3N0M0, stage IIA). Multiple liver metastases with portal thrombosis were found 8 weeks postoperatively. Despite combination chemotherapy with oral S-1 and gemcitabine, the patient died of hepatic failure with no effect of chemotherapy 14 weeks postoperatively. Correct diagnosis was difficult to determine preoperatively from the clinical, CT, and colonoscopy findings. Moreover, the disease was extremely aggressive even after curative resection. Physicians should consider pancreatic cancer in the differential diagnosis of similar cases

IL-10 Inhibits Transforming Growth Factor-ß-Induction of Type I Collagen mRNA Expression via Both JNK and p38 Pathways in Human Lung Fibroblasts

Transforming growth factor-ß (TGF-ß) is a key factor for understanding the pathogenesis of fibrotic disorders such as idiopathic pulmonary fibrosis (IPF). We have demonstrated that interleukin-10 (IL-10) suppresses TGF-ß-induced expression of type I collagen (COL1) mRNA in a human lung fibroblast cell line (WI-38). However, the inhibitory mechanism has not yet been clearly elucidated. Thus, in the current study, we investigate the effects of IL-10 blockade of TGF-ß signaling which regulates COL1 mRNA expression. In WI-38 cells, IL-10 inhibits TGF-ß-mediated phosphorylation of both, c-Jun HN2-terminal kinase (JNK) and p38, but does not suppress TGF-ß- mediated phosphorylation of Smad2 or affect TGF-ß-upregulation of Smad7 mRNA expression. In addition, SP600125 and SB203580, specific inhibitors of JNK and p38, respectively, attenuate TGF-ß-induced COL1 mRNA expression in WI-38 cells. These results suggest that IL-10 inhibits TGF-ß-induced COL1 mRNA expression via both JNK and p38 pathways but not Smad pathways in WI-38 cells. This inhibitory mechanism may provide a novel insight into therapeutic strategies for fibrotic disorders such as IPF

Extreme hyperglycemia and diabetic ketoacidosis occurring in a patient on chronic dialysis

Department of Urology, North medical center, Kyoto prefectural university of medicine, Kyoto, Japan.Department of Nephrology and Urology, Nishijin Hospital, Kyoto, Japan.Department of Internal medicine, Nishijin Hospital, Kyoto, Japan.Diabetic ketoacidosis (DKA) is a complication that is rarely reported in patients on chronic dialysis. Herein, we describe the case of a patient on chronic hemodialysis who presented to us with acute onset diabetic ketoacidosis. A 50-year-old man with insulin-dependent diabetes mellitus, who was on hemodialysis for 2 years, presented to us with altered consciousness. Laboratory data revealed the following results: blood sugar, 110.1 mmol/L (1984 mg/dL); serum sodium, 107 mmol/L; β -hydroxybutyric acid, 1991 μ M; pH, 7.048. A diagnosis of diabetic ketoacidosis was made, and insulin therapy and hemodialysis were initiated, following which his parameters including blood glucose, and serum potassium and sodium improved. High osmotic dehydration was not observed in our patient owing to his renal dysfunction. The patient’s consciousness normalized following the correction of hyperglycemia and DKA. This case report highlights the importance of early diagnosis of DKA, and prompt initiation of insulin therapy and hemodialysis in patients on chronic dialysis. Therefore, in patients with end stage renal disease, the blood glucose correction should be followed by the restoration of sodium and osmolality, guided by corrected sodium concentration and effective osmolality, and by the appropriate adjustment of insulin and dialysis