Performance Evaluation of Greenhouse Having Passive or Active Heating in Different Climatic Zones of India

Rosana G. Moreira, Editor-in-Chief; Texas A&M UniversityThis is a paper from International Commission of Agricultural Engineering (CIGR, Commission Internationale du Genie Rural) E-Journal Volume 9 (2007): Performance Evaluation of Greenhouse Having Passive or Active Heating in Different Climatic Zones of India. Manuscript EE 06 011. Vol. IX. May, 2007

Thermal Performance of an Adobe Structure Integrated with an Earth-Air Heat Exchanger: An Experimental Study

In this paper an attempt has been made to study annual thermal performance of an adobe structure with an effective area of 53 m2 located at solar energy park at Indian Institute of Technology Delhi, New Delhi ( 280 35' N,770 12' E ), India. Such houses are suitable for rural areas for various reasons e.g. storage of grains, low energy consumption, thermal comfort, made by local materials and environmental friendly. Experiments have been conducted during June 2004-May 2005 to measure hourly variation of room air temperature of room with an earth-air heat exchanger, untreated room and room with cross ventilation. Hourly variation of solar intensity, ambient temperature, inlet-outlet temperature of an earth-air heat exchanger has been measured. Analysis has been done by calculating average and maximum\minimum temperature of each room in each month. It has been found that room equipped with an earth-air heat exchanger gives best comfort among all other. It is seen that temperature of room with an earthair heat exchanger is 6.5 oC more and 3.0 oC less than temperature of untreated room in December and May month. Experimental uncertainties for December and May for room with an earth-air heat exchanger have been found out 11.9 and 3.0 % respectively

Microwave photovoltage and photoresistance effects in ferromagnetic microstrips

We investigate the dc electric response induced by ferromagnetic resonance in ferromagnetic Permalloy (Ni80Fe20) microstrips. The resulting magnetization precession alters the angle of the magnetization with respect to both dc and rf current. Consequently the time averaged anisotropic magnetoresistance (AMR) changes (photoresistance). At the same time the time-dependent AMR oscillation rectifies a part of the rf current and induces a dc voltage (photovoltage). A phenomenological approach to magnetoresistance is used to describe the distinct characteristics of the photoresistance and photovoltage with a consistent formalism, which is found in excellent agreement with experiments performed on in-plane magnetized ferromagnetic microstrips. Application of the microwave photovoltage effect for rf magnetic field sensing is discussed.Comment: 16 pages, 15 figure

The value of rapid functional assays of germline p53 status in LFS and LFL families

We have tested two rapid assays of p53 function, namely the apoptotic assay and the FASAY as means of detecting germline p53 mutations in members of Li–Fraumeni and Li–Fraumeni-like families. Results of the functional assays have been compared with direct sequencing of all 11 exons of the p53 gene. The results show good agreement between the two functional assays and between them and sequencing. No false-positives or negatives were seen with either functional assay although the apoptotic assay gave one borderline result for an individual without a mutation. As an initial screen the apoptotic assay is not only rapid but inexpensive and very simple to perform. It would be expected to detect any germline defect that leads to loss of p53 function. The apoptotic assay could be ideal as a means of prescreening large numbers of samples and identifying those that require further investigation. The FASAY detects mutations in exons 4–10, is rapid and distinguishes between functionally important and silent mutations. © 2000 Cancer Research Campaig

CHEK2 variants in susceptibility to breast cancer and evidence of retention of the wild type allele in tumours

We have recently shown that the CHEK2*1100delC mutation acts as a low penetrance breast cancer susceptibility allele. To investigate if other CHEK2 variants confer an increased risk of breast cancer, we have screened an affected individual with breast cancer from 68 breast cancer families. Five of these individuals were found to harbour germline variants in CHEK2. Three carried the 1100delC variant (4%). One of these three individuals also carried the missense variant, Arg180His. In the other two individuals, missense variants, Arg117Gly and Arg137Gln, were identified. These two missense variants reside within the Forkhead-associated domain of CHEK2, which is important for the function of the expressed protein. None of these missense variants were present in 300 healthy controls. Microdissected tumours with a germline mutation showed loss of the mutant allele suggesting a mechanism for tumorigenesis other than a loss of the wild type allele. This study provides further evidence that sequence variation in CHEK2 is associated with an increased risk of breast cancer, and implies that tumorigenesis in association with CHEK2 mutations does not involve loss of the wild type allele

