Current status of the CLIO project

CLIO (Cryogenic Laser Interferometer Observatory) is a Japanese gravitational wave detector project. One of the main purposes of CLIO is to demonstrate thermal-noise suppression by cooling mirrors for a future Japanese project, LCGT (Large-scale Cryogenic Gravitational Telescope). The CLIO site is in Kamioka mine, as is LCGT. The progress of CLIO between 2005 and 2007 (room- and cryogenic-temperature experiments) is introduced in this article. In a room-temperature experiment, we made efforts to improve the sensitivity. The current best sensitivity at 300 K is about $6 \times 10^{-21} /\sqrt{\rm Hz}$ around 400 Hz. Below 20 Hz, the strain (not displacement) sensitivity is comparable to that of LIGO, although the baselines of CLIO are 40-times shorter (CLIO: 100m, LIGO: 4km). This is because seismic noise is extremely small in Kamioka mine. We operated the interferometer at room temperature for gravitational wave observations. We obtained 86 hours of data. In the cryogenic experiment, it was confirmed that the mirrors were sufficiently cooled (14 K). However, we found that the radiation shield ducts transferred 300K radiation into the cryostat more effectively than we had expected. We observed that noise caused by pure aluminum wires to suspend a mirror was suppressed by cooling the mirror.Comment: 8 pages, 9 figures. Amaldi7 proceedings, J. Phys.: Conf. Ser. (accepted

Current status of Japanese detectors

Current status of TAMA and CLIO detectors in Japan is reported in this article. These two interferometric gravitational-wave detectors are being developed for the large cryogenic gravitational wave telescope (LCGT) which is a future plan for detecting gravitational wave signals at least once per year. TAMA300 is being upgraded to improve the sensitivity in low frequency region after the last observation experiment in 2004. To reduce the seismic noises, we are installing new seismic isolation system, which is called TAMA Seismic Attenuation System, for the four test masses. We confirmed stable mass locks of a cavity and improvements of length and angular fluctuations by using two SASs. We are currently optimizing the performance of the third and fourth SASs. We continue TAMA300 operation and R&D studies for LCGT. Next data taking in the summer of 2007 is planned. CLIO is a 100-m baseline length prototype detector for LCGT to investigate interferometer performance in cryogenic condition. The key features of CLIO are that it locates Kamioka underground site for low seismic noise level, and adopts cryogenic Sapphire mirrors for low thermal noise level. The first operation of the cryogenic interferometer was successfully demonstrated in February of 2006. Current sensitivity at room temperature is close to the target sensitivity within a factor of 4. Several observation experiments at room temperature have been done. Once the displacement noise reaches at thermal noise level of room temperature, its improvement by cooling test mass mirrors should be demonstrated.Comment: 6 pages, 5 figures, Proceedings of GWDAW-1

Evaluation of gene amplification and protein expression of HER-2/neu in esophageal squamous cell carcinoma using Fluorescence in situ Hybridization (FISH) and immunohistochemistry

