Charlotte Healthcare Insurance - Health Care All Year
http://www.healthcareallyear.com Health Care All Year 1801 North Tryon Street Ste. B-108 Charlotte, NC 28206 1-800-634-6669.
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Charlotte Healthcare Insurance - Health Care All Year - Video
Boehner #39;s Obamacare Lawsuit Explained
House Republicans filed a long-threatened lawsuit Friday against the Obama administration over unilateral actions on the health care law that they say are abuses of the president #39;s executive...
By: Secular Talk
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Health Care Rally
Thousands gathered on the lawn at Queens Park on Friday, November 21 to voice their displeasure over the health care in Ontario. That includes the Chatham-Kent Health Coalition, Members bussed...
By: 909sendme
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By LINDA A. JOHNSON and STEVE ROTHWELL
Associated Press
In a big year for deal making, the health care industry is a standout.
Large drugmakers are buying and selling businesses to control costs and deploy surplus cash. A rising stock market, tax strategies and low interest rates are also fueling the mergers and acquisitions.
It's all combining to make 2014 the most active year for health care deals in at least two decades. The industry has announced about $438 billion worth of mergers and acquisitions worldwide so far, about 14 percent of the $3.2 trillion total for all industries, according to data provider Dealogic. Overall, M&A is on track for its best year since 2007, the year before the financial crisis intensified.
"Health care has been a sleepy niche of M&A until recently, but the giant has been awakened," says Ken Menges, a senior partner handling M&A at law firm Akin Gump in New York.
To a large extent, the deals are being driven by "cost pressure on the entire health care system," as insurers and government health plans increasingly hold down or even reduce reimbursements to drug, device and service providers, says Ashtyn Evans, pharmaceutical and biotech analyst with investment firm Edward Jones in St. Louis, Missouri.
Companies also are looking to expand market share, and boost their portfolios in hot areas such as drugs for cancer and hepatitis C, she says.
Drugmaker Merck & Co., for example, agreed in June to pay nearly $4 billion for Idenix Pharmaceuticals Inc. to combine that company's hepatitis C medicines with its own.
Taxes are another reason behind the rush to the negotiating table.
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Health care mergers, acquisitions lead surge in global deals
In a big year for deal making, the health care industry is a standout.
Large drugmakers are buying and selling businesses to control costs and deploy surplus cash. A rising stock market, tax strategies and low interest rates are also fueling the mergers and acquisitions.
It's all combining to make 2014 the most active year for health care deals in at least two decades. The industry has announced about $438 billion worth of mergers and acquisitions worldwide so far, about 14 percent of the $3.2 trillion total for all industries, according to data provider Dealogic. Overall, M&A is on track for its best year since 2007, the year before the financial crisis intensified.
"Health care has been a sleepy niche of M&A until recently, but the giant has been awakened," says Ken Menges, a senior partner handling M&A at law firm Akin Gump in New York.
To a large extent, the deals are being driven by "cost pressure on the entire health care system," as insurers and government health plans increasingly hold down or even reduce reimbursements to drug, device and service providers, says Ashtyn Evans, pharmaceutical and biotech analyst with investment firm Edward Jones in St. Louis, Missouri.
Companies also are looking to expand market share, and boost their portfolios in hot areas such as drugs for cancer and hepatitis C, she says.
Drugmaker Merck & Co., for example, agreed in June to pay nearly $4 billion for Idenix Pharmaceuticals Inc. to combine that company's hepatitis C medicines with its own.
Taxes are another reason behind the rush to the negotiating table.
Some big, U.S. pharmaceutical, biotech and medical device companies have been trying to acquire overseas rivals, allowing them to move their headquarters to a country with a lower tax rate. The deals also give the buyer access to billions in overseas profits to invest in research and development, without having to bring those profits back to the U.S. and pay taxes on them.
Medical device maker Medtronic's $43 billion acquisition in June of Covidien, a Dublin, Ireland-based rival, is an example.
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As drugmakers and hospitals cut costs and sharpen focus, health care deals lead global surge
Ron Paul on Medicare, Medicaid, HMOs and the Decline the American Healthcare System
Take advantage of audible.com's special offer and start listening to audiobooks on your iPod or Smartphone today. Just click on the link Below. http://www.qk...
The Clinton health care plan, known officially as the Health Security Act, was a 1993 healthcare reform package proposed by the administration of President B...
http://www.RonPaul.com 05/31/2010 Introducing the Private Option Health Care Act by Ron Paul Most everyone agrees that health care in the United stated has m...