Analysis of CHK2 in vulval neoplasia

Structure and expression of the Rad53 homologue CHK2 were studied in vulval neoplasia. We identified the previously described silent polymorphism at codon 84 (A>G at nucleotide 252) in the germ-line of six out of 72, and somatic mutations in two out of 40 cases of vulval squamous cell carcinomas and none of 32 cases of vulval intraepithelial neoplasia. One mutation introduced a premature stop codon in the kinase domain of CHK2, whereas the second resulted in an amino acid substitution in the kinase domain. The two squamous cell carcinomas with mutations in CHK2 also expressed mutant p53. A CpG island was identified close to the putative CHK2 transcriptional start site, but methylation-specific PCR did not detect methylation in any of 40 vulval squamous cell carcinomas, irrespective of human papillomavirus or p53 status. Consistent with this observation, no cancer exhibited loss of CHK2 expression at mRNA or protein level. Taken together, these observations reveal that genetic but not epigenetic changes in CHK2 occur in a small proportion of vulval squamous cell carcinomas

The CHEK2*1100delC mutation has no major contribution in oesophageal carcinogenesis

In response to DNA damage, the cell cycle checkpoint kinase 2 (CHEK2) may phosphorylate p53, Cdc25A and Cdc25C, and regulate BRCA1 function, leading to cell cycle arrest and DNA repair. The truncating germline mutation CHEK2*1100delC abrogates kinase activity and confers low-penetrance susceptibility to breast cancer. We found CHEK2*1100delC in 0.5% of 190 oesophageal squamous cell carcinomas and in 1.5% of 196 oesophageal adenocarcinomas. In addition, we observed the mutation in 3.0% of 99 Barrett's metaplasias and 1.5% of 66 dysplastic Barrett's epithelia, both known precursor lesions of oesophageal adenocarcinoma. Since CHEK2*1100delC mutation frequencies did not significantly differ among oesophageal squamous cell carcinomas, adenocarcinomas and (dysplastic) Barrett's epithelia, as compared to healthy individuals, we conclude that the CHEK2*1100delC mutation has no major contribution in oesophageal carcinogenesis

Mutation analysis of the CHK2 gene in breast carcinoma and other cancers

BACKGROUND: Mutations in the CHK2 gene at chromosome 22q12.1 have been reported in families with Li-Fraumeni syndrome. Chk2 is an effector kinase that is activated in response to DNA damage and is involved in cell-cycle pathways and p53 pathways. METHODS: We screened 139 breast tumors for loss of heterozygosity at chromosome 22q, using seven microsatellite markers, and screened 119 breast tumors with single-strand conformation polymorphism and DNA sequencing for mutations in the CHK2 gene. RESULTS: Seventy-four of 139 sporadic breast tumors (53%) show loss of heterozygosity with at least one marker. These samples and 45 tumors from individuals carrying the BRCA2 999del5 mutation were screened for mutations in the CHK2 gene. In addition to putative polymorphic regions in short mononucleotide repeats in a non-coding exon and intron 2, a germ line variant (T59K) in the first coding exon was detected. On screening 1172 cancer patients for the T59K sequence variant, it was detected in a total of four breast-cancer patients, two colon-cancer patients, one stomach-cancer patient and one ovary-cancer patient, but not in 452 healthy individuals. A tumor-specific 5' splice site mutation at site +3 in intron 8 (TTgt [a → c]atg) was also detected. CONCLUSION: We conclude that somatic CHK2 mutations are rare in breast cancer, but our results suggest a tumor suppressor function for CHK2 in a small proportion of breast tumors. Furthermore, our results suggest that the T59K CHK2 sequence variant is a low-penetrance allele with respect to tumor growth