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This paper presents a vertical surface climbing robot for cleaning of dust from high rise building. Usually, people clean their wall of outer surface of building by human. Often it becomes risky and costly also. A portable robot having the ability to climb on vertical surface has been expected for a long time. To protect human’s life we designed a prototype of vertical surface climbing robot for cleaning and other multipurpose operation. Some combination of technology has been shown such as smart wireless control with all direction moving capability. Four Dc motors are used to move the robot and one Dc motor is used to rotate the cleaning brush. There is one Electric Ducted fan (EDF) which helps the robot to stick to the surface against gravitational force. An Arduino uno is used as a controller for different There is a Bluetooth modular which has been used to connect with smart phone and take command from user. Four motor helps it to move in up, down, right and left direction by the according commands given by smart phone. The full robot is power by using DC battery and AC to DC converted adapter combined. To observe the outcome of the project, we analyzed the performance of the robot by climbing in different surfaces with different nature. The climbing and stick to the surface differ because of grip. Griping is an important issue for this robot. Most of the surface except glass its performance satisfied us.

Summary We investigated the non-genomic effects of glucocorticoids (GCs) on inhibition of plasma membrane lipid raft formation in activated human basophils. Human basophils obtained from house dust mite (HDM)-sensitive volunteers were pretreated with hydrocortisone (CORT) or dexamethasone (Dex) for 30 min and then primed with phorbol 12-myristate 13-acetate (PMA, 10 ng/ml) or HDM (10 µg/ml). The expression of CD63, a basophil activation marker, was assessed by flow cytometry. Membrane-bound GC receptors (mGCRs) were analysed by flow cytometry and confocal laser microscopy. Lipid rafts were assessed using a GM1 ganglioside probe and visualization by confocal laser microscopy. Pretreatment of basophils with CORT (10−4 M and 10−5 M) and Dex (10−7 M) significantly inhibited CD63 expression 20 min after addition of PMA or HDM. The inhibitory effects of GCs were not altered by the nuclear GC receptor (GCR) antagonist RU486 (10−5 M) or the protein synthesis inhibitor cycloheximide (10−4 M) (P

1 Pulmonary inflammatory diseases such as asthma are characterized by chronic, cell-mediated inflammation of the bronchial mucosa. 2 Recruitment and activation of inflammatory cells is orchestrated by a variety of mediators such as cytokines, chemokines, or adhesion molecules, the expression of which is regulated via the transcription factor nuclear factor kappa B (NF-kappaB). 3 NF-kappaB signaling is controlled by the inhibitor of kappa B kinase complex (IKK), a critical catalytic subunit of which is IKK-beta. 4 We identified COMPOUND A as a small-molecule, ATP-competitive inhibitor selectively targeting IKK-beta kinase activity with a K(i) value of 2 nM. 5 COMPOUND A inhibited stress-induced NF-kappaB transactivation, chemokine-, cytokine-, and adhesion molecule expression, and T- and B-cell proliferation. 6 COMPOUND A is orally bioavailable and inhibited the release of LPS-induced TNF-alpha in rodents. 7 In mice COMPOUND A inhibited cockroach allergen-induced airway inflammation and hyperreactivity and efficiently abrogated leukocyte trafficking induced by carrageenan in mice or by ovalbumin in a rat model of airway inflammation. 8 COMPOUND A was well tolerated by rodents over 3 weeks without affecting weight gain. 9 Furthermore, in mice COMPOUND A suppressed edema formation in response to arachidonic acid, phorbol ester, or edema induced by delayed-type hypersensitivity. 10 These data suggest that IKK-beta inhibitors offer an effective therapeutic approach for inhibiting chronic pulmonary inflammation.

