2026 World Cup vote: Will Morocco or North America win?
Mladen Antonov, AFP | Italy's former defender Fabio Cannavaro displays the slip of Morocco during the Final Draw for the 2018 FIFA World Cup in Moscow on December 1, 2017.
FIFA members will decide on Wednesday whether the 2026 World Cup should be played in North America or in Morocco, taking football's global showpiece to Africa for just the second time.
The choice is clear - between a slick bid based on gleaming stadiums in the United States, Mexico and Canada or an ambitious attempt from Morocco based on as-yet largely unbuilt facilities.
On the eve of the 2018 World Cup in Russia, 207 FIFA member nations will cast their vote in a congress of world football's governing body.
Morocco's bid for 2026 was only cleared to advance to the runoff vote earlier this month, despite a FIFA evaluation report that classified the North African nation's stadiums, accommodation and transport as "high risk".
A FIFA summary of the bid taskforce's findings warned "the amount of new infrastructure required for the Morocco 2026 bid to become reality cannot be overstated".
Bid leader Carlos Cordeiro on Monday repeated a message he has hammered out again and again in recent months - vote on us, not Trump.
"We believe strongly that this decision will be made on its merits," Cordeiro said in a conference call with reporters. "This is not geopolitics, we're talking about football and what is fundamentally, at the end of the day, the best interest of football and our footballing community.... We've had no backlash."
"A football competition as big as the World Cup deserves to be in great places and if the US, Canada and Mexico get that it will be very special," Beckham said.
Morocco has tried, and failed, four times before, in votes for the 1994, 1998, 2006 and 2010 tournaments - it lost out in the latter to South Africa, the only African nation ever to have hosted football's global showpiece.
Morocco's bid leader Moulay Hafid Elalamy says the bid is based on the "fervour for football in the country and the entire African continent" and promises all the host cities will be less than an hour's flight apart.


Thanks to the deadline we mentioned earlier, a lot of players are signing arbitration-avoiding deals with their clubs today. None will be bigger than this one, however: Mookie Betts and the Red Sox have agreed to a one-year deal for $20 million.
Betts, who is just in his second year of arbitration-eligibility, made $10.5 million last season, so he'll nearly double his salary. He certainly earned it, after he hit .346/.438/.640 with 32 homers, 30 steals and 129 runs and won the AL MVP Award for the World Series champions.
Needless to say, this is record deal for a player in his second year of arbitration eligibility. Assuming he doesn't fall off a cliff in 2019, he'll shatter the third-year record too. Or, alternatively, he'll agree to a very, very lucrative long-term extension to keep him in Boston and away from the free agent market for a very, very long time.


text:
Metformin and Other Biguanides in Oncology: Advancing the Research Agenda
Michael Pollak
Retrospective studies that may be impractical to confirm prospectively suggest that diabetics treated with metformin have a substantially reduced cancer burden compared with other diabetics. It is unclear if this reflects a chemopreventive effect, an effect on transformed cells, or both. It also remains to be established if these data have relevance to people without diabetes. Laboratory models, however, provide independent impressive evidence for the activity of metformin and other biguanides in both cancer treatment and chemoprevention. Investigations of mechanisms of action of biguanides have revealed considerable complexity and have identified important gaps in knowledge that should be addressed to ensure the optimal design of clinical trials of these agents. Such trials may define important new indications for biguanides in the prevention and/or treatment of many common cancers. Cancer Prev Res; 3(9); 1060–5. ©2010 AACR.
The fascinating story leading to current interest in the use of metformin for cancer prevention and treatment began in medieval Europe. Herbalists of that time recognized that polyuria (excessive urination) could occasionally be alleviated by Galega officinalis (French lilac). Nothing was known concerning the active ingredient of the plant. Even the disease responsible for polyuria which responded to G. officinalis, diabetes mellitus, had not been defined. In the modern era, active fractions of the natural product were identified, leading to drug development efforts. After several false starts, the biguanides metformin, phenformin, and buformin were developed. Clinical experience showed that metformin has an excellent therapeutic index for diabetes, for which the drug was introduced in Europe in the 1970s and approved in the United States in 1995 (1).
Clinical trials showed that metformin has advantages over other agents used in the management of type II diabetes (2). This finding, in conjunction with the global diabetes epidemic, has made metformin one of the most frequently prescribed drugs on the planet, with an estimated 40 million prescriptions filled in the United States alone in 2008. Its safety has allowed further clinical trials, which documented effectiveness in other conditions including weight gain induced by antipsychotic medications (3), polycystic ovary disease (4), and diabetes prevention for subjects at a high risk (5). Early laboratory studies of biguanides explored antimicrobial activity, and biguanide derivatives are now widely used in applications ranging from swimming pool decontamination to contact lens sterilization and are under study for AIDS treatment (6). This review outlines the basis for current interest in potential applications of biguanides in oncology.
Mechanisms of Actions of Biguanides for Current Indications
The precise mechanism of action of biguanides in the therapy of type II diabetes remains an active research topic. As these compounds lower both the hyperglycemia and the hyperinsulinemia associated with this disease, early investigations explored the concept that biguanides enhance insulin-receptor activation and downstream signaling, thus reducing insulin resistance, which is a key aspect of type II diabetes pathophysiology. More recent work showed that biguanides impair mitochondrial adenosine-5′-triphosphate (ATP) production (7, 8), which results in the activation of the liver kinase B1 (LKB1)–5′ AMP-activated protein kinase (AMPK) signaling pathway. This pathway is central to the regulation of cellular energy homeostasis, and its activation under conditions of energy stress leads to physiologic downregulation of energy-consuming processes, such as protein synthesis and fatty acid synthesis, to restore ATP levels (9). This homeostatic system is conserved in evolution from yeast to humans, and LKB1 has previously been identified as a tumor suppressor gene (10).
In multicellular organisms, the LKB1-AMPK pathway has acquired further specialized roles in regulating energy metabolism at the level of the whole organism in addition to the cellular level. The system is involved in appetite control by the central nervous system (11), and in the special case of hepatocytes, activation of the LKB1-AMPK pathway downregulates gluconeogenesis, which represents the export of energy from hepatocytes to the organism in the form of glucose (12). This effect in turn reduces blood-glucose concentration, which results in a secondary decrease in insulin level. Although other mechanisms may also contribute, the inhibition of hepatic gluconeogenesis (by LKB1-AMPK activation and/or other processes; ref. 13) is now felt to be a key process underlying the utility of biguanides in the therapy of type II diabetes. Precise mechanisms of action in polycystic ovary disease and antipsychotic medication–induced obesity are unclear, but a reduction of insulin level is likely involved.
Metformin and Neoplastic Disease: Early Clues
Important early evidence suggesting that metformin is relevant to oncology came from population surveys examining the associations of diabetes and diabetes treatments with cancer. Several retrospective studies showed that diabetics had an increased cancer mortality compared with nondiabetics, and that diabetics on metformin had a substantially (∼40%) reduced cancer burden compared with diabetics on other treatments (reviewed in refs. 14, 15). Although such associations are hypothesis-generating rather than definitive, the consistency of findings among different independent studies certainly contributed to the justification for further research.
Early laboratory studies also were supportive. Experiments showed that, whereas metformin activates the LKB1-AMPK pathway to inhibit gluconeogenesis in hepatocytes (12), it activates this pathway with different consequences in mouse embryo fibroblasts and human prostate, colon, and breast cancer cell lines. In these cells, the consequences of LKB1-AMPK activation include inhibition of mammalian target of rapamycin (mTOR) and protein synthesis (consistent with the need to reduce energy expenditure) and thereby a reduction in proliferation (16–20). Of note, despite the early view that metformin might act as an "insulin sensitizer" in classic insulin target tissues, the aforementioned experimental systems revealed the opposite effect in cancer cells: metformin inhibited insulin-stimulated mTOR activation and proliferation in an AMPK-dependent manner. The mechanisms of metformin are discussed further by Engelman and Cantley elsewhere in this issue of the journal (21).
Recent Findings Suggesting Oncologic Applications of Biguanides
Many laboratory models (for example, those reported in refs. 16, 17, 22–35) have been used to show the antineoplastic activity of metformin, either as a single agent or in combinations. Not all of these studies rigorously defined mechanisms, but many have provided molecular correlates of activity. There is evidence indicating that the growth of untransformed epithelial cells and a subset of cancers is stimulated by insulin (reviewed in refs. 36, 37) and that the systemic insulin-lowering action of metformin might inhibit the proliferation of these cancers (22–24). The site of action of metformin that leads to insulin-lowering is the liver. Therefore, the insulin-lowering effect might operate in vivo even in the absence of detectable metformin in neoplastic tissue or, in the context of prevention, in at-risk tissue. This action of metformin shares mechanistic features with the manner by which caloric restriction inhibits the growth of certain cancers (38, 39). The antineoplastic action of biguanides attributable to insulin reduction is most likely to occur if the two following conditions are met: a lack of activating mutations in the signaling pathways downstream of the insulin receptor in neoplastic cells and hyperinsulinemia at baseline in the host. This mechanism might be relevant to prevention as well as treatment; indeed, the first condition is more likely to be satisfied in a prevention context.
