img src="http://cdn.thesuperficial.com//bfm_gallery/2008/12/1202 Brad Pitt Today/post_image/post_image-1202_brad_pitt_today_00.jpg" border="0"br Brad Pitt sat down for an interview this morning in New Orleans with a href="http://today.msnbc.msn.com/id/28000192/"The Today Show's/a Ann Curry (a href="http://thesuperficial.com/2008/12/brad_pitt_today_show.php"Video after the jump/a). He's currently in the 9th Ward building affordable solar-powered houses for Hurricane Katrina victims. But that shit's for suckers; Let's talk about those Brangelina babies! Here's some excerpts of the interviews including a fake one. See if you guess which one it is: strongOn raising six kids:/strong “I look at my sons and my daughters, and one's from Vietnam and one's from Cambodia and one's from Ethiopia, and ... they're all brothers and sisters. And they're fighting, they're laughing, they're going into hysterics and staying up late, and they're messing with their parents, and they're driving me crazy and I'm really proud." strongOn his reluctance to discuss his family in interviews:/strong “It just gets cheapened somehow, as it goes through the filters in the airwaves,” he explained. “And some things you just want to keep close.” strongOn the media:/strong "Listen, if I single-handedly rebuild New Orleans into a thriving metropolis complete with flying cars, then will you people please forget that I cheated on Jennifer Aniston and am criminally less sexy than that guy who writes The Superficial. It's embarrassing." strongOn getting married to Angelina Jolie:/strong “If we feel it’s important to our kids, we’ll do so.” Hope you put your thinking caps on! smallstrongAnswer:/strong “If we feel it’s important to our kids, we’ll do so.” Ha ha ha! No, seriously, who fell for that one? You might want to get checked for tumors./small div style="width: 425px; margin: 0 0 0 30px; padding: 0;"ul style="list-style-type: none; display: block; width: 425px; margin: 0; padding: 0;"li style="display: block; float: left; width: 90px; height: 134px; margin: 0; padding: 0 10px 10px 0;"a href="http://thesuperficial.com/2008/12/brad_pitt_today_show.php" style="display: block; width: 90px; height: 134px; background: #CCC; overflow: hidden; margin: 0; padding: 0;"img src="http://cdn.thesuperficial.com//bfm_gallery/2008/12/1202 Brad Pitt Today/gallery_thumb/gallery_thumb-1202_brad_pitt_today_00.jpg" style="display: block; border: 1px solid #cccccc; width: 88px; margin: 0; padding: 0;"/a/lili style="display: block; float: left; width: 90px; height: 134px; margin: 0; padding: 0 10px 10px 0;"a href="http://thesuperficial.com/2008/12/brad_pitt_today_show.php?bfm_index=1" style="display: block; width: 90px; height: 134px; background: #CCC; overflow: hidden; margin: 0; padding: 0;"img src="http://cdn.thesuperficial.com//bfm_gallery/2008/12/1202 Brad Pitt Today/gallery_thumb/gallery_thumb-1202_brad_pitt_today_01.jpg" style="display: block; border: 1px solid #cccccc; width: 88px; margin: 0; padding: 0;"/a/lili style="display: block; float: left; width: 90px; height: 134px; margin: 0; padding: 0 10px 10px 0;"a href="http://thesuperficial.com/2008/12/brad_pitt_today_show.php?bfm_index=2" style="display: block; width: 90px; height: 134px; background: #CCC; overflow: hidden; margin: 0; padding: 0;"img src="http://cdn.thesuperficial.com//bfm_gallery/2008/12/1202 Brad Pitt Today/gallery_thumb/gallery_thumb-1202_brad_pitt_today_02.jpg" style="display: block; border: 1px solid #cccccc; width: 88px; margin: 0; padding: 0;"/a/lili style="display: block; float: left; width: 90px; height: 134px; margin: 0; padding: 0 10px 10px 0;"a href="http://thesuperficial.com/2008/12/brad_pitt_today_show.php?bfm_index=3" style="display: block; width: 90px; height: 134px; background: #CCC; overflow: hidden; margin: 0; padding: 0;"img src="http://cdn.thesuperficial.com//bfm_gallery/2008/12/1202 Brad Pitt Today/gallery_thumb/gallery_thumb-1202_brad_pitt_today_03.jpg" style="display: block; border: 1px solid #cccccc; width: 88px; margin: 0; padding: 0;"/a/li/uldiv style="clear: left;"/div/div div class = "credit"Photos: a href="http://www.splashnewsonline.com"Splash News/a/div pa href="http://feedads.googleadservices.com/~a/lC4o6jO5Tsb0jxFCa9V9zlMcZxI/a"img src="http://feedads.googleadservices.com/~a/lC4o6jO5Tsb0jxFCa9V9zlMcZxI/i" border="0" ismap="true"/img/a/pimg src="http://feedproxy.google.com/~r/thesuperficial/SNxk/~4/WqNwYsIc8Xk" height="1" width="1"/

