Transmission control protocol (TCP) and Ethernet have been widely used in readout systems. These protocols are de facto standards and have been implemented on standard operating systems. However, ...some small devices, e.g., front-end devices and detectors, are not capable of employing these protocols because of hardware size limitations. This paper describes a TCP processor for gigabit Ethernet with a circuit size suitable for implementing on a single field programmable gate array. The only peripheral device required is a single Ethernet physical layer device. The hardware was implemented and its TCP throughput was measured. The throughputs in both directions simultaneously were at the upper limits of gigabit Ethernet. A mechanism for slow control over user datagram protocol (UDP) is also provided. The processor described here allows adoption of TCP/Ethernet in small devices that have hardware size limitations.
Hyper Suprime-Cam: Camera dewar design Komiyama, Yutaka; Obuchi, Yoshiyuki; Nakaya, Hidehiko ...
Publications of the Astronomical Society of Japan,
01/2018, Letnik:
70, Številka:
SP1
Journal Article
Recenzirano
Abstract
This paper describes the detailed design of the CCD dewar and the camera system which is a part of the wide-field imager Hyper Suprime-Cam (HSC) on the 8.2 m Subaru Telescope. On the 1.°5 ...diameter focal plane (497 mm in physical size), 116 four-side buttable 2 k × 4 k fully depleted CCDs are tiled with 0.3 mm gaps between adjacent chips, which are cooled down to −100°C by two pulse tube coolers with a capability to exhaust 100 W heat at −100°C. The design of the dewar is basically a natural extension of Suprime-Cam, incorporating some improvements such as (1) a detailed CCD positioning strategy to avoid any collision between CCDs while maximizing the filling factor of the focal plane, (2) a spherical washers mechanism adopted for the interface points to avoid any deformation caused by the tilt of the interface surface to be transferred to the focal plane, (3) the employment of a truncated-cone-shaped window, made of synthetic silica, to save the back focal space, and (4) a passive heat transfer mechanism to exhaust efficiently the heat generated from the CCD readout electronics which are accommodated inside the dewar. Extensive simulations using a finite-element analysis (FEA) method are carried out to verify that the design of the dewar is sufficient to satisfy the assigned errors. We also perform verification tests using the actually assembled CCD dewar to supplement the FEA and demonstrate that the design is adequate to ensure an excellent image quality which is key to the HSC. The details of the camera system, including the control computer system, are described as well as the assembling process of the dewar and the process of installation on the telescope.
Abstract
The Hyper Suprime-Cam (HSC) is an 870 megapixel prime focus optical imaging camera for the 8.2 m Subaru telescope. The wide-field corrector delivers sharp images of 0${^{\prime\prime}_{.}}$2 ...(FWHM) in the HSC-i band over the entire 1${^{\circ}_{.}}$5 diameter field of view. The collimation of the camera with respect to the optical axis of the primary mirror is done with hexapod actuators, the mechanical accuracy of which is a few microns. Analysis of the remaining wavefront error in off-focus stellar images reveals that the collimation of the optical components meets design specifications. While there is a flexure of mechanical components, it also is within the design specification. As a result, the camera achieves its seeing-limited imaging on Maunakea during most of the time; the median seeing over several years of observing is 0${^{\prime\prime}_{.}}$67 (FWHM) in the i band. The sensors use p-channel, fully depleted CCDs of 200 μm thickness (2048 × 4176 15 μm square pixels) and we employ 116 of them to pave the 50 cm diameter focal plane. The minimum interval between exposures is 34 s, including the time to read out arrays, to transfer data to the control computer, and to save them to the hard drive. HSC on Subaru uniquely features a combination of a large aperture, a wide field of view, sharp images and a high sensitivity especially at longer wavelengths, which makes the HSC one of the most powerful observing facilities in the world.