Efforts to establish if the separate direct mechanism of action of metformin (involving LKB1-AMPK pathway activation within tumor cells described in vitro; refs. 16–20) also operates in vivo, have yielded surprising results. This mechanism may indeed play a role in vivo, but evidence also suggests that metformin could inhibit the growth of LKB1-deficient tumors by a separate mechanism involving the induction of cellular energy deficiency. In the context of LKB1 deficiency, the metformin-induced decrease in mitochondrial ATP production fails to trigger a fully compensatory decrease in energy expenditure in some models, resulting in an energy crisis and necrosis (40). Confirmation of this mechanism would imply an attractive therapeutic index of metformin for tumors with loss of LKB1 tumor suppressor gene function and in Peutz-Jeghers syndrome; it also would suggest that agents which reduce ATP production have advantages over direct activators of AMPK (41). This implication is conceptually similar to a prior finding of enhanced activity of metformin in cancers with loss of function of p53 (25), as p53 is involved in mediating the antiproliferative, energy-conserving response to AMPK activation, and its loss accentuates metformin-induced energy stress.
The laboratory demonstration that dose and route influence benefit of metformin in the context of a lung cancer prevention model (reported in this issue of the journal; ref. 26) reminds us that pharmacokinetic considerations need to be addressed: one cannot assume that regimens optimized for diabetes control will be optimal for possible future oncology indications. Although this study (26) provides evidence that the observed indirect effect of metformin on levels of insulin and IGF-I, circulating hormones known to be involved in cancer risk (reviewed in ref. 36), is mechanistically important in prevention, a separate encouraging colon cancer prevention model favored a role for direct AMPK activation (27). The proposed direct and indirect mechanisms of action of metformin are not mutually exclusive. Factors including molecular pathology of tumors (or at-risk tissues), drug concentrations at the sites of action, and host characteristics such as the presence of hyperinsulinemia and/or diabetes) might define settings where direct, indirect, both or neither mechanisms may operate, and which subjects will benefit. Results concerning the role of host metabolic factors provide an example of the uncertainties at this stage of investigation: although some experimental systems (such as that described in ref. 26) show the activity of metformin in the absence of documented host metabolic derangements, different models (for example, see refs. 22–24) suggest that maximal benefit is seen in hyperinsulinemic hosts.
Additional data of interest are provided by recent population studies. A retrospective study showed that the rate of pathologically complete response to neoadjuvant chemotherapy in patients with diabetes and breast cancer was significantly higher for patients taking metformin than for those taking other antidiabetic therapies (42), suggesting a role for metformin in sensitizing cancers to chemotherapy.
Support for investigations of metformin for breast cancer prevention is provided by a provocative study that found a 56% decrease in breast cancer among diabetics receiving metformin compared with diabetics on other therapies (43). This study is not definitive, however, as it involved a small sample size and was retrospective.
Gaps in Knowledge
The collective effect of the findings summarized here is to raise enthusiasm for further investigations of biguanides for cancer prevention and treatment, not only because the data suggest activity, but also because they identify important gaps in knowledge. Several key questions need to be addressed before clinical studies can be optimally designed.
What are the important mechanisms of action? What is the optimum compound and dosing regimen?
The question of mechanism is not merely academic because clarification of mode of action could facilitate clinical development. Candidate mechanisms are complex and involve both systemic (for example, insulin lowering) and direct effects. We know with certainty from diabetes experience that conventional metformin doses are sufficient to achieve concentrations in the liver that reduce glucose production, and, secondarily, reduce insulin levels for those patients who have hyperinsulinemia at baseline. One strategy to evaluate the importance of the systemic insulin-lowering actions of metformin will be to compare its efficacy with that of specific small molecule receptor tyrosine kinase inhibitors of the insulin/insulin-like growth factor 1 (IGF-I) receptor family (36). These agents block all the relevant receptors, whereas the systemic action of metformin merely reduces insulin levels, with little effect on IGF-I or IGF-II. Therefore, any in vivo evidence suggesting that the activity of metformin is superior to that of specific insulin-IGF receptor family inhibitors would imply mechanisms of action for biguanides beyond reduction of concentration of circulating insulin. A related point is that, particularly for indications involving short-term treatment, any forthcoming evidence defining settings in which the insulin-lowering actions of metformin are mechanistically important will suggest applications for insulin/IGF-I receptor–blocking drugs, which may reduce signal transduction more effectively than would a decrease in concentration of one of the relevant ligands.
If the direct mechanism of action is important, there is a clear need for human pharmacokinetic and pharmacodynamic studies to identify the best compounds and dosing regimens for effects in extrahepatic tissues. The presence of the organic cation transporter 1 (OCT1) membrane transporter (44) may be important for cellular uptake of metformin, but less so for other biguanides, which may enter the cell in the absence of active transport. There are data implying that phenformin might be superior to metformin in activity for oncologic indications (28), and this may be due to differences in potency and pharmacokinetics. Although phenformin was withdrawn from the market because its risk of toxicity was felt to be unacceptable for long-term treatment of diabetes, it is safer than many antineoplastic agents in common use today. For cancer therapy, the toxicity risk of phenformin would likely be justified if it offered benefits over metformin in terms of efficacy, particularly if duration of therapy was limited, as might be the case in combinations with chemotherapy or radiotherapy. On the other hand, the risk of toxicity in the prevention setting must be minimal, and here, metformin has an obvious advantage, with large databases showing its long-term safety and tolerability; metformin is considered by many to be the safest available pharmacologic treatment for diabetes and to be safe enough for prevention indications (2, 5).
Last, the possibility of novel mechanisms of action of biguanides, including immune system modulation (45), should be considered.
Are there rational combinations to investigate?
Early results and theoretical considerations suggest that biguanides might be more effective in combinations than as single agents for cancer treatment, combined not only with chemotherapy (29) and radiotherapy (30), but also with rapalogs (rapamycin-related compounds) or with other agents targeting energy metabolism (31). Many combinations might be effective in relatively short-term treatment durations, whereas single-agent treatment might be practical for longer durations, similar to current hormonal therapies for prostate or breast cancer. The improved rate of pathologic complete response to neoadjuvant chemotherapy in the presence of metformin (42) implies that at least some benefits of this biguanide do not require long-term exposure.
Metformin deserves investigation for prostate cancer therapy in the special context of preventing the hyperinsulinemia that arises as a consequence of castration (46), which might contribute to the progression to castration-resistant disease (47).
Combinations in the prevention setting are unexplored.
What are the relevant predictive host or tumor biomarkers?
The identification of predictive host or tumor biomarkers represents a critical issue in the contexts of both prevention and treatment, but few data are available. Possibilities include phosphatidylinositol 3-kinase, and LKB1-AMPK functional status in neoplastic tissue, and/or baseline fasting or postprandial serum insulin levels.
Because metformin has little effect on normal insulin levels, high baseline levels might predict an increased chance of any benefit mediated by a reduction in insulin concentration. Constitutive activation of phosphatidylinositol 3-kinase is an example of a tumor characteristic that would be expected to confer resistance to the insulin-lowering effects of metformin, but not necessarily to its direct actions involving mTOR inhibition. Indeed, metformin might have some advantages over rapamycin because its inhibition of mTOR does not seem to be associated with increased AKT activation in some in vitro models (32).
The functional status of the LKB1-AMPK pathway in neoplastic tissue may also predict activity, although it is difficult to predict the direction. Tumors or at-risk tissue in which this tumor suppressor pathway is operational might respond via the AMPK activation mechanism. On the other hand, if drug concentration is adequate, tumors or at-risk tissue with loss of function of this pathway might be sensitive to the mechanism involving metformin-induced energy stress.
Do studies of cancer incidence and mortality among diabetics in relation to metformin use have implications for nondiabetics? Do they imply a chemopreventive action?
The available population studies should be interpreted with caution as they are retrospective and, even more important, are confined to diabetics, in whom risk and prognostic factors that are relatively unimportant in the general population may have dominant roles. At present, we have no clinical evidence, even retrospective, for antineoplastic activity of biguanides in nondiabetics. Phase II clinical trials that address this issue will be of key importance in guiding subsequent clinical research.
Only a few in vivo models have treated host metabolic status as a variable to study its influence on the antineoplastic activity of biguanides. These models (22–24) suggest that metformin is most active in the context of a high-energy diet that leads to hyperinsulinemia. If confirmed, this finding would suggest that the insulin-lowering action of metformin is important and that hyperinsulinemic subjects would be of special interest for clinical trials.
Available data suggest that metformin-associated reductions in cancer mortality are similar in magnitude to reductions in cancer incidence, raising the possibility that the main effects may be preventive, notwithstanding the experimental evidence that biguanides have antiproliferative activity for established cancers.
What potential clinical oncologic applications of biguanides deserve study?
Available data suggest that biguanides have potential applications not only for adjuvant and palliative cancer treatment, but also in cancer prevention. Apart from this broad agenda, there is the challenge (and opportunity) related to the apparent general rather than organ-specific effects of biguanides. Preclinical data justify, as a minimum, further research in treating or preventing colon, prostate, breast, and lung cancer. Although many cancer research efforts are organized on a strictly organ-specific basis, coordination of biguanide research across disease sites might accelerate progress.
For all indications, one of the key challenges in clinical trial design is deciding who is likely enough to benefit to be included in a trial. One possibility, using the available epidemiologic clues, would be to confine early studies to diabetics. In practice, however, this would be difficult for many reasons, including the possibility that some physicians or patients would not be at equipoise for a randomization that might exclude metformin. A subgroup in which randomization might be acceptable, and in which biguanides might have a higher chance of efficacy than in an unselected population, would be individuals with insulin resistance and hyperinsulinemia but no formal diabetes diagnosis. Of course, it is easiest to carry out trials in unselected populations, but such studies must be large if they are to have sufficient power to detect benefits that are confined to subgroups of special interest, such as hyperinsulinemic individuals or, in an extreme example, people with Peutz-Jeghers syndrome.