Spanish golf legend Seve Ballesteros is stable following a fourth and "scheduled" brain operation at Madrid's La Paz hospital as he battles back from a malignant tumor.img src="http://feedproxy.google.com/~r/rss/edition_sport/~4/dCFlBzLNOOk" height="1" width="1"/

iAdvances in experimental medicine and biology, Vol. 630 (2008), pp. 35-51./ibr /br /Cancer is one of the leading causes of human death and belongs to the group of main chronic noncommunicable diseases (NCD). Certain specific features ofNCD have raised the concept of 'normal' and 'successful' aging. The apparent paradox of simultaneous increase with aging of the diseases connected with estrogen deficiency as well as with estrogenic excess can be explained by the existence of the phenomenon of the switching of estrogen effects. An isolated or combined with the weakening of hormonal effect increase in genotoxic action of estrogens can modify the course ofage-associated pathology. In particular, such changes in estrogen effect may alter the biology of tumors to make them less favorable/more aggressive. Two other endocrine-genotoxic switchings (EGS) involving phenomena ofJanus (dual) function of glucose and adipogenotoxicosis may produce similar influences on tumor and other NCD biology. These three phenomena form a'basic triad' and can act independently of each other or in concert. EGS and their inductors may serve as targets for prevention and, probably, treatment of main noncommunicable diseases. The measures to correct components of the 'triad' can be divided into several groups aimed to optimally orchestrate the balance between endocrine and DNA-damagingeffects of estrogens, glucose and adipose tissue-related factors.br /iLM Berstein/i

iCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, Vol. 11, No. 10 Pt 1. (October 2002), pp. 953-971./ibr /br /Animal experiments and in vitro studies have shown that compounds found in tobacco smoke, such as polycyclic hydrocarbons, aromatic amines, and N-nitrosamines, may induce mammary tumors. The findings of smoking-specific DNA adducts and p53 gene mutations in the breast tissue of smokers also support the biological plausibility of a positive association between cigarette smoking and breast cancer, as does the detection of carcinogenic activity in breast fluid. However, epidemiological studies conducted over the past few decades have variably shown positive, inverse, or null associations. To help reconcile the discrepant findings, epidemiologists have paid increasing attention to measures of exposure to tobacco smoke that might be of the greatest etiological importance, to aspects of the smoker that might modify the association between smoking and breast cancer risk, and to the potentially different associations that might exist with different types of breast tumors, such as those with and without estrogen or progesterone receptors. Overall, the results of these studies suggest that smoking probably does not decrease the risk and indeed suggest that there may be an increased breast cancer risk with smoking of long duration, smoking before a first full-term pregnancy, and passive smoking. These findings require confirmation in future studies, as do suggestions of increased risk among women with certain genotypes.br /iPD Terry, TE Rohan/i

