Human papillomavirus detected in female breast carcinomas in Japan

To investigate the aetiological role of human papillomavirus (HPV) in breast cancer, we examined the presence, genotype, viral load, and physical status of HPV in 124 Japanese female patients with breast carcinoma. Human papillomavirus presence was examined by PCR using SPF10 primers, and primer sets targeting the E6 region of HPV-16, -18, and -33. The INNO-LiPA HPV genotyping kit was used to determine genotype. Human papillomavirus DNA was detected in 26 (21%) breast carcinomas. The most frequently detected HPV genotype was HPV-16 (92%), followed by HPV-6 (46%), HPV-18 (12%), and HPV-33 (4%). In 11 normal epithelium specimens adjacent to 11 HPV-16-positive carcinomas, 7 were HPV-16-positive. However, none of the normal breast tissue specimens adjacent to HPV-negative breast carcinomas were HPV-positive. The real-time PCR analysis suggested the presence of integrated form of viral DNA in all HPV-16-positive samples, and estimated viral load was low with a geometric mean of 5.4 copies per 104 cells. In conclusion, although HPV DNA was detected in 26 (21%) breast carcinomas and, in all HPV-16-positive cases, the HPV genome was considered integrated into the host genome, their low viral loads suggest it is unlikely that integrated HPV is aetiologically involved in the development of Japanese breast carcinomas that we examined

Human papillomavirus in high- and low-risk areas of oesophageal squamous cell carcinoma in China

To examine the potential roles of human papillomavirus (HPV) in oesophageal squamous cell carcinoma (ESCC) development, we examined the presence of HPV DNA in paraffin-embedded ESCC tissues collected from two areas with different ESCC incidence rates in China, that is, Gansu (n=26) and Shandong (n=33), using PCR with SPF10 primers, or PCR with GP5+/GP6+ primers combined with Southern blot hybridisation. HPV genotype was determined by the INNO-LiPA HPV genotyping kit. HPV DNA was detected in 17 cases (65%) in Gansu, where ESCC incidence is much higher than in Shandong, where HPV was positive in two samples (6%). HPV genotypes 16 and 18 were detected in 79 and 16% of HPV-positive samples, respectively. Real-time PCR analysis suggested the presence of integrated form of HPV DNA in all the HPV-16-positive samples, but its viral load was estimated to be only <1–2 copies cell−1. We could not detect HPV 16/18 E6 protein expression by immunostaining in any of the HPV-16-positive samples. Neither p16INK4a nor p53 expression was related to HPV presence in ESCCs. Further studies seem warranted to examine the possible aetiological roles of HPV in ESCC

A mobile sensor network to map carbon dioxide emissions in urban environments

A method for directly measuring carbon dioxide (CO2) emissions using a mobile sensor network in cities at fine spatial resolution was developed and tested. First, a compact, mobile system was built using an infrared gas analyzer combined with open-source hardware to control, georeference, and log measurements of CO2 mixing ratios on vehicles (car, bicycles). Second, two measurement campaigns, one in summer and one in winter (heating season) were carried out. Five mobile sensors were deployed within a 1 × 12. 7 km transect across the city of Vancouver, BC, Canada. The sensors were operated for 3.5 h on pre-defined routes to map CO2 mixing ratios at street level, which were then averaged to 100  ×  100 m grid cells. The averaged CO2 mixing ratios of all grids in the study area were 417.9 ppm in summer and 442.5 ppm in winter. In both campaigns, mixing ratios were highest in the grid cells of the downtown core and along arterial roads and lowest in parks and well vegetated residential areas. Third, an aerodynamic resistance approach to calculating emissions was used to derive CO2 emissions from the gridded CO2 mixing ratio measurements in conjunction with mixing ratios and fluxes collected from a 28 m tall eddy-covariance tower located within the study area. These measured emissions showed a range of −12 to 226 CO2 ha−1 h−1 in summer and of −14 to 163 kg CO2 ha−1 h−1 in winter, with an average of 35.1 kg CO2 ha−1 h−1 (summer) and 25.9 kg CO2 ha−1 h−1 (winter). Fourth, an independent emissions inventory was developed for the study area using buildings energy simulations from a previous study and routinely available traffic counts. The emissions inventory for the same area averaged to 22.06 kg CO2 ha−1 h−1 (summer) and 28.76 kg CO2 ha−1 h−1 (winter) and was used to compare against the measured emissions from the mobile sensor network. The comparison on a grid-by-grid basis showed linearity between CO2 mixing ratios and the emissions inventory (R2 = 0. 53 in summer and R2 = 0. 47 in winter). Also, 87 % (summer) and 94 % (winter) of measured grid cells show a difference within ±1 order of magnitude, and 49 % (summer) and 69 % (winter) show an error of less than a factor 2. Although associated with considerable errors at the individual grid cell level, the study demonstrates a promising method of using a network of mobile sensors and an aerodynamic resistance approach to rapidly map greenhouse gases at high spatial resolution across cities. The method could be improved by longer measurements and a refined calculation of the aerodynamic resistance