A substantial body of evidence justifies further research regarding oncologic applications of biguanides, but considerable gaps remain in the knowledge base required to optimize designs of clinical trials of these agents. We need to ascertain the best biguanide or related compound, determine the appropriate dose, and determine biologically based eligibility criteria that define subpopulations likely to benefit before conducting a costly phase III trial involving thousands of patients and prolonged follow-up. Therefore, early steps should include small-scale trials involving pharmacokinetic and pharmacodynamic end points and acceleration of ongoing laboratory and epidemiologic studies. These steps may yield data that will not only contribute to the rationale for major phase III trials, but may also help optimize their design.
The role of the private sector in the exploration of new indications for metformin might be problematic because the drug is off-patent, but mechanisms have been proposed to justify investment in new indications for approved agents (48). On the other hand, there is a clear incentive from an intellectual property perspective to screen libraries of biguanides and related compounds to identify patentable molecules that may have advantages over metformin for cancer treatment.
With respect to cancer prevention, it is noteworthy that a recently reported pilot clinical trial (49) provides preliminary evidence that even low-dose metformin (250 mg once daily) can supress aberrant crypt formation in the colon. If confirmed, this will represent an important milestone in translational research concerning applications of metformin in oncology. However, this study also points to the need for more data with respect to pharmacokinetics. The half-life of metformin is approximately 6 hours (50), and a typical dose in diabetes is 500 mg three times daily, so the tissue drug concentrations (and therefore the mechanisms) responsible for the observed effect on aberrant crypts are unclear. The gastrointestinal tract may be a special case, as there is indirect evidence from FDG PET scanning (showing metformin-stimulated glucose uptake by normal colon, as would be expected following AMPK activation) that metformin might act locally from the lumen following oral administration (51). Would the slow-release metformin preparations developed for dosing convenience (for example, see ref. 50) enhance benefits by achieving more continuous exposure? Would higher doses achieve more impressive effects? As is the case with other potential applications of biguanides in oncology, design of definitive clinical trials capable of measuring maximal achievable benefits will be facilitated when optimal dosing regimes are clarified using forthcoming pharmacokinetic, pharmacodynamic- and even pharmacogenomic (52, 53) data in the context of mechanism.
Metformin may have broad activity against carcinogenesis in general, unlike intensively studied compounds that have utility only for a specific site (e.g., tamoxifen or raloxifene for the breast and finasteride or dutasteride for the prostate). If such broad spectrum activity is confirmed, metformin could become a far more attractive chemoprevention agent than are disease site–specific compounds. Metformin also may have benefits in the context of aging-related diseases (33) in addition to known benefits in diabetes prevention and treatment. Therefore, if the next research steps provide sufficient justification for large-scale cancer prevention trials, end points should include overall health outcomes. Such trials would be most justifiable, however, if future research provides criteria to identify a specific high-risk population in which metformin is expected to provide benefit.
We now have both motivating data and the tools of epidemiology, laboratory studies, and translational research to pursue specific settings in which biguanides might be useful for cancer control.
The author has consulted for Merck, Novo-Nordisk, Lilly, Pfizer, and Sanofi-Aventis.
Grant Support: Dr. Pollak holds the Alexander-Goldfarb Research Chair at McGill University and his lab is supported by Prostate Cancer Canada, the Prostate Cancer Foundation (Santa Monica), NIH, and the Canadian Cancer Society Research Institute.
Revision received July 27, 2010.
Accepted July 27, 2010.
Bailey CJ,
Turner RC
. Metformin. N Engl J Med 1996;334:574–9.
Wu RR,
Zhao JP,
Jin H,
. Lifestyle intervention and metformin for treatment of antipsychotic-induced weight gain: a randomized controlled trial. JAMA 2008;299:185–93.
Palomba S,
Falbo A,
Zullo F,
Orio F Jr..
Evidence-based and potential benefits of metformin in the polycystic ovary syndrome: a comprehensive review. Endocr Rev 2009;30:1–50.
Knowler WC,
Barrett-Connor E,
Fowler SE,
. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393–403.
Thakkar N,
Pirrone V,
Passic S,
. Persistent interactions between biguanide-based compound NB325 and CXCR4 result in prolonged inhibition of human immunodeficiency virus type 1 infection. Antimicrob Agents Chemother 2010;54:1965–72.
Hawley SA,
Ross FA,
Chevtzoff C,
. Use of cells expressing gamma subunit variants to identify diverse mechanisms of AMPK activation. Cell Metab 2010;11:554–65.
El Mir MY,
Nogueira V,
Fontaine E,
Averet N,
Rigoulet M,
Leverve X
. Dimethylbiguanide inhibits cell respiration via an indirect effect targeted on the respiratory chain complex I. J Biol Chem 2000;275:223–8.
Kahn BB,
Alquier T,
Carling D,
Hardie DG
. AMP-activated protein kinase: ancient energy gauge provides clues to modern understanding of metabolism. Cell Metab 2005;1:15–25.
Shackelford DB,
Shaw RJ
. The LKB1-AMPK pathway: metabolism and growth control in tumour suppression. Nat Rev Cancer 2009;9:563–75.
Minokoshi Y,
Furukawa N,
. AMP-kinase regulates food intake by responding to hormonal and nutrient signals in the hypothalamus. Nature 2004;428:569–74.
Foretz M,
Hebrard S,
Leclerc J,
. Metformin inhibits hepatic gluconeogenesis in mice independently of the LKB1/AMPK pathway via a decrease in hepatic energy state. J Clin Invest 2010;120:2267–70.
Giovannucci E,
Harlan DM,
Archer MC,
. Diabetes and cancer: a consensus report. CA Cancer J Clin 2010;60:207–21.
Johnson JA,
. Insulin, glucose and the increased risk of cancer in patients with type 2 diabetes. Diabetologia. Epub 2010 Jul 20.
Dowling R,
Sonenberg N,
. Metformin is an AMP kinase-dependent growth inhibitor for breast cancer cells. Cancer Res 2006;66:10269–73.
Gwinn DM,
Egan DF,
. AMPK phosphorylation of raptor mediates a metabolic checkpoint. Mol Cell 2008;30:214–26.
Engelman JA,
Cantley LC
. Chemoprevention meets glucose control. Cancer Prev Res 2010;3:1049–52.
Blouin M-J,
. Metformin attenuates the stimulatory effect of a high energy diet on in vivo H59 carcinoma growth. Endocr Relat Cancer 2008;15:833–9.
Amrein L,
Panasci L,
. Metformin blocks the stimulative effect of a high energy diet on colon carcinoma growth in vivo and is associated with reduced expression of fatty acid synthase. Endocr Relat Cancer 2010;17:351–60.
Fox MM,
Evans R,
. Dietary energy availability affects primary and metastatic breast cancer and metformin efficacy. Breast Cancer Res Treat. Epub 2009 Nov 22.
Mercado JR,
Maier CR,
Kawabata S,
Fox SD,
. Metformin prevents tobacco carcinogen-induced lung tumorigenesis. Cancer Prev Res 2010;3:1066–76.
Hosono K,
Endo H,
Takahashi H,
. Metformin suppresses azoxymethane-induced colorectal aberrant crypt foci by activating AMP-activated protein kinase. Mol Carcinog 2010;49:662–71.
. Important role of the LKB1-AMPK pathway in suppressing tumourigenesis in PTEN deficient mice. Biochem J 2008;412:211–21.
Hirsch HA,
Iliopoulos D,
Tsichlis PN,
Struhl K
. Metformin selectively targets cancer stem cells, and acts together with chemotherapy to block tumor growth and prolong remission. Cancer Res 2009;69:7507–11.
Sanli T,
Rashid A,
. Ionizing radiation activates AMP-activated kinase (AMPK): a target for radiosensitization of human cancer cells. Int J Radiat Oncol Biol Phys. Epub 2010 Jul 7.
Ben S,
Laurent I,
Giuliano K,
. Targeting cancer cell metabolism: the combination of metformin and 2-deoxyglucose induces p53-dependent apoptosis in prostate cancer cells. Cancer Res 2010;70:2465–75.
Piura E,
. Metformin and rapamycin have distinct effects on the AKT pathway and proliferation in breast cancer cells. Breast Cancer Res Treat 2010;123:271–9.
Anisimov VN,
Egormin PA,
Bershtein LM,
. Metformin decelerates aging and development of mammary tumors in HER-2/neu transgenic mice. Bull Exp Biol Med 2005;139:721–3.
Pollak MN
. The effects of adiponectin and metformin on prostate and colon neoplasia involve activation of AMP-activated protein kinase. Cancer Prev Res (Phila Pa) 2008;1:369–75.
Vazquez-Martin A,
Oliveras-Ferraros C,
Menendez JA
. The antidiabetic drug metformin suppresses HER2 (erbB-2) oncoprotein overexpression via inhibition of the mTOR effector p70S6K1 in human breast carcinoma cells. Cell Cycle 2009;8:88–96.
. Insulin and insulin-like growth factor signalling in neoplasia. Nat Rev Cancer 2008;8:915–28.
Law JH,
Habibi G,
Hu K,
. Phosphorylated insulin-like growth factor-1/insulin receptor is present in all breast cancer subtypes and is related to poor survival. Cancer Res 2008;68:10238–46.
. Do cancer cells care if their host is hungry? Cell Metab 2009;9:401–3.
Kalaany NY,
Sabatini DM
. Tumours with PI3K activation are resistant to dietary restriction. Nature 2009;458:725–31.
. Host metabolic factors and tumor molecular pathology (including LKB1 status) interact to determine the antineoplastic action of metformin and similar compounds. Proceedings of International LKB1-AMPK Congress, Marseilles. 2010, http://www.lkb1.com/.