iInternational journal of cancer. Journal international du cancer, Vol. 122, No. 8. (15 April 2008), pp. 1832-1841./ibr /br /The association between alcohol consumption and an increased risk of breast cancer has been established. It is still unclear however, whether this relationship differs across the estrogen receptor (ER) and progesterone receptor (PR) tumors subtypes. To provide a quantitative assessment of the association between alcohol intake and the risk of ER-/PR-defined breast cancer, we conducted a meta-analysis of cohort and case-control studies. Studies were identified by a literature search of PubMed through April 20, 2007 and by searching the reference lists of relevant articles. Summarized risk estimates (REs) with 95% confidence intervals (CIs) were calculated using random-effects models. The summarized results of the meta-analysis comparing the highest versus the lowest consumption categories showed statistically significant higher risks of developing all ER+ (27%), all ER- (14%), ER+PR+ (22%) and ER+PR- (28%), but not ER-PR- tumors. The dose-response meta-analysis showed that an increase in alcohol consumption of 10 g of ethanol per day was associated with statistically significant increased risks for all ER+ (12%), all ER- (7%), ER+PR+ (11%) and ER+PR- (15%), but not ER-PR-. A statistically significant heterogeneity of the REs across all ER+ versus ER-PR- was observed (p(heterogeneity) = 0.02). The summarized results from studies with adjustment for postmenopausal hormone use, body mass index and family history of breast cancer were higher and statistically significantly different from those without. The observed positive associations with alcohol for ER+PR+ and ER+PR- tumors cannot be explained by estrogen-dependent pathway only. Further studies need to clarify the biological mechanisms.br /iR Suzuki, N Orsini, L Mignone, S Saji, A Wolk/i

iNutrition and cancer, Vol. 21, No. 2. (1994), pp. 113-131./ibr /br /International variations in cancer rates have been attributed, at least in part, to differences in dietary intake. Recently, it has been suggested that consumption of soyfoods may contribute to the relatively low rates of breast, colon, and prostate cancers in countries such as China and Japan. Soybeans contain a number of anticarcinogens, and a recent National Cancer Institute workshop recommended that the role of soyfoods in cancer prevention be investigated. In this review, the hypothesis that soy intake reduces cancer risk is considered by examining relevant in vitro, animal, and epidemiological data. Soybeans are a unique dietary source of the isoflavone genistein, which possesses weak estrogenic activity and has been shown to act in animal models as an antiestrogen. Genistein is also a specific inhibitor of protein tyrosine kinases; it also inhibits DNA topoisomerases and other critical enzymes involved in signal transduction. In vitro, genistein suppresses the growth of a wide range of cancer cells, with IC50 values ranging from 5 to 40 microM (1-10 micrograms/ml). Of the 26 animal studies of experimental carcinogenesis in which diets containing soy or soybean isoflavones were employed, 17 (65%) reported protective effects. No studies reported soy intake increased tumor development. The epidemiological data are also inconsistent, although consumption of nonfermented soy products, such as soymilk and tofu, tended to be either protective or not associated with cancer risk; however, no consistent pattern was evident with the fermented soy products, such as miso. Protective effects were observed for both hormone- and nonhormone-related cancers. While a definitive statement that soy reduces cancer risk cannot be made at this time, there is sufficient evidence of a protective effect to warrant continued investigation.br /iMJ Messina, V Persky, KD Setchell, S Barnes/i