Why are insurance rates so high? Will more regulation and Universal Care Help? Experts say No! Patriots United counters the Obamacare plan! Hosts Health Care Panel Discussion in Crystal...
06/14/2010 - http://www.RonPaul.com Obamacare Is Bad For Your Health by Ron Paul The administration's terrible health care reform bill is now law. But the de...
This video gives easy-to-understand explanations for various types of accounts as they relate to health plans and tax implications. It also shows the differe...
National Health Care Reform ( or Health Insurance Regulations) Evans, GA (By Anibal Ibarra) - Free clinics are still not being considered in either of the dr...
The march after the "Rally Against Greed" at City Hall, in Colorado Springs, October 13, 2009. In the mid-1980s, under Raygun, Medicare also began encouragin...
Max Baucus grills Kathleen Sebelius on the implementation of the Affordable Care Act. Max Baucus had single payer advocates arrested at a hearing. Baucus adm...
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Sri Lankan health workers wear protective gear as they attend a preparedness program for Ebola at the Infectious Disease Hospital for fever in Colombo, Sri Lanka, Tuesday, Oct.28, 2014. Airports in Asia have stepped up their defenses: screening passengers who have travelled from affected countries, taking any with high temperature for observation and trying to keep contact them with for 21 days, the incubation period. According to the World Health Organization, more than 10,000 people have been infected with Ebola and nearly half of them have died. (AP Photo/Eranga Jayawardena)
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By Elias Meseret, The Associated Press
ADDIS ABABA, Ethiopia - More than 5,000 additional health care workers are needed to fight Ebola in the three most affected countries in West Africa, the president of the World Bank said Tuesday.
Jim Yong Kim said he is worried about where those health care workers can be found given the Ebola fear factor. The World Bank president spoke in Ethiopia alongside U.N. Secretary-General Ban Ki-moon and African Union chairwoman Nkosazana Dlamini-Zuma.
Ban said the transmission of the virus continues to outpace the international community's response. He appealed for African Union member states not to impose Ebola-related travel restrictions or close their borders.
"We need to have a steady stream of health care workers from Africa coming into the three affected countries. The head of the U.N. Mission for Ebola Emergency Response, David Nabarro, has told us that we need at least 5,000 health workers from outside the region," Jim said.
"Right now, I'm very much worried about where we will find those health care workers. With the fear factor going out of control in so many places, I hope health care professionals will understand that when they took their oath to become a health care worker it was precisely for moments like this," he said.
Dlamini-Zuma said African Union states have pledged to send more than 2,000 health care workers into West Africa. She did not say when the workers would arrive.
"The disease, which is not new to the world, and its manifestations in these countries, has caught us by surprise. With the wisdom of hindsight, our responses at all levels continental, global and national were slow, and often knee-jerk reactions that did not always help the situation," Dlamini-Zuma said.
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Stem Cell Cure for "Bubble Baby" Disease (SCID), Pioneered by UCLA #39;s Don Kohn
On November 18th, 2014, a UCLA research team led by Donald Kohn, M.D., announced a breakthrough gene therapy and stem cell cure for "bubble baby" disease, or severe combined ...
By: California Institute for Regenerative Medicine
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Stem Cell Cure for "Bubble Baby" Disease (SCID), Pioneered by UCLA's Don Kohn - Video
3rd International Conference and Exhibition on Cell Gene Therapy
3rd International Conference and Exhibition on Cell Gene Therapy, October 27-29, 2014 at Las Vegas, USA. Cell Therapy conference is an outstanding event co...
By: Srinu Babu Gedela
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3rd International Conference and Exhibition on Cell & Gene Therapy - Video
THANK YOU from Saving Eliza!
THANK YOU to all the supporters of Saving Eliza and helping make history! YOU did it! You #39;ve made a significant impact on stopping Sanfilippo Syndrome for this generation and future generations!...
By: SavingEliza.com
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HOPE, HYPE REALITY: ZINC FINGER GENE THERAPY TO CONTROL OR CURE HIV
A video to answer your questions about a gene therapy approach to an HIV cure. On Nov 5, 2014, the defeatHIV Community Advisory Board hosted a talk with Dr. Philip D. Gregory (Chief Scientific...