Cool B,
Zinker B,
Chiou W,
. Identification and characterization of a small molecule AMPK activator that treats key components of type 2 diabetes and the metabolic syndrome. Cell Metab 2006;3:403–16.
Jiralerspong S,
Palla SL,
Giordano SH,
. Metformin and pathologic complete responses to neoadjuvant chemotherapy in diabetic patients with breast cancer. J Clin Oncol 2009;27:3297–302.
Bodmer M,
Meier C,
Krahenbuhl S,
Jick SS,
Meier CR,
Meier CR
. Long-term metformin use is associated with decreased risk of breast cancer. Diabetes Care 2010;33:1304–8.
Pearce EL,
Walsh MC,
Cejas PJ,
. Enhancing CD8 T-cell memory by modulating fatty acid metabolism. Nature 2009;460:103–7.
Smith MR,
Lee H,
Nathan DM
. Insulin sensitivity during combined androgen blockade for prostate cancer. J Clin Endocrinol Metab 2006;91:1305–8.
Cox M,
Gleave M,
. Insulin receptor expression by human prostate cancers. Prostate 2009;69:33–40.
. More patent protection for medicines with a new purpose. Nature 2010;465:1005.
. Metformin suppresses colorectal aberrant crypt foci in a short-term clinical trial. Cancer Prev Res 2010;3:1077–83.
Gusler G,
Gorsline J,
Levy G,
. Pharmacokinetics of metformin gastric-retentive tablets in healthy volunteers. J Clin Pharmacol 2001;41:655–61.
Gontier E,
Fourme E,
Wartski M,
. High and typical 18F-FDG bowel uptake in patients treated with metformin. Eur J Nucl Med Mol Imaging. 2008;35:95–9.
Gambineri A,
Tomassoni F,
Gasparini DI,
. Organic cation transporter 1 polymorphisms predict the metabolic response to metformin in women with the polycystic ovary syndrome. J Clin Endocrinol Metab 2010 Jul 21. [Epub ahead of print].
Becker ML,
Visser LE,
van Schaik RH,
Hofman A,
Uitterlinden AG,
Stricker BH,
. Interaction between polymorphisms in the OCT1 and MATE1 transporter and metformin response. Pharmacogenet Genomics 2010;20:38–44.
You are going to email the following Metformin and Other Biguanides in Oncology: Advancing the Research Agenda
Immune Responses and Triple-negative Breast Cancer
Anticancer Pharmacology of WA in Breast Cancer
OPSCC Is Now the Most Common HPV-associated Cancer
Show more Review

redpajama_set_name: RedPajamaCommonCrawl


A blonde mermaid in pink covers both sides of this retractable, pocket tape measure. Tropical flowers are on the back side and a coordinating pink ribbon encircles the piece. Attached to the tape's pull tab is a silver mermaid charm and a flower button decorates the front.


Grand Isle County has the distinction of being the least populous county in Vermont. Grand Isle County vital records are available from the North Hero town clerk. Office hours are 8 am to 4:30 pm, Monday, Tuesday, and Thursday; 8 am to noon Wednesday, Friday, and Saturday. The clerk may be contacted by phone (802-372-6926), fax (802-372-3806) email (townclerk@northherovt.com) or mail. The Vermont State Archives and every town clerk maintains birth, death, and marriage vital records; Grand Isle county towns are Alburg, Grand Isle, Isle La Motte, and South Hero. Divorce records are obtained from the clerk of the court where the divorce was granted.


text:
Home Page RSS Register Login
Posts Tagged 'Political Malignancy'
To kill a beast.
Let's be clear: if Trump is not politically killed off once and for all, he will become a MAGA Dracula, rising from the dead to haunt US politics for years to come and giving inspiration to his wretched family of grifters and thousands of deplorables well into the next decade. So what is needed now is a stake in his black heart, or a silver bullet, so long as whatever the means employed, it kills the beast.
The process of doing so is more akin to cancer surgery than supernatural intervention, but before proceeding to the discussion let me explain why Trump's political death sentence is recognised as necessary.
The Democrats know what he is so I shall not discuss the logics by which they came to the conclusion that he needs to be extirpated from the body politic. It is the Republicans who are decisive here. They–by that I mean the Republican National Committee, US congressional delegations, state governments and legislatures, and the corporate interests that influence and fund Republican causes and candidates–have to come to grips with simple facts.
Trump was never a "true" Republican. Not only is he not a blue-blood old monied elite with stakes in traditional Republican ventures like oil, automobiles and finance. He was not a member of the party until he switched allegiance in 2010. From the get-go, his politics have been more of the George Wallace meets Barry Goldwater type rather than of the Nixon-Reagan-Rockefeller variant. His victory in the 2016 presidential primaries was a slap in the face by an upstart vulgarian to the Republican establishment, which he then proceeded to eviscerate by using their own opportunism against them. He offered the GOP "family" tax breaks, deregulation, a return to Anglo-Saxon heterosexist patrirachical Christian values and shirt-sleeve patriotism. They responded with political support. That support was contingent on his staying in his lane and understanding the limits on his authority and the boundaries of his power.
He did not. Instead, he picked needless fights at home and abroad over matters both inconsequential and important. He alienated allies and he cultivated American enemies. Rather than work to heal old wounds he picked the scab of racism and bigotry until it festered and burst into the public square in places like Charlottesville, Portland and Kenosha (the last two where he joined rightwing conspiracists in claiming that Black Lives Matter protests over the murder of unarmed black men by police were an Antifa-Socialist plot).
Meanwhile, he drove a wedge within the GOP by forcing out non-MAGA types and replacing them with national-populists who would do his bidding. That fractured the Republicans, and yet the marriage of convenience between the GOP establishment and Trump continued until 2020. However, at that point his erratic behaviour and incompetent, some might say delusional approach to the Covid-19 crisis turned a bad situation into a world-leading case study in governmental dysfunction. He turned a public health crisis into an internecine ideological war about masks and lockdowns. He refused to listen to scientists and increasingly relieved on conspiracy theorists for advice on the pandemic and more. In doing so he became bad for business even as the financial markets remained optimistic that at some point he would come to his senses.
He did not. He ran a dog-whistling re-election campaign marked by Covid super-spreader rallies. He impugned the integrity of the electoral process months before the vote was held. He tried to manipulate votes by filling the US Postal Service with partisan hacks who attempted to suppress absentee (mail-in) ballots by reducing collection points and sorting facilities. He urged Republican state election officials to challenge minority voting rights and to limit access to voting facilities in areas that traditionally went Democratic on Election Day. He did everything in his power to tip the scales, skew the results and delegitimise any outcome other than his win.
He lost anyway. Not by hundreds of thousands or a few million votes. He lost by nearly 8 million votes. It is true that he garnered 74 million votes himself, but that was on the back on the highest voter turn out in over a century (60.66 percent). Joe Biden won close to 82 million votes, so in the end even with those 74 million votes cast for Trump, the race was not close.
Rather than concede gracefully, Trump well and truly jumped out of his lane. He denounced without evidence fraud in the electoral system and specifically those in contested swing states. He spoke of dark forces operating behind the scenes to cheat him out of his rightful victory. He decried foreign (but non- Russian) interference. He mounted over sixty specious legal challenges to the results in several states, losing all but one of them. And then he crossed the biggest line of all: he incited a seditious insurrectionary attack on the US Capitol in order to prevent the Electoral College results from being certified by Congress. People were killed and injured in the mass assault and occupation of the Legislative branch. Politicians were forced to flee for their lives and take cover as the mob swarmed the debating chamber and halls baying for blood. And rather than appeal for calm, Trump watched it unfold on TV.
Whether they recognise it or not, that was the point when he crossed a Republican bridge too far. The assault on the Capitol was aimed not just at Democrats but at Republicans as well (people chanted "Hang Mike Pence," among other niceties). In the days leading up to, during and after the siege, Republican lawmakers were harassed and threatened in public spaces, social media and via personal communications (including Mitt-Romney (R-UT) and Lyndsey Graham (R-SC), as were Democrats (House Speaker Nancy Pelosi (D-CA) and congresswoman Alexandria Ocasio Cortez (D-NY) were singled out for particularly violent misogynistic abuse). The attack may have been originally driven by partisan rage stoked by Trump and his minions, but became a broad-brushed assault on an institutional pillar of the American Republic.
Because many of the insurrectionists were wrapped in body armour and armed with blunt and other street-level weapons like Mace and bear spray (there were also firearms and explosives cached near the Capitol), which they used to fight sworn law enforcement officers defending the complex, the assault was an attack on the sovereignty of the US government itself. That is because one of the foundations of sovereignty–the core of what it is to be a "sovereign"–is legal monopoly over organised violence within defined territorial limits (the definition is from Max Weber but the origins of the notion of sovereignty as having a coercive core dates back to Thomas Hobbes).
It has now been established that, cloaked by the larger crowd who attended the Trump "Stop the Steal" rally and then walked to the capitol after Trump urged them to, members of various militias were acting in a coordinated fashion to the extent that some used walkie-talkies and their phones to organise aspects of the attack such as blocking the underground tunnels below the Capitol that are used as escape routes for congresspeople in times of crisis. Once they violently engaged the Capitol and DC Police on the steps and interior of the legislature, they challenged the sovereignty of the Federal Government and the components parts of its repressive apparatus.
For any nation-state, much less a supposed superpower, that cannot stand. Regardless of partisan orientation, no individual is above the Institution. As the saying goes, the Nation is one of laws, not people. Sovereignty cannot be contested because if it does, the Republic is at risk. The State is sacrosanct so long as it performs its core functions.