Mitogen-activated protein kinase (MAPK) kinases (MKKs, also called MAPK/extracellular signal-regulated kinase [ERK] kinase [MEK]) are constituents of numerous signal transduction pathways involved in growth, differentiation, and stress response. One of its members, MKK4, directly phosphorylates and activates the c-Jun terminal kinases (also called stress-activated protein kinase [SAPK]) in response to stress and pro-inflammatory cytokines. Recent evidence suggest that control of MKK4 activity may provide a novel approach for the treatment of cancer or as anti-inflammatory therapy. To screen for novel low-molecular-weight inhibitors of MKK4, we established a quantitative, non-radioactive in vitro kinase assay. Human MKK4 was expressed as fusion protein with glutathione S-transferase (GST) in Escherichia coli. Co-expression of a constitutive active fragment of the MAPK/ERK kinase kinase-1 yielded active GST-MKK4 using GST-SAPK alpha-kinase-negative (KN) mutant as substrate. We determined the kinetic constants for ATP and GST-SAPK alpha-KN. The apparent Km value for GST-SAPKalpha-KN was 3.7 microM, while the apparent Km value for ATP was 0.17 microM. Staurosporine inhibited GST-MKK4 with an IC50 of 70 nM. The kinase assay was adapted to a 384-well non-radioactive format. After the kinase reaction the phosphorylated product was captured onto a streptavidin-coated microtiter plate, and phosphorylation was detected with a europium-labeled anti-phosphotyrosine antibody, which allowed time-resolved fluorescence measurement.

AMP and adenosine are found in all cell types and can be released by cells or created extracellularly from the breakdown of ATP and ADP. We have identified an orphan G protein-coupled receptor with homology to the P2Y family of nucleotide receptors that can respond to both AMP and adenosine. Based on its ability to functionally bind the nucleotide AMP, we have named it P2Y15. Upon stimulation, P2Y15 induces both Ca2+ mobilization and cyclic AMP generation, suggesting coupling to at least two different G proteins. It is highly expressed in mast cells and is found predominantly in the tissues of the respiratory tract and kidneys, which are known to be affected by AMP, adenosine, and adenosine antagonists. Until now, the effects of AMP have been thought to depend on its dephosphorylation to adenosine but we demonstrate here that P2Y15 is a bona fide AMP receptor by showing that it binds [(32)P]AMP. Because AMP and adenosine have bronchoconstrictive effects that can be inhibited by theophylline, we tested whether theophylline and other adenosine receptor antagonists can block P2Y15. We found inhibition at a theophylline concentration well within the therapeutic dose range, indicating that P2Y15 may be a clinically important target of this drug.

We cloned, expressed, and characterized in vitro and in vivo the gene encoding the rat ortholog of chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2), a G protein-coupled receptor for prostaglandin D 2 (PGD 2 ). Quantitative reverse transcription-polymerase chain reaction analysis demonstrated highest CRTH2 expression in the lung, brain, ovary, and spleen. Pharmacologically, rat CRTH2 stably transfected in mouse preB lymphoma L1.2 cells behaved very similar compared with the mouse and human orthologs, showing a binding affinity for PGD 2 of 11 nM, a functional calcium mobilization when exposed to agonist, and similar sensitivity to agonists and antagonists. In vivo, selective activation of CRTH2 by 13,14-dihydro-15-keto (DK)-PGD 2 injection into rats led to a dose- and time-dependent increase of the number of leukocytes in the peripheral blood. Specifically, eosinophils, lymphocytes, and neutrophils were recruited with maximum effects seen 60 min after the injection of 300 μg of DK-PGD 2 per rat. Pretreatment of the animals with the CRTH2/thromboxane A 2 receptor antagonist, ramatroban, completely abrogated DK-PGD 2 -induced eosinophilia, suggesting that CRTH2 might have a physiological and/or pathophysiological role in controlling leukocyte migration.

IkappaB kinase beta (IKK-beta) is a serine-threonine protein kinase critically involved in the activation of the transcription factor Nuclear Factor kappa B (NF-kappaB) in response to various inflammatory stimuli. We have identified a small molecule inhibitor of IKK-beta. Optimization of the lead compound resulted in improvements in both in vitro and in vivo potency, and provided IKK-beta inhibitors exhibiting potent activity in an acute cytokine release model (LPS-induced TNFalpha).