Dual-specificity phosphatase 4 (DUSP4), a MAP kinase phosphatase, has been regarded as a tumor suppressor gene in several cancers. However, high-level expression of DUSP4 is occasionally observed in ...specific cancers and its functional significance in carcinogenesis is not fully understood. In the present study, we showed that downregulation of DUSP4 suppressed the proliferation of cancer cell lines exhibiting high expression of DUSP4 by inducing apoptosis and cell cycle arrest at G2/M phase. Expression microarray analyses and pathway analyses revealed that downregulation of DUSP4 activated the p53 signaling pathway, and might be involved in cell growth suppression. Aberrant accumulation of p53 and induction of p53 downstream target genes were further investigated. Furthermore, cell growth suppression following downregulation of DUSP4 was markedly attenuated in p53-deleted cells established using the CRISPR/Cas9 system. These findings suggest that constitutive expression of DUSP4 in cancer cells contributes to enhanced proliferation through escape from apoptosis and cell cycle arrest. We propose that DUSP4 could be a novel therapeutic target for cancers overexpressing it.
•Downregulation of DUSP4 leads to growth suppression in DUSP4-overexpressing cancer cells, independently of MAP kinase.•Cell cycle arrest and apoptosis are induced by downregulation of DUSP4.•Activation of p53 signaling pathway is involved in the growth suppression by downregulation of DUSP4.
It is widely accepted that aberrant activation of the Wnt signaling pathway is responsible for the development of precursor lesions of colorectal cancer (CRC). However, the molecular mechanisms ...involved in the process of progression from these precursor lesions to invasive lesions of CRC are not fully understood. Recently, we reported that constitutive activation of MAPK accompanied by downregulation of dual‐specificity phosphatase 4 (DUSP4), a MAPK phosphatase, contributes to the progression of precursor lesions in the pancreas. In this study, we found that downregulation of DUSP4 was related to constitutive activation of ERKs in CRC cells. Restoration of DUSP4 resulted in inactivation of ERKs, leading to suppression of both proliferation and invasiveness, as shown by treatment with an MEK inhibitor. Furthermore, immunohistochemistry revealed that DUSP4 expression was upregulated in the superficial region of CRC tissue, whereas it was significantly downregulated in the deep region. In contrast, ERKs in the deep region were markedly hyperactivated compared to those in the superficial region. These results suggest that activation of the MAPK signaling pathway caused by downregulation of DUSP4 is responsible for progression of CRCs and would be a promising therapeutic target.
DUSP4 was weakly and focally expressed in the nuclei of normal epithelium adjacent to cancer tissues, but was strongly and diffusely detected in nuclei of colorectal cancer cells in the superficial region. In contrast, nuclear expression of DUSP4 was significantly reduced in cells located in the deep region.
Constitutive activation of the mitogen‐activated protein kinase (MAPK) signaling pathway is essential for tumorigenesis of pancreatic ductal adenocarcinoma (PDAC). To date, however, almost all ...clinical trials of inhibitor targeting this pathway have failed to improve the outcome of patients with PDAC. We found that implanted MIA Paca2, a human PDAC cell line sensitive to a MAPK inhibitor, PD0325901, became refractory within a week after treatment. By comparing the expression profiles of MIA Paca2 before and after acquisition of the refractoriness to PD0325901, we identified clusterin (CLU) as a candidate gene involved. CLU was shown to be induced immediately after treatment with PD0325901 or expressed primarily in more than half of PDAC cell lines, enhancing cell viability by escaping from apoptosis. A combination of PD0325901 and CLU downregulation was found to synergistically or additively reduce the proliferation of PDAC cells. In surgically resected PDAC tissues, overexpression of CLU in cancer cells was observed immunohistochemically in approximately half of the cases studied. Collectively, our findings highlight the mechanisms responsible for the rapid refractory response to MEK inhibitor in PDAC cells, suggesting a novel therapeutic strategy that could be applicable to patients with PDAC using inhibitor targeting the MAPK signaling pathway and CLU.
Our findings highlight the mechanisms responsible for the rapid acquisition of resistance to MEK inhibitor in PDAC cells, suggesting a novel therapeutic strategy that could be applicable to patients with PDAC using inhibitor targeting the MAPK signaling pathway and CLU.