That is why Trump must be excised. He has undermined the basic foundations of the constitutional Republic and thereby challenged fundamental notions of the US as a sovereign State. He has divided the Nation and manipulated his supporters into becoming a riotous seditious mob. He has put himself before God, Flag and Country even while wrapping himself in them.
If not in public, in their hearts Republicans know this.
Removal of Trump's malignant political presence is a three step process. One is via his Senate trial and banishment, one involves the prosecution and punishment of his seditious supporters, and one is a form of legal chemotherapy that will hopefully prevent him from returning to the political scene. This is what needs to happen. It does not mean that it will happen. We can only be hopeful.
Senate Minority Mitch McConnell (R-KY) seems to understand the situation. With his bleating about "rigged" elections in Georgia, Trump contributed to the GOP losing both Senate seats in that state (to a Jew and an African-American!). That cost McConnell his majority leadership. He now has an incentive to see Trump finished off because among other things it will pull the rug out from under and bring to heel would-be pretenders to the MAGA throne like Marco Rubio, Ted Cruz and Josh Hawley.
The impeachment charge against Trump is incitement of the attack. In asking for two extra weeks for Trump's lawyers to "prepare, " McConnell may in fact be giving Democrats more time to uncover irrefutable evidence that the Trump White House colluded with insurrectionists on how to storm the Capitol. The New York Times and Wall Street Journal have uncovered evidence that some of the "rioters" were paid staff on Trump's campaign and were in contact with members of Trump's entourage, including family members and people like Rudy Giuliani. With the articles of impeachment now tabled, more evidence may be uncovered before the Senate court proceedings begin. People can be subpoenaed to testify under oath or offered immunity in exchange for their testimony. Unlike his first impeachment, Trump cannot offer presidential protection to those called as witnesses (as he did when he ordered various officials not to testify). Things are about to get real and that reality is ugly for Trump.
17 Republicans need to cross the aisle and vote in favour of conviction in order for Trump to be impeached. McConnell has said that he has whatever numbers he needs to go either way. If the evidence is compelling then it will be easier to convict on "institutions over individuals" grounds. Doing so will be the start of the de-Trumpification process. Although that is necessary, it is not sufficient. More needs to be done by way of follow ups.
If Trump is convicted he then can be banned from political life by a simple majority vote in the Senate. The decision to vote on a lifetime ban is called by the Democratic majority. Given his long-standing repudiation of Trump, Mitt Romney will gladly provide the cross-over vote but there are others who will be willing to do so as well.
In order to make the ban stick, the second step is a form of legal chemotherapy. He needs to be sued and charged in civil and criminal courts at the state and federal levels, along with family members and others, like Giuliani, who conspired with him during his time in business and government. The constant barrage of lawsuits and prosecutions will exhaust him financially and perhaps mentally and will open space for people to turn on him in order to escape or receive lesser punishment themselves. So long as he is occupied in this fashion he will have relatively little resources, time or energy to try and mount some sort of political re-birth under different guise.
The final part of this process involves the prosecution and serious punishment of those charged with offences related to the assault on the Capitol. These include murder; conspiracy to commit murder; grievous bodily harm; conspiracy to commit grievous bodily harm; inter-state transport of weapons with the intention of committing crime; looting; vandalism; theft of government property; theft and distribution of classified material; rioting; affray; sedition; treason and more. The charges must be as serious as possible and the sentences must be as severe as legally permissible.
The reason for this hard line approach is not just the punitive value it has on those who perpetrated the attack on the Capitol. Its main value is deterrent. It provides a palpable indicator of the boundaries of the "no go" zone when it comes to political dissent and legitimate protest. Adopting a judicial hard-line will help deter copycats or those who think that just because some politicians, even the president, say it is OK, seditious insurrection in fact is not OK as far as the constitutional State is concerned.
The three-tiered approach to extirpating the Trump malignancy from US politics is the only way that we can be reasonably assured that the treatment will work (and yes, I recognise that I am borrowing some of that "organic" language used by the Argentina junta when referring to its victims. But if the shoe fits, then why not wear it?). In the end, Trump is an existential threat to the very notion of the US as a nation-state, and must be treated as the domestic terrorist inspiration and enabler that he is. Not to put too fine a point on it, but he is no better and more likely a bit worse than one of Osama bin-Laden's drivers in Pakistan. If so, and those guys wound up in Guantanamo or dead for their efforts, why should he be treated appreciably differently than they were?
One can only hope that Mitch McConnell and the GOP recognise that Trump is just another data point on that anti-democratic continuum, but one that is far more dangerous to the US than any Islamicist chauffeur.
Tags: Impeachment, insurrection, Political Malignancy, Trump
Posted in Authoritarianism, comparative politics, Crime, Democracy, elections, governance, History, identity, National identity, Politics, Rebuild, Uncategorized, USA | 18 Comments | Read More »
A democratic peace or a feminist peace?
Indigenous socialism with a Chilean face.
The incremental shift.
The unshackled straitjacket.
Warnings versus threats in foreign relations.
Media Link: "A View from Afar" year-end review.
Chinese influence and American hate diffusion.
Random Retweets: Pandemic mitigation.
Positive Feedback.
Media Link: "A View from Afar" on supply chain bottlenecks, commodity (over) concentration and the need for post-pandemic structural reform.
Media Link: "A View from Afar" on PRC-Taiwan tensions.
Raucous AUKUS Ruckus.
Ideational and ideological in the construction of "isms."
The supermarket stabbing spree was not a terrorist act.
9/11, forever wars and the end of liberal internationalism.
Pablo on A democratic peace or a feminist peace?
Di Trower on A democratic peace or a feminist peace?
Edward Main on Indigenous socialism with a Chilean face.
Pablo on Indigenous socialism with a Chilean face.
James Green on Indigenous socialism with a Chilean face.
Robert Miles on The incremental shift.
Pablo on The incremental shift.
Edward Main on The incremental shift.
Barbara Matthews on The incremental shift.
Tom Hunter on The incremental shift.
Di Trower on The incremental shift.
Act Authoritarianism Barack Obama Chris Trotter Crime Democracy Don Brash DPF Election 2011 Elections Foreign policy/affairs GCSB Greens Helen Clark Hone Harawira identity politics Idiot/Savant Intelligence International relations John Key Kiwiblog Labour Maori Party Media media theory National NZDF NZ Herald open government Participation Phil Goff photography Police Propaganda racism Radio NZ National Referenda Representation Security symbolic politics Terrorism The Standard Tino Rangatiratanga Trump USA
An inclusive society
Chrischurch
cultural difference
Intelligence and Security
NZ foreign policy
NZ Security
NZDF
Take Māori
working class politics
Auckland Trains
BK Drinkwater
Boganette
Bowalley Road
Capitalism Bad; Tree Pretty
Ethical Martini
Fatal Paradox
Frogblog
From the Morgue
G.Blog
Gordon Campbell at Scoop
Ideologically Impure
Idle Thoughts of an Idle Fellow
Imperator Fish
Inquiring Mind
Just Left
Kumara Republic
Laws 179: Elephants and the Law
Lefthandpalm
Luddite Journo
Mars 2 Earth
Maui Street
Media Law Journal
Monkeyswithtypewriter
Mydeology
pollywannacracka
Prog Blog
Sciblogs
Still Truckin'
The Dim-Post
The Fundy Post
The Hand Mirror
The Opinionated Diner
TV3 Political News
TVNZ Political News
BagNews Notes
Brian Easton
Campaign for MMP
Nicky Hager
© 2008 Kiwipolitico
StarScape Theme (1.5.6: Scorpius) | Design by: GDragoN
Powered by: Wordpress Valid XHTML Valid CSS


Helping you revolutionize the world.
Technology companies are changing the way we live our lives and interact with the world around us. Every industry—from transportation to education to telecommunications, energy, and public safety—is being affected. Often, these transformative technologies require access to high-speed, high-bandwidth, low-latency networks in order to reach their full potential. These innovators need the ability to adapt and scale quickly with the assurance that there will be adequate infrastructure to support their biggest ambitions.
If you're one of these technology companies, we are uniquely positioned to support your continued innovation. We have over 40,000 towers, approximately 70,000 route miles of fiber and 65,000 small cells on air or under contract—all managed under a shared infrastructure model, so we're your single source for all network infrastructure needs. We have 25 years of experience building and deploying end-to-end network solutions of all types and sizes. With nearly 100 offices nationwide, there's someone nearby who will be there at every step of your project to make sure it gets done quickly, efficiently, and according to your needs.
We'll work with you to understand your business and build a plan that works for your unique needs. We offer flexible terms and manageable startup costs that are based on your business model, so you can be sure we'll find a solution that works for you. We'll work with you to create a realistic timeline, and give you full access to our proprietary tools that will help you identify the best locations to suit your needs.
Communications infrastructure is our core business, so you can count on us to be the last owner of our assets—a partner who will be with you for the long haul. With nearly 100 offices around the country, we are an extension of your team. From network planning—including identifying markets and developing deployment strategies—to navigating the regulatory environment with our municipal relationships at the state and city level, our expertise can save you time and money. Once your project is completed, our state-of-the-art Network Operations Centers provide ongoing support, 24/7 site monitoring, and local service teams to ensure we can act quickly if a problem arises.
To learn more about how Crown Castle can support your innovation, fill out the form below and we'll be in touch.
What types of companies do you serve?
We work with a wide variety of technology companies and understand the unique needs of everyone from small start-ups to multi-national companies. Our partnerships span across a variety of companies including utilities, WISPs, broadcasters, sensors, internet of things, edge computing, unmanned air vehicles, and more. Contact us to learn more about how we can help you.
How will Crown Castle work with my team?