<p>Abstract</p> <p>Background</p> <p>Esophageal squamous cell carcinoma (ESCC) is the sixth most frequent neoplasia in Brazil. It is usually associated with a poor prognosis because it is often at an advanced stage when diagnosed and there is a high frequency of lymph node metastases. It is important to know what prognostic factors can facilitate diagnosis, optimize therapeutic decisions, and improve the survival of these patients. A member of the epidermal growth factor receptor (EGFR) family, c-erbB-2, has received much attention because of its therapeutic implications; however, few studies involving fluorescence <it>in situ </it>hybridization (FISH) analysis of HER-2/neu gene amplification and protein expression in ESCC have been conducted. The aim of this study was to verify the presence of HER-2/neu gene amplification using FISH, and to correlate the results with immunohistochemical expression and clinical-pathological findings.</p> <p>Methods</p> <p>One hundred and ninety-nine ESCC cases were evaluated using the Tissue Microarray (TMA) technique. A polyclonal antibody against c-erbB-2 was used for immunohistochemistry. Analyses were based on the membrane staining pattern. The results were classified according to the Herceptest criteria (DAKO): negative (0/1+), potential positive (2+) and positive (3+). The FISH reactions were performed according to the FISH HER2 PharmDx (DAKO) protocol. In each case, 100 tumor nuclei were evaluated. Cases showing a gene/CEN17 fluorescence ratio ≥ 2 were considered positive for gene amplification.</p> <p>Results</p> <p>The c-erbB-2 expression was negative in 117/185 cases (63.2%) and positive in 68 (36.8%), of which 56 (30.3%) were 2+ and 12 (6.5%) were 3+. No significant associations were found among protein expression, clinicopathological data and overall survival. Among the 47 cases analyzed, 38 (80.9%) showed no gene amplification while 9 (19.1%) showed amplification, as demonstrated by FISH. Cases that were negative (0/1+) and potential positive (2+) for c-erbB-2 expression by immunohistochemistry showed no gene amplification. However, all cases with gene amplification were positive (3+) by immunohistochemistry. According to univariate analysis, there was a significant difference (p = 0.003) in survival rates when cases with and without HER-2/neu amplification were compared.</p> <p>Conclusion</p> <p>Our data demonstrate the correspondence between gene amplification and protein expression of HER-2/neu. Gene amplification is an indicator of poor prognosis in ESCC.</p

Mutations in the TRKA/NGF receptor gene in patients with congenital insensitivity to pain with anhidrosis

Congenital insensitivity to pain with anhidrosis (CIPA; MIM 256800) is an autosomal-recessive disorder characterized by recurrent episodes of unexplained fever, anhidrosis (absence of sweating) and absence of reaction to noxious stimuli, self-mutilating behaviour and mental retardation1−3. The genetic basis for CIPA is unknown. Nerve growth factor (NGF) induces neurite outgrowth and promotes survival of embryonic sensory and sympathetic neurons4. Mice lacking the gene for TrkA, a receptor tyrosine kinase for NGF5,6, share dramatic phenotypic features of CIPA, including loss of responses to painful stimuli, although anhidrosis is not apparent in these animals7. We therefore considered the human TRKA homologue as a candidate for the CIPA gene. The mRNA and genomic DNA encoding TRKA were analysed in three unrelated CIPA patients who had consanguineous parents. We detected a deletion-, splice- and missense-muta-tion in the tyrosine kinase domain in these three patients. Our findings strongly suggest that defects in TRKA cause CIPA and that the NGF−TRKA system has a crucial role in the development and function of the nociceptive reception as well as establishment of thermoregulation via sweating in humans. These results also implicate genes encoding other TRK and neurotrophin family members as candidates for developmental defect(s) of the nervous system

Can human amblyopia be treated in adulthood?

Amblyopia is a common visual disorder that results in a spatial acuity deficit in the affected eye. Orthodox treatment is to occlude the unaffected eye for lengthy periods, largely determined by the severity of the visual deficit at diagnosis. Although this treatment is not without its problems (poor compliance, potential to reduce binocular function, etc) it is effective in many children with moderate to severe amblyopia. Diagnosis and initiation of treatment early in life are thought to be critical to the success of this form of therapy. Occlusion is rarely undertaken in older children (more than 10 years old) as the visual benefits are considered to be marginal. Therefore, in subjects where occlusion is not effective or those missed by mass screening programs, there is no alternative therapy available later in life. More recently, burgeoning evidence has begun to reveal previously unrecognized levels of residual neural plasticity in the adult brain and scientists have developed new genetic, pharmacological, and behavioral interventions to activate these latent mechanisms in order to harness their potential for visual recovery. Prominent amongst these is the concept of perceptual learning—the fact that repeatedly practicing a challenging visual task leads to substantial and enduring improvements in visual performance over time. In the normal visual system the improvements are highly specific to the attributes of the trained stimulus. However, in the amblyopic visual system, learned improvements have been shown to generalize to novel tasks. In this paper we ask whether amblyopic deficits can be reduced in adulthood and explore the pattern of transfer of learned improvements. We also show that developing training protocols that target the deficit in stereo acuity allows the recovery of normal stereo function even in adulthood. This information will help guide further development of learning-based interventions in this clinical group