Chronic pancreatitis (CP) is characterized by irreversible damage that engenders fibrosis and necrosis of pancreatic tissue, with the consequent loss of endocrine and exocrine function of the pancreas. The clinical course of CP engenders a high rate of morbidity and mortality over a 20-25-year period. In view of this fact, current efforts emphasize the establishment of early diagnosis to commence intervention that can positively affect the natural course of the disease. Endoscopic ultrasonography (EUS) is a well-established and less-invasive modality for CP diagnosis. The higher imaging resolution provided by EUS enables detection of subtle pancreatic abnormalities, not only parenchymal but also ductal changes, that are undetectable using other modalities. This review presents an overview of the endosonographic diagnosis of chronic pancreatitis.

未治療の口腔, 上顎洞, 口峡咽頭原発の扁平上皮癌患者35名に対し, シスプラチンとその拮抗剤であるチオ硫酸ナトリウムを用いた2経路注入法とビンブラスチンとペプロマイシンの静脈内投与から成るネオアジュバント化学療法を施行し, その治療効果について検討した。化学療法の奏効率は91.4%で, CR率は57.1%であった。非担癌他病死例を除外すると, 累積5年生存率はCR群では100%であり, PR+NC群では87.5%であった。本化学療法は適正な支持療法を行うことにより, 短期間で遂行することが可能である。20名のCR患者の内12名に縮小手術が施されたが, 全ての患者が非担癌で良好な口腟機能を保持している。これらのデータは, この化学療法のレジメンが頭頸部癌の治療により効果的であることを示している。この結果はまだ予備的なものであり, さらに症例を加えて検討する必要がある。

In a search for genetic markers of duodenal ulcer, serum pepsinogen I level, ABO blood groups and secretor status were determined in 89 siblings of 34 duodenal ulcer families. Duodenal ulcer patients were likely either to have hyperpepsinogenemia I or to be non-secretors on a familial basis, but not to have an increased frequency of blood group O. The frequency of duodenal ulcer in the siblings was highest in hyperpepsinogenemia I/non-secretor and lowest in normopepsinogenemia I/secretor. Therefore, the influence of two genes, hyperpepsinogenemia I and non-secretor, on the risk of duodenal ulcer is multiplicative. These results provide evidence on the hypothesis of polygenic inheritance of duodenal ulcer.

Three patients with diffuse sclerosing osteomyelitis of the mandible who had been treated by intra-arterial infusion of urokinase and antibacterial agents including fosfomycin were evaluated. All patients underwent decortication at the same time. They were all free from symptoms an average of 3 years 7 months after treatment.Urokinase and fosfomycin may cause the dissolution of biofilm, which prevents contact between antibacterial agents and causative organism. Thus, the intra-arterial infusion of urokinase, fosfomycin, and other antibacterial agents can efficiently eradicate bacteria in sclerotic bone in osteomyelitis.

1 Pulmonary inflammatory diseases such as asthma are characterized by chronic, cell-mediated inflammation of the bronchial mucosa. 2 Recruitment and activation of inflammatory cells is orchestrated by a variety of mediators such as cytokines, chemokines, or adhesion molecules, the expression of which is regulated via the transcription factor nuclear factor kappa B (NF-kappaB). 3 NF-kappaB signaling is controlled by the inhibitor of kappa B kinase complex (IKK), a critical catalytic subunit of which is IKK-beta. 4 We identified COMPOUND A as a small-molecule, ATP-competitive inhibitor selectively targeting IKK-beta kinase activity with a K(i) value of 2 nM. 5 COMPOUND A inhibited stress-induced NF-kappaB transactivation, chemokine-, cytokine-, and adhesion molecule expression, and T- and B-cell proliferation. 6 COMPOUND A is orally bioavailable and inhibited the release of LPS-induced TNF-alpha in rodents. 7 In mice COMPOUND A inhibited cockroach allergen-induced airway inflammation and hyperreactivity and efficiently abrogated leukocyte trafficking induced by carrageenan in mice or by ovalbumin in a rat model of airway inflammation. 8 COMPOUND A was well tolerated by rodents over 3 weeks without affecting weight gain. 9 Furthermore, in mice COMPOUND A suppressed edema formation in response to arachidonic acid, phorbol ester, or edema induced by delayed-type hypersensitivity. 10 These data suggest that IKK-beta inhibitors offer an effective therapeutic approach for inhibiting chronic pulmonary inflammation.