We have extensive expertise that complements your own team's efforts—helping you to continue growing while minimizing potential roadblocks. We can help with everything from business and network planning to navigating the regulatory environment at the site and city level. For those at very early stages, we consultatively assist in identifying markets and developing deployment strategies to get you on air—on time and on budget. Our turnkey offering means that we can take on all aspects of a project, eliminating the need for you to maintain the large amount of resources necessary to deploy a network.
What site development services do you provide that can help me get on air?
While we do not require that you use Crown Castle for your site services, we offer a range of solutions based around your company's needs. This can range from simple application entry to a full turnkey solution taking your project all the way to network integration.
How much does it cost to work with Crown Castle?
We design customized, flexible programs based on each individual request. Please contact us and we'll work to find a solution that works for you.
Reach out to your area market sales manager to start the conversation around the specific needs and requirements of your build. We've provided some information below that will help us get started, but is not required.
How soon can I be on air?
We have a customized process for technology companies to help accelerate your network deployment and get you on air quickly and efficiently, while following all local zoning and permitting requirements.
Can I see where your assets are located?
Yes, fill out our form here and someone will be in touch soon to complete your registration for CCIsites, our proprietary database tool, where you can explore, evaluate, and select available sites.
What type of backhaul connectivity do your sites have?
Many of our sites are connected via fiber, although some rural sites may have T1 connectivity. However, we're constantly expanding and upgrading our footprint. Contact us to ensure you have the most updated information about your area.


text:
Cayman skier fastest 15-yr-old in Downhill & Super G
Blackadder1 | 24/04/2012
(CNS): Very strong late season finishes in senior FIS races at Telluride, Park City and Vail and two excellent runs in the Downhill and Super G at Mount Bachelor in Oregon in April have catapulted Caymanian Dean Travers to the world No 1 position in the International Ski Federation rankings for 15-year-olds in Downhill and Super G, two of the four Alpine disciplines published today. Dean is the first person from any Caribbean nation to achieve this. Speaking from Dean's Winter training headquarters in Colorado, the young skier's mother, MaryAnne Travers, said, "Everyone here is just amazed by these results. Dean has been the fastest 15-year-old in the US in Super G but he has now reached an entirely new level.v"The results are the more remarkable because Dean had to recover from a bad injury early in the season, which kept him off the slopes for 6 weeks.
As a result, when it was time to race he had no start points.
"We decided to ignore the junior races favored by the European junior skiers and entered Dean in the late season senior races just to gain experience," said MaryAnn Travers. "This was a big challenge for him because he had start positions in the 90's, inevitably on rutted and soft courses. It also meant he had to race 15 to 30 year olds, including the senior European racers at US colleges. But he started to surprise everyone with some tremendous finishes in the top 20 and then just got faster and faster."
In some races Dean finished within just a second or two of the winner, which meant meaningful points on the FIS system, and he is now ranked ahead of the Austrian and Swiss racers of his age, as well as the North Americans. In one sensational Giant Slalom run in Park City, Dean beat the entire senior field. As a result of the Mt Bachelor Downhills, Dean moved from being ranked as the 240th 15-year-old in the world in Downhill to 1st , to add to his No 1 world ranking in Super G.
Dean has been clocked at over 70mph in the Downhill. He attributes his success to his coach, former World Cup and Olympic racer Jake Zamansky, and to his strength coach Ray Cook.
"Thanks to my coach and trainer I am very happy with the way the season ended," Dean said. "I am pleased that I have been able to build on my Gold Medal in the Super G at Whistler Cup last season and the Downhill, ranking the best. It doesn't matter to me how steep or icy the course. In fact, the steeper the better — I like to accelerate on the steeps."
Dean has worked very hard on a specifically designed strength programme. "I put in two hours in the gym most days," he said, "and then spend about three hours on the training hill at Aspen before we do the video analysis. The video allows my coach, Jake, to pinpoint any problems in technique so I can correct after every training run. The core and leg strength have also been essential. The longer senior FIS runs are much more physically demanding because they generate much higher speeds. But Ray has focused on this and it means that I can holdmy angles at higher speeds and get much more energy out of the ski."
Coach Zamansky won't change the approach, he said. "Next season we will continue to race Dean against the seniors. He has certainly surprised a lot of more experienced competitors already. These FIS rankings in these two disciplines are a great indication of potential, so we are very encouraged. This could turn out to be something special."
Dean, who races in Cayman colours and his custom sting ray and turtle helmet added, "Next season I should rank with the top seeds in Downhill and Super G. This means I will start on clean harder courses, which should be a second or two faster. Some of these late season courses in soft snow have been very difficult. For now, though, after I catch up on my homework I'm looking forward to a rest on the beach at Rum Point before I head to New Zealand for more training in July."
great to see this.
Cool running's bo!
Great job keep up the good work even though we have some bad minded people here in cayman who's giving you thumbs down
This is an amazing achievement Dean, we are all very proud of you!
Congratulations Dean, great news and keep up the good work.
Peter Milburn says:
Keep up the good work Dean.We are all proud of you here.
Concerned Caymanain says:
We are proud of you Dean! Thank you for helping to put Cayman on the map – in a good way!!
Congrats buddy!
You're definitely making a few "firsts" in your sport.
It sounds like a pretty intense workout / practice regime as well – keep it up.
A friend of the family says:
Congrats to Dean on an amazing feat for a 15 year old. Myself and all of cayman [I'm sure]
are proud of you. like we were when Sadone won her gold, and all the young athletes who
brought home medals from other games. And thanks for parents like Tony and Mary Ann.
splendid Dean you have made Cayman proud, keep up the great acheivements!
fantastic well done Dean!
Cheese Face says:
Why on earth does that comment have a thumbs down???
Some really sad bitter and twisted folks on here.
Well done to the lad.
« Cayman sprinter breaks national record at ACC race
Big win for Cayman at the Big Game »


An eerie animated prop can authentically recreate that frightful skin crawling feeling with sudden motion or startling animation. To make sure your house is the most haunted one on the block this Halloween, be sure to include lots of our animated props they really go bump in the night!
Party& Occasions Patio& Garden Pets Pharmacy Photo Center Sports Lunging Reaper Animated Prop Halloween Decoration. Product Image. Price 213. 12. Product Title. Lunging Reaper Animated Prop Halloween Decoration. Product Haunting Ghost Trio Animated Halloween Decoration.
Product Image. Price 188. 05. Product Title. A rocking chair that rocks all by itself? These push button or motion sensor activated animated Halloween props make your porch come alive with scary ghosts, ghouls, spiders, and flapping bats. Find great deals on eBay for Animated Halloween Props in Halloween Props.
Shop with confidence. Download halloween party stock photos. Affordable and search from millions of royalty free images, photos and vectors. Find Animated Halloween Props& Decorations at the lowest price guaranteed.
Buy today& save plus get free shipping offers on all Halloween home decor at OrientalTrading. com! Browse Halloween Party pictures, photos, images, GIFs, and videos on Photobucket Animated Halloween fun webisodes, stories, games, downloads and more for kids and entire family Party& Occasions Patio& Garden Pets Pharmacy Photo Center Sports& Outdoors Toys Video Games.
Walmart Halloween. Fun Express. See more brands. Width. Less Than 6 ft. 6 8 ft. 8 10 ft. 10 12 ft. 12 18 ft. Halloween Props Animated. Showing 40 of 1047 results that match your query. Search Product Result.


text:
Team Onboarding
Acceleration & Restart
Onboarding and Transition Testimonials
Onboarding Tools
Risk Calculator
Why The P.S. Is So Important For Introverts
Executive Onboarding, Onboarding
Let's start with the premise that you want everyone's best ideas – whether or not you choose to accept or act on them. Let's further presume that you have meetings for participants to learn, contribute and decide. The problem is that meetings, by definition, are geared to extroverts and run the risk of leaving introverts behind. If you want the best ideas for introverts you must, must, must, give them things to mull over in advance and must give them a chance to weigh in after the meeting close with a p.s. with the rest of their ideas – and often, their best ideas.
Extroverts like me think with our mouths. We do best ratcheting up good ideas while sparring with other extroverts. We're happy to float really bad ideas to prompt a discussion and debate so others can come up with better ideas in turn prompting our own better ideas, their even better ideas, our even better ideas and so on. Extroverts feed off each other.
I'm told (though I personally find it hard to understand how this is possible) that introverts think with their brains. They like to absorb information and then let it bounce around in their heads until it emerges as fully-formed ideas.
All kidding aside, you need both. You need everyone's best ideas – however they got there.
Now do you see the problem with meetings? Almost inevitably, the first people to open their mouths on any topic will be the extroverts. The second people to chime in will be….other extroverts. The extroverts will bounce off each other leaving no air space for the introverts.
A skilled leader or facilitator will try to bring the introverts into the conversation at some point. But it won't work. The information coming out of the mouths of the extroverts will be bouncing around in the introverts' heads like unpopped kernels of popcorn not yet ready to see the light of day.
You've got to give introverts a chance to pre-think their ideas. (Pre-pop their popcorn?) Do this by giving them pre-reads in advance with enough information to prompt their thinking. Tell them what the main topics of conversation are going to be so they can mull things over in advance. This way they'll be ready to share their ideas in the company of extroverts.
How do you know in advance which are the introverts and which are the extroverts? The bad news is that it's hard to tell on the margins. The good news is that it doesn't matter. Send everyone the pre-reads. The introverts will love it. They'll dig into the pre-reads and be ready for the meeting. The extroverts won't pay any attention to it. They'll wait to engage with others in the meeting. This way, both will be ready to contribute to their fullest potential.
