The significance of recent interest rates movements

Interest rates

Another recession, but different

Recessions

A primer on the consumer price index

Consumer price indexes

The link between money and prices : 1971-76

Money theory ; Money ; Prices

Real money balances: a misleading indicator of monetary actions

Money ; Monetary policy - United States

Real money balances: a good forecasting device and a good policy target?

Money ; Monetary policy - United States

Curbing price expectations: the key to inflation control

Inflation (Finance)

Isoprene Emission and Carbon Dioxide Protect Aspen Leaves from Heat Stress

High temperature, especially above 35oC, is known to reduce leaf photosynthetic rate in many tree species. This study investigated the effect of high temperature on isoprene-emitting (aspen) and non- emitting (birch) trees under ambient and elevated CO2 under open field conditions. Aspen trees tolerate heat better than birch trees and elevated CO2 protects both species against moderate heat stress. The increased thermotolerance in aspen trees compared to the birch trees may result from the aspen's ability to produce isoprene. Elevated CO2 increased carboxylation capacity, photosynthetic electron transport capacity and triose phosphate use in both birch and aspen trees. High temperature decreased all of these parameters in birch regardless of CO2 treatment but only photosynthetic electron transport and triose phosphate use at ambient CO2 were reduced in aspen. As temperature rises, non-isoprene-emitting trees will be at a disadvantage and biological diversity and species richness might be lost in some ecosystems. Our results indicate that isoprene emitting tree species will have an advantage over non-isoprene emitting ones under high temperatures

Association between human papillomavirus and primary lung cancer – a systematic review and pilot study

In this systematic review conducted on 73 studies that provided information on HPV prevalence in primary lung cancer tissue examined by PCR the overall HPV prevalence detected was 13.6 %. This rate was lower than in most systematic reviews made. A possible explanation might be that only studies using PCR were included while studies using ISH are discussed to detect higher prevalence. The HPV prevalence was analyzed for Europe, Asia and The Americas since no studies from Australia or Africa met the inclusion criteria. The highest HPV prevalence was detected in Asia followed by The Americas and Europe. This is in concordance with the information available in the literature even though no explanation has been found to this day. A geographic distribution as well as an ethnic component to HPV infection in lung cancer have been discussed. In a subgroup analysis researching HPV 16 and 18 prevalence in the three continents of which studies were included the difference was statistically significant in all of them. HPV 16 prevalence was higher on all three continents. Overall HPV prevalence 16 and 18 was 6.0 % and 3.2 % respectively which was statistically highly significant as well (p<0.01). In our review HPV detection was more strongly associated with SCC than with AC. The difference was statistically significant. (18.6 % vs. 9.6 %, p<0.01) Even though the tissue processing method (FFPE vs. fresh frozen) did not result in a statistical difference in the detected HPV prevalence the time-period in which the analysis was made (1990s vs. 21st century) resulted in a statistically highly significant difference in the HPV prevalence that was detected (p=0.9 vs. p<0.01 respectively). The difference between HPV prevalence in the cancer and the control group in our analysis was statistically highly significant (31.3 % vs. 5.4 %, p<0.01) This result has been found in other systematic reviews as well which has led many authors to discuss a possible association between primary lung cancer and HPV infection. Still the most important modifiable risk factor for lung cancer is smoking. Therefore smoking cessation has to remain one of the most important goals in lung cancer prevention. Mechanisms behind lung cancer development are still not fully understood. Neither are there established screening methods that allow earlier diagnosis. The information in our systematic review and in other publications suggests that HPV infection could play a role in lung cancer development but many questions are still unanswered. Most of the studies published used PCR on HPV DNA to determine the HPV prevalence in primary lung cancer specimens. Proof of HPV DNA in tumor samples is not enough evidence to prove a causal relationship between HPV and lung cancer development. One way to collect further information is to test for oncoprotein expression or mRNA. Another way is to confirm that HPV DNA is in fact integrated into the tumor genome. Only few studies using these methods have been done and more data will have to be gathered before a definitive decision can be made. Another point that cannot yet be answered is why there seems to be a geographic difference in HPV prevalence in lung cancer. All of the published systematic reviews and meta-analysis published found the highest HPV prevalence in Asia which is in concordance with our own results. No explanation for this has been found. Some studies have discussed whether HPV is not an independent risk factor for lung cancer but a co-factor. In many studies HPV is more strongly related with SCC which is known to have a strong correlation with smoking. The very low detection of HPV in SCLC which has a very strong correlation with smoking behavior as well can be considered as a counterargument. In contrast other studies have found a very high HPV prevalence in nonsmoking females with adenocarcinoma. Many different possible infection routes have been discussed. Based on todays knowledge HPV infection does not cause viremia even though that seems to be the most likely way of infection. Because of the given anatomy a direct infection of the bronchial epithelium seems unlikely. The way in which HPV enters host cells has not yet been fully understood either. Further research should be done on the large heterogeneity of HPV prevalence worldwide. Some of the possible influencing factors might be e.g. different PCR protocols, different PCR primers used or differences in the host factors. In conclusion further research has to be done most of all to examine the causality of HPV prevalence in lung cancer