By: defeatHIV
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HOPE, HYPE & REALITY: ZINC FINGER GENE THERAPY TO CONTROL OR CURE HIV - Video
Gene Therapy advance online publication 6November2014; doi: 10.1038/gt.2014.95
P FForde1,3, L JHall2,3, Mde Kruijf1, M GBourke1, TDoddy1, MSadadcharam1 and D MSoden1
The current standard of care for cancer uses surgery, radiation and chemotherapy to achieve local tumour control and reduce the risk of disease recurrence. 1 Immunotherapy is potentially a new therapeutic pilar, which can complement the current standard of care and can reduce risk of disease recurrence.2, 3, 4, 5
Immunotherapy-based therapies have the potential to activate a tumour antigen-specific response, which can help to eradicate the tumour and reduce the risk of disease recurrence.6, 7, 8, 9 Delivering immunotherapies clinically can be achieved through a number of approaches including the use of gene therapy, which has many applications and methodologies already developed for cancer treatment.10, 11, 12, 13 For gene therapy to be successful, safe and efficient gene delivery is critical. 12 In current cancer gene therapy studies, viral vectors are used in the majority of gene delivery approaches, as they have high-efficiency transfection.14, 15 However, there are a number of significant drawbacks that include efficiency of production, host immunogenicity, integration and safety. 15, 16 An alternative option to viral vectors is plasmid DNA. Toxicity is generally very low, and large-scale production is relatively easy. 17 However, a major obstacle that has prevented the widespread application of plasmid DNA is its relative inefficiency in gene transfection.17, 18 Therefore, most applications for plasmid DNA have been limited to vaccine studies, with a few exceptions.18, 19 Consequently, methods that can significantly increase plasmid DNA transfection efficiency will greatly extend the utility of this promising mode of gene transfer. The technique of electroporation is widely used in vitro to effectively introduce DNA and other molecules into eukaryotic cells and bacteria. Application of short electrical pulses to the target cells permeabilises the cell membrane, thereby facilitating DNA uptake.20 A number of studies, preclinical and clinical, have shown highly successful responses with electroporated plasmid DNA encoding immune genes and also chemotherapeutic drugs.21, 22, 23, 24, 25 Recently, we have shown that applying electroporation to a range of tissue types using a new electroporation system, EndoVe in a large pig model. This will significantly enhance the application of electrogene therapy. 26
Several cytokines have demonstrated significant antitumour effects. Among these, granulocytemacrophage colony-stimulating factor (GmCSF) is one of the most potent, specific and long-lasting inducers of antitumour immunity. GmCSF can mediate its effect by stimulating the differentiation and activation of dendritic cells (DCs) and macrophages, and by increasing the antigen presentation capability.27 For optimal antigen presentation, engagement of the T-cell receptor with an antigen/major histocompatibility complex requires the costimulatory molecule such as B7-1 (CD80) and B7-2 (CD86). 27, 28 Subsequently, DC and macrophages process and present tumour antigens to T cells, and to both CD4+ and cytotoxic (CD8+) T cells, by augmenting the antitumour response.28 As such, GmCSF is particularly effective in generating systemic immunity against a number of poorly immunogenic tumours. 27
We recently characterised a non-viral vector therapy system: EEV plasmid (pEEV) with a vastly superior expression capacity when compared with a standard control vector. 26 The purpose of this study was to test the therapeutic potential of the pEEV system. We hypothesised that pEEV has the capability to reach the therapeutic threshold for the treatment of solid tumours. We present here the use of pEEV as a gene therapy vector carrying murine GmCSF and human b7-1 genes (pEEVGmCSF-b7.1). We used electroporation as a means to facilitate the delivery of the pEEV and assessed the efficacy and immune induction in primary and secondary responses to treatment in murine colon adenocarcinoma and melanoma cancer models.