Click here for a list of my Forbes articles (of which this is #612) and a summary of my book on executive onboarding: The New Leader's 100-Day Action Plan.
Don't forget the P.S. There's no way for the introverts to get the benefit of extroverts' thinking before the meeting. This is because the extroverts do their best thinking and make their best contributions in the company of others. This means there will be new information bouncing around inside introverts' heads. They need time to process that.
Hence the P.S. Give everyone a chance to contribute even more ideas after the meeting closes. Do this with an invitation in the final notes.
Putting this all together gets to the following basic steps for a meeting.
Prelude:
One person responsible.
Single overall objective set.
Agenda set with clear expectations for learning, contributions and decisions by item, with time allocated to match what's needed.
Attendees include those needed and no one else (with substitutes allowed for those who can't make it).
Appropriate pre-work, analysis, and pre-reading to people far enough in advance for all to learn/contribute to their fullest potential.
Delivery/Moment of Impact:
Meeting participation and timing facilitated to optimize learning, contributions, and action-oriented decisions, ending when overall objective is achieved.
Follow-through:
Meeting notes out promptly to memorialize decisions and actions, inviting other ideas to improve best current thinking, and kicking off the preparation for the next meeting.
« The Pillars Of Interpersonal Leadership – Structure, Leverage And Confidence
Onboarding Digital Natives Into Executive Roles »
PrimeGenesis > External Articles > Onboarding > Why The P.S. Is So Important For Introverts
BRAVE Leadership
Forbes Executive Onboarding Notes
Strategic Inflection Points
© 2019 PrimeGenesis | BETTER RESULTS FASTER Since 2003
Email Jeff
Former CEO, President, COO, and CTO in public and private equity backed companies. CEO at On Campus Marketing, President at Accuity, COO at GAIN Capital, CTO at Thomson Financial. Strong track record as a leader in complex transitions in information, media, and retail businesses with emphasis on digital transformations and M&A integration. BS University of Dayton; MBA University of Maryland.
Thomas Yang
Email Thomas
Formerly President, International Callaway, SVP International Starbucks, senior leadership positions internationally with Coca-Cola, Procter & Gamble, and Clorox. Board of Advisors University of San Diego Business School. Board of Governors of Gemological Institute of America. BS University of Colorado; Masters Degree for the American Graduate School of International Management (Thunderbird).
Tony Botterill
Partners with executives to drive change across a range of business sectors, supporting them through high-stakes transitions. Tony supports leaders and teams in onboardings, new team start-ups, team integration, major project performance and trouble-shooting, leveraging dozens of client engagements – including BP, Petrofac, Talisman Sinopec, HBOS, Reuters, Cisco Systems and Lloyds Banking Group.
Susanne Pennella
Email Susi
An Austrian native with 20+ years of Management, Human Resource and Legal experience in Europe and the United States. Her rare ability to think cross-functionally as well as cross-culturally led to outstanding successes at Procter & Gamble in both brand management and human resources. Susanne was also a Law Professor and Assistant District Attorney. Doctorate in Law, Salzburg University.
Mary Vonnegut
Email Mary
Formerly President Gumps Catalog & SVP Marketing Hanover Direct, VP Marketing Ross-Simons and COO Passport Internationale. Experience in strategic planning, database marketing, direct response merchandising and merchandise fulfillment operations. Diverse categories from high-end jewelry to moving and storage franchise services in entrepreneurial and corporate environments. BA Middlebury College; MBA Harvard.
Mark Anderson
Operating executive with experience in Europe and Asia. Leadership roles at Pearson, including Managing Director UK, Managing Director Europe and Strategy-International. Executive positions for Spalding Evenflo in Asia Pacific and Patientline in the UK. Non-executive director of Hubbub and sits on the appeal board of the children's charity Buttle UK. Author of The Leadership Book and a Cambridge Fellow in Science & Policy.
Linda Hlavac
Human Resources leader supporting leaders and teams during transitions across industries and geographies. Helps executives improve their personal impact and performance in leading change, developing teams and delivering results. At Catalent Pharma Solutions, created a global HR function for the pre-IPO company. Previous experience at LexisNexis, Dun & Bradstreet and Westinghouse. B.A. Susquehanna University; MBA Ohio University.
Joe Durrett
Former CEO of Information Resources, Broderbund Software and Advo. Senior line positions at Kraft General Foods including SVP of Sales and President of Grocery Products, and Procter & Gamble. Throughout his career, Joe has driven dramatic increases in revenue, profitability and value for companies he has served on the boards of, run, worked in and consulted to. BA Duke; MBA Wharton.
Email Ed
Diverse organizational development consulting experience across retail, telecommunications, electronics, manufacturing, health care, financial services and the utility industry. Served in senior leadership roles at both Mercer Human Resources, as a worldwide partner, and at Watson Wyatt as worldwide leader for performance management services. BA at Lake Forest College; Masters, Loyola University, Chicago.
John Lawler
Former CEO of three private equity backed companies. Group President of Emerging Markets at LexisNexis after long career at Dun & Bradstreet. Proven transformational CEO, board member, consultant and coach with a strong track record supporting leaders and teams through complex transitions. Extensive experience in Americas, Europe and Asia. BA Williams College; MBA University of Virginia.
Jayme Check
Partner & Co-Founder
Email Jayme
CEO of Quantum Global Partners and co-founder of PrimeGenesis. Developed world-class leaders for such companies as Cisco, Kellogg's, Blue Shield, Johnson & Johnson, Panasonic, LexisNexis, DaVita, Anthem, GMAC and Kimberly-Clark. Instrumental in building tech company named one of "SoCal's 50 Fastest Growing Companies." Developed nation's first medical franchise. Expertise in structuring innovative equity-based venture transactions. BS Syracuse; MBA UCLA.
George Bradt
Email George
Led the revolution in how people start new jobs. Prior to founding PrimeGenesis, George served as chief executive of J.D. Power's Power Information Network spin off and in general management, marketing and sales at Coca-Cola in Europe and Asia, Procter & Gamble and Unilever. Principal of CEO Connection and contributes a weekly column to Forbes.com, The New Leader's Playbook. AB Harvard; MBA Wharton.
Susan Lawler
Email Susan
Change leader with particular expertise in strategy, marketing, executive communications and coaching. Transformed disparate local groups into a cohesive, award winning global marketing team at D&B. Led strategic plan process, re-branded the company, and drove growth initiatives, setting the path for 6-fold growth in shareholder value. ICA Executive Coach. B.A. Union, MBA; Columbia University.
George Olcott, PhD
Current non-executive director of Denso Corporation and Hitachi Chemical and Affiliate Professor at the Department of Business and Commerce at Keio University. He was formerly Managing Director, Head of Equity Capital Markets for UBS Warburg in Tokyo. Previous roles at Shell and Swire. Author of "Conflict and Change: Foreign Ownership and the Japanese Firm." Fluent in Japanese. Oxford undergraduate, INSEAD MBA, PhD from Cambridge.
Roger Neill
CEO/Managing Partner of Lintas Australia, Synectics Corporation, Center for Creativity – City University London. Helped Sam Wanamaker re-build Shakespeare's Globe in London. Started his working life as a professional rock musician. Roger is one of the world's thought leaders on innovation and creativity. Based in London, UK, he writes, speaks and conducts masterclasses and workshops around the world and is a principal of Per Diem Consulting.
Harry Kangis
President of P&G's Millstone gourmet coffee subsidiary, GM of the Home Entertainment Network, VP Marketing for Kenner Toys and COO for Nutrition Technology Corp. A 25+ year marketing and general management veteran, who has managed a broad range of challenges from mature consumer packaged goods brands to a wide variety of innovative service and product start-ups and is a principal of One Page Solutions. BA Williams; MBA Wharton.
Rob Gregory
CEO with an unusual mix of senior experience in both the private and public sectors and an extraordinary record of success managing both large profitable companies and turnaround situations. As President of VF Corporation, he and his team tripled its sales to $3B and grew its profit 500%+ to turn it into the largest and most profitable publicly held apparel company in the world at that time. Served on the boards of over a dozen companies including Gitano, London Fog, Promus Hotels, Frisby International and USF&G. BA Wofford; law degree U. South Carolina; AMP Harvard.
Bill Berman, PhD
A clinical and consulting psychologist, worked with a number of public and private companies, including Xerox, Unilever, Clinical Communications Group, Diageo, and Kaiser-Permanente. He is co-author of 3 books and over 50 articles on a variety of psychology and business topics. He is a fellow of the American Psychological Association, board-certified by the American Board of Professional Psychology, has taught at Cornell Medical College and Fordham University and is a principal of Berman Leadership Development. AB Harvard; PhD Yale.
[caldera_form id="CF5caa7db7b764d"]


text:
Keyword: krueger
Former Obama economic adviser Alan Krueger dead at 58 [Top Clinton & Obama Advisor]
05/05/2019 10:34:26 PM PDT · by NoLibZone · 65 replies
https://nypost.com/2019/03/19/former-obama-economic-adviser-alan-krueger-dead-at-58/ ^ | 4-19-19 | By Lia Eustachewich
Alan Krueger, a Princeton University economist who served as a top adviser to Presidents Bill Clinton and Barack Obama, died Saturday, according to the university. The 58-year-old committed suicide, his family said in a separate statement released by the school Monday. "It is with tremendous sadness we share that Professor Alan B. Krueger, beloved husband, father, son, brother, and Princeton professor of economics took his own life over the weekend," the family said. "The family requests the time and space to grieve and remember him." Krueger served as a Labor Department economist under Clinton, then as a top Treasury official...
Why did Obama and Clinton economic adviser, 58, take his own life ...