Primary cutaneous nocardiosis of the face is a rare diease in Japan. A 58-year-old woman visited our department due to post-traumatic facial swelling. Clinical exaination revealed a 2×3 cm induration with skin redness and a few small whitish pustules at the right side of the mental region. Nocardia brasiliensis was isolated from aspirated pus. Although N. brasiliensis was resistant to many antibiotics on sensitivity testing, the lesions disappeared relatively soon after the oral administration of sulfamethoxazole-trimethoprim combination therapy followed by minocyclin.

We have integrated a high speed and high density 6T-SRAM cell (0.998 /spl mu/m/sup 2/) for system-on-a-chip (SOC) using enhanced 100 nm CMOS logic technology. This is achieved by a systematic integration methodology, which includes high-NA ArF lithography, optimized optical proximity correction (OPC) CAD, narrow well isolation, poly-buffered shallow trench isolation (STI), offset spacer transistor, and 9-level Cu interconnect and low-k dielectric technologies with the lithographically scalable SRAM cell design.

Nineteen-hour variation of subjective sleepiness, performance and physiological indices were assessed during sleep deprivation. Longitudinal data of each index had its characteristic curve through which the values changed from day level to night level. A comparison of the time when each curve crossed its mid-range (50% value of its range) showed that those of subjective sleepiness and heart rate were significantly earlier than those of tracking error and coefficient of variation of R-R interval (CVR-R), P < 0.01. That of rectal temperature was located at between 1:00 and 4:00 am. These temporal relationships were reproducible under two lighting conditions. These results will be useful in considering the occurrence of human errors by night-time workers in the early morning.

Several mutants of quinoprotein glucose dehydrogenase (GDH) in Escherichia coli were obtained and characterized. Of these, significant mutants were further characterized by kinetic analysis after purification or by site-directed mutagenesis to introduce different amino acid substitutions. H775R and H775A showed a pronounced reduction of affinity for a prosthetic group, pyrroloquinoline quinone (PQQ), suggesting that His-775 may directly interact with PQQ. D730N and D730A showed low glucose oxidase activity without influence on the affinity for PQQ, Mg2+, or substrate, but D730R showed reduced affinity for PQQ. The spectrum of tryptophan fluorescence revealed that the local structure surrounding PQQ was not changed by D730N mutation. Based on these data, we assume that Asp-730 may occur close to PQQ and function as a proton (and also electron) donor to PQQ or acceptor from PQQH2. Substitutions of Gly-689, that are located at the end of a unique segment of GDH among homologous quinoprotein dehydrogenases, directed reduction of the affinity for PQQ or GDH activity. Therefore, the unique segment and Asp-730 may play a specific role for GDH, which might be related to the intramolecular electron transfer from PQQ to ubiquinone.

We analyzed environmental factors, family history of peptic ulcer, gastric acid secretion, and serum levels of pepsinogen I (PG I) and gastrin in 56 juvenile patients with duodenal ulcer and 39 normal teenage subjects. Basal acid output and maximal acid output were significantly higher in our duodenal ulcer patients than in controls without ulcer (both, p0.01), and patients with duodenal ulcer showed significantly higher serum levels of PG I and gastrin than the controls (both, p0.001). There were no significant differences in any environmental factor between the patients and controls. Fifteen of the 17 patients who had one or both parents with hyperpepsinogenemia I had high serum PG I levels. Over half of the duodenal ulcer patients had high serum gastrin levels, irrespective of family history of hypergastrinemia. Our findings suggest that hyperpepsinogenemia I and hypergastrinemia are important characteristics and that genetic background, particularly the inheritance of a gastric mucosal trait expressed as hyperpepsinogenemia I, is frequently involved in the pathogenesis of juvenile duodenal ulcer.

Nineteen-hour variation of postural sway, alertness and rectal temperature during sleep deprivation were studied. Alertness decreased gradually at night and remained low until morning. Postural sway in the eyes-closed condition increased during early morning. In six of the eight subjects the greatest sway was observed during the 3-h period when rectal temperature was at its minimum. It is suggested that unbearable sleepiness during sleep deprivation will give rise to measurable impairment of postural balance especially during the time zone of temperature nadir.