iJAMA : the journal of the American Medical Association, Vol. 295, No. 6. (8 February 2006), pp. 629-642./ibr /br /CONTEXT: The hypothesis that a low-fat dietary pattern can reduce breast cancer risk has existed for decades but has never been tested in a controlled intervention trial. OBJECTIVE: To assess the effects of undertaking a low-fat dietary pattern on breast cancer incidence. DESIGN AND SETTING: A randomized, controlled, primary prevention trial conducted at 40 US clinical centers from 1993 to 2005. PARTICIPANTS: A total of 48,835 postmenopausal women, aged 50 to 79 years, without prior breast cancer, including 18.6% of minority race/ethnicity, were enrolled. INTERVENTIONS: Women were randomly assigned to the dietary modification intervention group (40% [n = 19,541]) or the comparison group (60% [n = 29,294]). The intervention was designed to promote dietary change with the goals of reducing intake of total fat to 20% of energy and increasing consumption of vegetables and fruit to at least 5 servings daily and grains to at least 6 servings daily. Comparison group participants were not asked to make dietary changes. MAIN OUTCOME MEASURE: Invasive breast cancer incidence. RESULTS: Dietary fat intake was significantly lower in the dietary modification intervention group compared with the comparison group. The difference between groups in change from baseline for percentage of energy from fat varied from 10.7% at year 1 to 8.1% at year 6. Vegetable and fruit consumption was higher in the intervention group by at least 1 serving per day and a smaller, more transient difference was found for grain consumption. The number of women who developed invasive breast cancer (annualized incidence rate) over the 8.1-year average follow-up period was 655 (0.42%) in the intervention group and 1072 (0.45%) in the comparison group (hazard ratio, 0.91; 95% confidence interval, 0.83-1.01 for the comparison between the 2 groups). Secondary analyses suggest a lower hazard ratio among adherent women, provide greater evidence of risk reduction among women having a high-fat diet at baseline, and suggest a dietary effect that varies by hormone receptor characteristics of the tumor. CONCLUSIONS: Among postmenopausal women, a low-fat dietary pattern did not result in a statistically significant reduction in invasive breast cancer risk over an 8.1-year average follow-up period. However, the nonsignificant trends observed suggesting reduced risk associated with a low-fat dietary pattern indicate that longer, planned, nonintervention follow-up may yield a more definitive comparison. CLINICAL TRIALS REGISTRATION: ClinicalTrials.gov Identifier: NCT00000611.br /iRL Prentice, B Caan, RT Chlebowski, R Patterson, LH Kuller, JK Ockene, KL Margolis, MC Limacher, JE Manson, LM Parker, E Paskett, L Phillips, J Robbins, JE Rossouw, GE Sarto, JM Shikany, ML Stefanick, CA Thomson, L Van Horn, MZ Vitolins, J Wactawski-Wende, RB Wallace, S Wassertheil-Smoller, E Whitlock, K Yano, L Adams-Campbell, GL Anderson, AR Assaf, SA Beresford, HR Black, RL Brunner, RG Brzyski, L Ford, M Gass, J Hays, D Heber, G Heiss, SL Hendrix, J Hsia, FA Hubbell, RD Jackson, KC Johnson, JM Kotchen, AZ LaCroix, DS Lane, RD Langer, NL Lasser, MM Henderson/i