In the current study, we investigated the therapeutic efficacy of pEEVGmCSF-b7.1 when compared with a standard vector also expressing GmCSF-b7.1. To test this, two tumour types (CT26 murine colorectal and B16F10 metastatic melanoma) were treated by electroporating tumours with pMG (standard plasmid backbone), pGT141GmCSF-b7.1 (standard plasmid therapy), pEEV (backbone) and pEEVGmCSF-b7.1 ( Figure 1). As expected, the volumes of all non-electroporated (untreated) CT26 tumours and those treated with the empty plasmids, pMG and pEEV, significantly increased (P<0.01) in size ( Figure 1a). However, we did observe that the empty pEEV plasmid inhibited growth of the CT26 tumour between days 8 and 12, which we have observed previously.26 Both therapeutic plasmids delayed the growth rate of the CT26 tumour. Importantly, the growth of pEEVGmCSF-b7.1-treated tumours was significantly more inhibited compared with pGT141GmCSF-b7.1-treated tumours (P<0.002) and untreated control tumours (P<0.0004). By day 26 post-treatment, the untreated and the pMG- and pEEV-treated groups of animals were euthanised because of tumour size ( Figure 1b). Although the standard therapy pGT141GmCSF-b7.1 did inhibit tumour growth, all animals from this group were killed by day 36 when the tumours reached the ethical size of 1.7cm3. One mouse was removed from the pEEVGmCSF-b7.1-treated group on day 36 and again at day 45 because of tumours exceeding the ethical size; however, the remaining 66% of the mice survived up until day 150 post-treatment when they were then killed for subsequent immune analysis. To further test the efficacy of pEEVGmCSF-b7.1 therapy, we used the B16F10 melanoma cell line because of its aggressive nature. Following the same experimental protocol as described for the CT26 model ( Figure 1c), we again observed that untreated tumours grew exponentially with the killing of the mice from day 12 onwards (because of tumour size). Again, we observed that pEEVGmCSF-b7.1 treatment delayed tumour growth when compared with the untreated group (P<0.0001) and pGT141GmCSF-b7.1 (P<0.0001). In terms of survival, the pMG, pEEV, untreated and pGT141GmCSF-b7.1-treated group of animals were killed by day 28 (Figure 1d). Notably, we observed an even greater survival efficacy for the pEEVGmCSF-b7.1 (when compared with the CT26 model) in that 100% mice survived and all remained tumour free for 150 days post-treatment until they were removed for subsequent immune analysis. Similar results were obtained in both tumour types treated based on a range of tumour sizes (Supplementary Figure S2). Taken together, these data indicate that pEEVGmCSF-b7.1 treatment is able to significantly reduce (in the CT26 model) or prevent (B16F10 model) primary tumour growth.
Therapeutic effect on established CT26 and B16F10 solid tumours. (a) Representative CT26 tumour growth curve: each Balb/C mouse was subcutaneously injected with 5 105 CT26 cells in the flank. On day 14 posttumour inoculation, tumours were treated with pMG (), pGT141GmCSF-b7.1 (), pEEV () and pEEVGmCSF-b7.1 () or untreated (). Six mice per groups were used and the experiment was performed two times. Tumour volume was calculated using the formula: V=ab2/6. Data are presented as the meanss.e.m. It was observed that the pEEVGmCSF-b7.1 therapy delayed the growth of the tumours most effectively in comparison with the other groups. At 17 days post-treatment, pEEVGmCSF-b7.1 significantly delayed tumour growth compared with untreated tumour (***P<0.0004) standard therapy vector pGT141GmCSF-b7.1 (**P<0.002). (b) Representative KaplanMeier survival curve of CT26-treated tumours was measured. Only mice treated with pEEVGmCSF-b7.1 survived. Sixty-six per cent of mice survived up to 150 days. All other groups were killed by day 36. (c) Representative growth curve of B16F10 tumour. Each C57BL/6J was subcutaneously injected with 2 x105 B16F10 cells in the flank of the mice. On day 15 posttumour inoculation, tumours were treated with pMG (), pGT141GmCSF-b7.1 (), pEEV () and pEEVGmCSF-b7.1 () or untreated (). Six mice per groups were used and the experiment was performed two times. At 12 days post-treatment, pEEVGmCSF-b7.1 significantly delayed tumour growth compared with untreated tumour (**P<0.0001) standard therapy vector pGT141GmCSF-b7.1 (*P<0.0001). (d) Representative KaplanMeier survival curve of B16F10 showing pEEVGmCSF-b7.1 had 100% survival up to 150 days post-treatment with all other groups killed by day 28. Similar results were obtained in two independent experiments.