We herein report a case of melanoma differentiation-associated gene 5 (MDA5) antibody-positive dermatomyositis that developed in a patient with refractory gingivitis. The diagnosis of anti-MDA5 ...antibody-positive dermatomyositis was made based on a characteristic skin rash, weakness of proximal muscles, interstitial pneumonia, and positivity for anti-MDA5 antibody. The patient was started on triple therapy with high-dose prednisolone, tacrolimus, and intravenous cyclophosphamide. After treatment, the refractory gingivitis disappeared, and the other skin rash and interstitial lung disease also improved. In the diagnosis and treatment of anti-MDA5 antibody-positive dermatomyositis, it is necessary to pay attention to the intraoral findings, including the gingiva.
Background
Mongolia has the highest mortality rate of gastric cancer. The early detection of cancer and down-staging screening for high risk patients are essential. Therefore, we aimed to validate ...serum markers for stratifying patients for further management.
Methods
Endoscopy and histological examination were performed to determine high risk and gastric cancer patients. Rapid urease test, culture and histological tests were performed to diagnose
Helicobacter pylori
infection. Serum pepsinogen (PG) I and II and anti-
H. pylori
IgG were measured by ELISA. Receiver Operating Characteristic analysis was used to extract the best cut-off point.
Results
Totally 752 non-cancer and 50 consecutive gastric cancer patients were involved. The corpus chronic gastritis (72%: 36/50 vs. 56.4%: 427/752), corpus atrophy (42.0%: 21/50 vs. 18.2%: 137/752) and intestinal metaplasia (IM) (64.0%: 32/50 vs. 21.5%: 162/752) were significantly higher in gastric cancer than non-cancer patients, respectively. Therefore, corpus chronic gastritis, corpus atrophy and IM were considered as high risk disease. The best serum marker to predict the high risk status was PGI/II < 3.1 (sensitivity 67.2%, specificity 61%) and PGI/II further reduced to < 2.2 (sensitivity 66%, specificity 65.1%) together with PGI < 28 ng/mL (sensitivity 70%, specificity 70%) were the best prediction for gastric cancer. The best cut-off point to diagnose
H. pylori
infection was anti-
H. pylori
IgG > 8 U/mL. Multivariate analysis showed that anti-
H. pylori
IgG > 8 U/mL and PGI/II < 3.1 increased risk for high risk status and PGI/II < 3.1 remained to increase risk for gastric cancer.
Conclusion
The serum diagnosis using PGI/II < 3.1 cut-off value is valuable marker to predict high risk patients for population based massive screening.
We encountered a 78-year-old Japanese man with IgG4-related sialoadenitis complicated with marked eosinophilia. We diagnosed him with IgG4-RD (related disease) with a submandibular gland tumor, serum ...IgG4 elevation, IgG4-positive plasma cell infiltration, and storiform fibrosis. During follow-up after total incision of the submandibular gland, the peripheral eosinophil count was markedly elevated to 29,480/μL. The differential diagnosis of severe eosinophilia without IgG4-RD was excluded. The patient exhibited a prompt response to corticosteroid therapy. His peripheral blood eosinophil count was the highest ever reported among similar cases. We also review previous cases of IgG4-RD with severe eosinophilia.
Gastric cancer is an inflammation-related malignancy related to long-standing acute and chronic inflammation caused by infection with the human bacterial pathogen Helicobacter pylori. Inflammation ...can result in genomic instability. However, there are considerable data that H. pylori itself can also produce genomic instability both directly and through epigenetic pathways. Overall, the mechanisms of H. pylori-induced host genomic instabilities remain poorly understood. We used microarray screening of H. pylori-infected human gastric biopsy specimens to identify candidate genes involved in H. pylori-induced host genomic instabilities. We found upregulation of ATM expression in vivo in gastric mucosal cells infected with H. pylori. Using gastric cancer cell lines, we confirmed that the H. pylori-related activation of ATM was due to the accumulation of DNA double-strand breaks (DSBs). DSBs were observed following infection with both cag pathogenicity island (PAI)-positive and -negative strains, but the effect was more robust with cag PAI-positive strains. These results are consistent with the fact that infections with both cag PAI-positive and -negative strains are associated with gastric carcinogenesis, but the risk is higher in individuals infected with cag PAI-positive strains.
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