Some researchers at Microsoft have been a href="http://www.nytimes.com/2008/11/25/technology/internet/25symptoms.html?_r=1"studying cyberchondria/a, the phenomenon of people searching the web for medical info, then concluding they've got some horrible disease or affliction. They conclude that "Web search engines have the potential to escalate medical concerns." That seems like something a href="http://www.techdirt.com/articles/20040203/1117235.shtml"we already knew/a, but the researchers suggest one potential way to deal with the issue would be to teach search engines to recognize when they're being used as a medical diagnostic tool, and get them to respond with something other than pages about brain tumors, rare diseases and other worst-case-scenario maladies. One suggestion is a list of possible issues related to the symptom a user searches for, ranked in order of likelihood. That sounds fine, except, is that really all that different than the situation today? If a susceptible user searches for the cause of a headache, and something like a brain tumor gets mentioned, whether in passing or at the bottom of a ranked list, won't they fixate on it or some other serious condition? While online health information could certainly be made more useful, trying to change it so as to carve out cyberchondria seems pretty pointless, as the hypochondriacs will simply find another source to feed their anxiety.p style="border-top: 1px #aaaaaa dashed;padding-top: 5px;margin-top: 10px;"emCarlo Longino is an expert at the a href="http://www.insightcommunity.com/"Insight Community/a. To get insight and analysis from Carlo Longino and other experts on challenges your company faces, a href="http://www.insightcommunity.com/"click here/a./em/p br /br /a href="http://techdirt.com/articles/20081125/1653442951.shtml"Permalink/a | a href="http://techdirt.com/articles/20081125/1653442951.shtml#comments"Comments/a | a href="http://techdirt.com/article.php?sid=20081125/1653442951op=sharethis"Email This Story/abr / br style="clear: both;"/ a href="http://www.pheedo.com/click.phdo?s=c58b798ebcf70c44e57e3d1ba243a4abp=1"img alt="" style="border: 0;" border="0" src="http://www.pheedo.com/img.phdo?s=c58b798ebcf70c44e57e3d1ba243a4abp=1"//a img src="http://www.pheedo.com/feeds/tracker.php?i=c58b798ebcf70c44e57e3d1ba243a4ab" style="display: none;" border="0" height="1" width="1" alt=""/div class="feedflare" a href="http://feeds.techdirt.com/~f/techdirt/feed?a=fE14o"img src="http://feeds.techdirt.com/~f/techdirt/feed?i=fE14o" border="0"/img/a /divimg src="http://feeds.techdirt.com/~r/techdirt/feed/~4/471768677" height="1" width="1"/

I am pleased to announce that Aura Biosciences a US/Spanish biotech company that is developing ground breaking nanotechnology for the targeted delivery of drugs has moved to the offices of Jazzya, my holding company. The company was founded by my former student Elisabet de los Pinos and has developed the Nanotsmart Technology. Aura joins mobile internet start up Tooio who just raised 1.5 million euros in spite of extremely adverse market conditions and is also at our offices.

Nanosmart uses the advantage of viruses that can cross the membrane and deliver the therapeutic load into the cells. Unlike other technologies which use full viruses with their genetic material which is a big bio-safety issue, the Nanosmart structure is a hollow nanoparticle that resembles the viral shell but does not carry any viral genome making it a safe and disrupting technology for the delivery of a wide array of drugs and novel molecules like siRNA and microRNA.

In the field of Oncology Nanosmart enables the selective delivery of classic chemotherapy drugs. Chemotherapy drugs have been selected for their activity against proliferating cells but they do not discriminate between normal cells and tumor cells undergoing rapid division; this drugs cause unspecific damage (hair and nail loss, nausea, vomit and ulcer) side effects which can be life threatening. Nanosmart allows the chemotherapy to target only tumor cells thus enhancing its efficacy and reducing the side effects due to its systemic exposure. Chemotherapy drugs represent a market of 9.6 billion USD in the seven major markets and it is expected that this products will lose patent protection within the next five years.

After founding Medicorp Sciences while at school in 1985 but having been out of the company for many years now it is great to be back in contact with the sector and be able to help Aura put together their business strategy.

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iEndocr Relat Cancer, Vol. 11, No. 3. (September 2004), pp. 497-522./ibr /br /It is widely believed that ductal breast cancer dissemination involves a succession of clinical and pathological stages starting with carcinoma in situ, progressing into invasive lesion and culminating in metastatic disease. Such changes have frequently been attributed to the sequential acquisition of various alterations in a single cell followed by clonal selection and expansion, thus leading to intra-tumor diversity. According to this multi-step view, extensive genotype and phenotype (marker expression, grade) shift may occur in the same tumor during progression; this may lead to the co-existence of molecularly and/or pathologically different areas within the same lesion. An increasing amount of data of various natures now appear to challenge this concept: only a few distinct 'portraits', in relation to estrogen receptor (ER) status and grade, may be found among tumors. Moreover, although undergoing increasing genetic alteration, most individual lesions largely maintain their phenotype when they evolve from in situ to the metastatic state. While many of the data presented here are related to ductal tumors, lobular cancer is also discussed.br /iM Lacroix, RA Toillon, G Leclercq/i

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