As already indicated, for optimal cancer therapy, robust immune responses must be induced; thus, to determine immune cell recruitment, we performed a comprehensive immune population profile of spleens and tumours 72h post-treatment. CT26 tumour mice treated with pEEVGmCSF-b7.1 had a significantly greater percentage of splenic CD19+ (B cells), DX5+/CD3+ (natural killer T (NKT) cells), DX5+/CD3 (NK cells) and CD8+ (cytotoxic T cells) as shown in Table 1. Within the tumour environment, we observed that the percentage of all cell types examined (with the exception of CD4+ cells (T cells)) were significantly greater in pEEVGmCSF-b7.1-treated tumours when compared with untreated tumours. Importantly, when the therapeutic plasmid treatments were compared, we observed that pEEVGmCSF-b7.1-treated mice had significantly more splenic and tumour CD19+ cells (P<0.05) and significantly greater number of tumour DX5+/CD3 (P<0.001), F4/80+ (macrophages) (P<0.001) and CD8+ (P<0.001) cells than control pGT141GmCSF-b7.1-treated mice. We observed a similar immune profile for the B16F10-treated mice ( Figure 2b). Splenic and tumour CD19+ (P<0.001), DX5+/CD3+ (P<0.01), DX5+/CD3 (P<0.01), CD11c+ (DCs) (P<0.001), F4/80 (P<0.001) and CD8+ (P<0.001) cells were all significantly higher for the pEEVGmCSF-b7.1-treated mice than for untreated animals. However, we did not observe any significant differences in CD4+ or T-cell receptor +/CD3+ ( T cells) (data not shown). Notably, when the standard pGT141GmCSF-b7.1 therapy was compared with pEEVGmCSF-b7.1, the percentage of CD19+ (P<0.001), DX5+/CD3+ (P<0.01), CD11c+ (P<0.001) and CD8+ (P<0.001) cells were all significantly greater, indicating that pEEVGmCSF-b7.1 recruits a superior immune recruitment locally at the tumour site. The spleen data had a similar trend as the tumour data with the percentage of CD19+ (P<0.01), DX5+/CD3+ (P<0.001), CD11c+ (P<0.001), F4/80 (P<0.001) and CD8+ (P<0.001) cells all significantly greater in the pEEVGmCSF-b7.1-treated mice when compared with the standard therapy. These data indicate that treatment with pEEVGmCSF-b7.1 induces robust recruitment of innate and adaptive immune cell populations in both colorectal and metastatic melanoma models.
Percentage of the respective T cells found locally at the site of the B16F10 tumours treated with pMG, pEEV, pGT141GmCSF-b7.1 and pEEVGmCSF-b7.1 or untreated. (a) Represents data obtained for the CD4+CD25+FoxP3+cells and (b) CD4+CD25FoxP3+ cells. Data represent the mean of the respective cells. Error bars show s.d. from four animals. The asterisks (*) indicate significant values of *P <0.05 and **P <0.01 as determined by one-way analysis of variance (ANOVA) following Bonferronis multiple comparison of pEEVGmCSF-b7.1 compared with untreated tumour. The asterisks () indicate significance values of P<0.05 as determined by one-way ANOVA following Bonferronis multiple comparison of pEEVGmCSF-b7.1 compared with the standard vector pGT141GmCSF-b7.1. The asterisks () indicate significant values of P<0.05 as determined by one-way ANOVA following Bonferronis multiple comparison of pEEVGmCSF-b7.1 compared with pMG. The asterisks (*) indicate significant values of *P<0.05 as determined by one-way ANOVA following Bonferronis multiple comparison of untreated compared with pEEV. Similar results were obtained in two independent experiments.
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Night of Violence (Futurist Remix)
Night of Violence Futurist Remix Alec Empire Alec Empire 2005 Digital Hardcore Recordings Ltd. Released on: 2005-05-23 Composer: Alec Empire Lyricist: Alec...
By: Alec Empire - Topic
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Interview with Michael Strzenberger of the Freedom Party Germany Nov 21 2014
By: Vlad Tepes
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Interview with Michael Strzenberger of the Freedom Party Germany Nov 21 2014 - Video
The Wonder of Freedom through Christ
November Miracle and Revival event.
By: DCLMHQ
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Let #39;s Play Monster Hunter Freedom Unite Part 255 Kellogs und Red Bull
Wer sich schon immer gefragt hat, warum der Teostra und die Lunastra im Vergleich zu den anderen Drachenltesten so komisch aussieht: Hier erfahrt ihr die Antwort. -------------------------------...
By: DeusNemesiX
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Let's Play Monster Hunter Freedom Unite Part 255 Kellogs und Red Bull - Video
FCS Day 50 - Freedom! Channel Spotlight
Freedom! Channel Spotlight, day 50! - To get a spotlight leave a comment below help your fellow partners! Today #39;s featured channels: RusherZ https://www.youtube.com/user/GamingRush123/featur.
By: Freedom!
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Mr Hollywood Four Story #1 | Rewritten Freedom Fighters
The Rewritten Freedom Fighters take down a Mr Hollywood Four Story.
By: Rewritten Freedom Fighters
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Mr Hollywood Four Story #1 | Rewritten Freedom Fighters - Video
Churchill: Champion of Freedom
Made in 1965 and narrated by Wynford Vaughan-Thomas, "Champion of Freedom" is a documentary covering the life of Sir Winston Churchill.
By: Rod Willerton
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