03/19/2019 3:29:50 PM PDT · by Candor7 · 124 replies
Daily Mail ^ | 11:49 EDT, 19 March 2019 | Updated: 15:51 EDT, 19 March 2019 | By Jennifer Smith and Associated Press and Ariel Zilber For Dailymail.com
The suicide of Alan Krueger, a former Obama and Clinton adviser who killed himself this weekend, has shocked the worlds of politics and business where he was universally revered. Krueger, 58, had a new book coming out in June and was still a member of faculty at Princeton University in New Jersey. He lived at home with his wife Lisa, with whom he has two children, Benjamin, 28, and Sydney, 26. He is survived by them, his elderly parents and siblings. The family confirmed that he killed himself in a statement that was released by Princeton on Monday but no...
Alan Krueger, former White House economist, dead at 58 from suicide
03/18/2019 4:32:15 PM PDT · by John W · 121 replies
nydailynews.com ^ | March 18, 2019 | Gina Salamone
Alan Krueger, a Princeton University economist and a top adviser under two Presidents, has died at age 58 after taking his own life. "It is with tremendous sadness we share that Professor Alan B. Krueger, beloved husband, father, son, brother, and Princeton professor of economics took his own life over the weekend," a statement from his family reads. "The family requests the time and space to grieve and remember him. In lieu of flowers, we encourage those wishing to honor Alan to make a contribution to the charity of their choice." His passing was initially announced Monday by Princeton, which...
Top Obama Economic Aide Cuts and Pastes His Statements
02/04/2013 7:45:10 AM PST · by Hoodat · 8 replies
White House Dossier ^ | February 4, 2013, 8:40 am | Keith Koffler
White House Council of Economic Adviser Chair Alan Krueger has begun his monthly statements on the nation's employment situation with nearly the exact same sentences almost every month since November 2011, just after he was installed as one of Obama's most senior economic advisers. With the exception of some variation in the May 2012 statement, Krueger has mailed it in every month, not bothering to change a thing in the opening lines of his commentary on the statistic that is perhaps more important to Americans. Krueger's statements are released by the White House the morning the latest employment numbers become...
A Deep Faith in What's Been Proved (Obama by the numbers - Perry by faith)
New York Times ^ | September 1, 2011 | CHRYSTIA FREELAND | REUTERS -- Letter to Editor
NEW YORK — You might call it the cognitive divide — the split between an evidence-based worldview and one that is rooted in faith or ideology — and it is one of the most important fault lines in the United States today. President Barack Obama called attention to the cognitive divide, and reminded us...when he chose the Princeton University economist Alan Krueger to lead his Council of Economic Advisers. Mr. Krueger is a labor economist, and at first blush, that focus may seem the important part of his résumé......his mastery of data and his utter commitment to the truths it...
Obamanomics stays on path to failure with Krueger
08/30/2011 9:26:58 AM PDT · by freespirited · 14 replies
Washington Examiner ^ | 08/29/11 | Editorial Board
Any hopes that President Obama might somehow recognize the utter failure of his economic policies and seek new ideas and directions were dashed by his selection Monday of Princeton University economist Alan E. Krueger to succeed Austan D. Goolsbee as chairman of the Council of Economic Advisers. Krueger previously served as an assistant secretary of the Treasury under Timothy Geithner. Obama praised Krueger's work during the first two years of his administration, and said Krueger's chief task in the new job will be to help develop policy recommendations to get the stagnating economy growing again. Don't expect any new ideas...
Obama to prod Congress on jobs
08/29/2011 3:42:35 PM PDT · by ColdOne · 42 replies
Politico44 ^ | 08/29/11 | MATT NEGRIN
President Obama formally announced that Alan Krueger will be his newest economic adviser Monday morning, also suggesting in a Rose Garden statement that he's about finished with his jobs plan that he'll announce next week. "I will be laying out a series of steps that Congress can take immediately to put more money in the pockets of working families and middle-class families,
White House to nominate Krueger as top economist
08/29/2011 5:33:23 AM PDT · by sunmars · 71 replies
Reuters ^
President Barack Obama on Monday will announced he has chosen Princeton University labor economist Alan Krueger to become the top White House economist, a White House official said. Krueger would succeed Austan Goolsbee as chairman of the Council of Economic Advisers. The decision comes as Obama prepares to unveil a jobs package in a speech planned for shortly after the September 5 Labor Day holiday. With U.S. unemployment at a stubbornly high 9.1 percent and amid fears the economy could slide back into recession, Obama is under pressure to show he is doing all he can to bolster growth. Goolsbee,...
The Fallen at Fort Hood - Amy Krueger
11/06/2009 9:14:17 PM PST · by Saije · 10 replies · 707+ views
Washington Post ^ | 11/6/2009 | Staff
Amy Krueger joined Army in aftermath of Sept. 11 attacks. In Kiel, Wis., a rural community of 3,200, feeling for the military runs so strong that, every Veterans Day, the high school invites local vets to lunch. So it was not entirely surprising that the week after Amy Krueger, a college student preparing to be a social worker, watched the Sept. 11, 2001, terrorist attacks on television, she and her roommate walked into an Army recruiting office to enlist. She felt she needed to be "an army of one," a story in the local Tri-County Times quoted Krueger as saying...
Kiel Native Killed in Fort Hood Shootings
WBAY ^ | 11/6/2009 | Emily Matesic
A 1998 graduate of Kiel High School is among the 13 people killed Thursday when 39-year-old Major Nidal Hasan opened fire on his fellow soldiers at Fort Hood, Texas, getting ready to deploy overseas. Thirty people were wounded. Staff Sergeant Amy Krueger was killed at Fort Hood. The first thing the mayor of Kiel did Friday morning when he heard the news about 29-year-old Amy Krueger was to order all the flags in the city lowered to half-staff. The mayor, who's too close to the Krueger family to speak on-camera, told us he feels overwhelmed and he still can't believe...
Seeds of Doubt [New Orleans ACORN office shutting down?]
09/20/2009 6:14:20 PM PDT · by Ebenezer · 38 replies · 2,798+ views
The (New Orleans) Times-Picayune ^ | September 20, 2009 | Bruce Nolan
ACORN, a social justice organization with roots in [New Orleans], battles a string of scandals. The announcement stuck to a wall outside the entrance to ACORN's local office in the 2600 block of Canal Street quietly signals the trouble afoot. In English and Spanish, the Association of Community Organizations for Reform Now tells walk-up clients that ACORN's housing office has shut itself down for two weeks to immerse itself "in an intensive training program." The sign is a symptom of a tumultuous week in the history of a controversial poor people's social justice movement -- one founded by a New...
BILL WOULD BE STEP BACK FOR N.Y. HUNTERS
04/16/2009 4:30:04 PM PDT · by neverdem · 19 replies · 573+ views
NY Post ^ | April 12, 2009 | KEN MORAN
ONE of the high notes this past hunting season was the success of the new Junior Big-Game hunting license authorized by Gov. David A. Paterson, which allows 14- and 15-year-olds to hunt big game for the first time. State Senator Liz Krueger (D-N.Y.) is trying to undo the positive steps taken by the state legislature last year by introducing Senate Bill 3598, which would raise the hunting age across the board. Specifically, the bill increases the minimum age for obtaining a hunting license from 16 to 18 years of age, and would require anyone under the age of 20 to...
Freddy Krueger Wannabe Slashes Friend, Gets Slammer
04/06/2007 7:31:59 AM PDT · by bedolido · 7 replies · 389+ views
TMZ ^ | 4-6-2007 | staff writer
Call it "A Nightmare on Bulwer Road." A British man, Jason Moore, could spend the rest of his life in the clink for attacking his friend John-Paul Skamarski with a knife-equipped glove -- much like the one Freddy Krueger used to snag his prey in the "Nightmare on Elm Street" horror flicks.
January 24, 1935: First canned beer goes on sale
01/24/2007 12:34:36 PM PST · by fgoodwin · 11 replies · 475+ views
The History Channel ^ | January 24, 2007 | anon
January 24, 1935: First canned beer goes on salehttp://www.history.com/tdih.do?action=tdihVideoCategory&id=52350 Canned beer makes its debut on this day in 1935. In partnership with the American Can Company, the Gottfried Krueger Brewing Company delivered 2,000 cans of Krueger's Finest Beer and Krueger's Cream Ale to faithful Krueger drinkers in Richmond, Virginia. Ninety-one percent of the drinkers approved of the canned beer, driving Krueger to give the green light to further production. By the late 19th century, cans were instrumental in the mass distribution of foodstuffs, but it wasn't until 1909 that the American Can Company made its first attempt to can beer....
Talk radio host, producer sue KNBR over firing
10/24/2005 9:25:55 PM PDT · by Roberts · 9 replies · 399+ views
San Francisco Chronicle ^ | 10/24/05 | Phillip Matier, Andrew Ross
Fired KNBR sports talk jock Larry Krueger and ex-morning show producer Tony Rhein have filed a pair of blistering lawsuits against their former employer -- saying they were fired after the infamous "brain-dead Caribbean hitters" flap simply so the station could keep its deal to broadcast Giants games. Just when it looked like the storm might pass with a weeklong suspension for Krueger and an apology from the mike man, KNBR's morning crew rained on the parade six days later by playing comedy bits from "South Park" and from Dana Carvey's "Church Lady'' to mock Alou for calling Krueger a...


Up! Up! And away we go in a... a balloonhouse.
Pixar's going to lift your spirits.
Wheee! Not only do I want to see "Up", the trailer also made me want to watch ALL of the Pixar masterpieces again as soon as possible.
Decemberists, live, tonight on NPR.