AAPS: PHOENIX VA

New Obamacare Endgame: the VA for All May 26, 2014 By Richard Amerling, M.D. author Physicians' Declaration of Independence Scandal at the Phoenix Veterans Administration lifted the curtain of secrecy on the VA’s secret waiting lists. The VA lies while patients die. This is by no means a new phenomenon. The nation’s single-payer system for veterans has long been greatly overloaded. Congress tried to fix it in 1996 by passing a law requiring that any veteran needing care had to be seen within 30 days. The VA is supposed to have a wonderful electronic medical records system, and the EMR is supposed to be the magic formula for efficiency and quality. The VA gamed the electronic system to hide the waiting lists. Readers of the British press will be struck by the similarities between fudging waiting lists at VA hospitals and stacking patients in ambulances outside UK hospitals. Finding it impossible to comply with a National Health Service mandate that all patients admitted to an emergency room be seen within four hours, ho spitals kept patients waiting in ambulances outside the ER! Britain’s NHS and our VA system are both administratively top-heavy, command-and-control bureaucracies. All such systems tend to expand, along with their budgets, as administrators hire more and more people to do what they were supposed to be doing. There is no competition, and virtually no accountability. Every problem is always someone else’s responsibility. Mandates and quotas, rather than incentives, are used to motivate those in the trenches. Physicians working in the VA system, like the NHS, are mostly salaried employees. There are many fine doctors in both systems, but the incentives in place do not reward them for going the extra mile, seeing the additional patient, or doing another procedure if it means going past their shift. Inevitably, these systems create backlogs and lengthening queues for care. Americans need to take a close look at the VA—and not only because of their concern about poor treatment of our wounded warriors. It is the prototype for Obamacare. The intent behind Obamacare is to completely centralize control over health care, and thus turn American health care into one huge Veterans’ Administration. In 2011 I wrote that Obamacare was designed as Medicaid for all. Medicaid expansion is a key component of the law. If Congress wanted to expand coverage to the ten million or so individuals who fall through the cracks of the private/public health system, this could have been accomplished easily by offering them Medicaid or Medicare. These creaky systems could be made to work better simply by eliminating the price controls on physicians and allowing them to balance bill patients for the difference between payment and the cost of providing service. But expanding coverage was not the goal. The stated goal of government central planners, and of many medical elites, is to abolish traditional fee-for-service medicine. They wrongly blame FFS for out of control health care spending. This is absurd on its face. FFS medicine pre-dates the massive health spending inflation that was largely brought on by Medicare and Medicaid, and the domination by third-party payers. The lack of price transparency and the removal of most disincentives to utilization of health services are what led to the incredible over-spending on health care that we’ve seen since the ‘60s. FFS is the only way to insure the prompt delivery of needed care. But what central planners want is for all physicians to be salaried employees of either the government or of large hospital systems. Then planners could centrally control care through “payment-for-performance” algorithms built into electronic records. The promptness and quality of care will suffer. Obamacare is already becoming like the VA. A kidney transplant patient suddenly developed blurred vision. This alarming symptom could signal a brain tumor or other serious diagnosis. I would have arranged for an MRI to be done the same day. Her new Obamacare plan, however, offered a specialist appointment two weeks hence. The shameful backlog in our VA system could be remedied overnight by either giving veterans vouchers for care in the private, FFS system, or by building incentives into the VA payment structure. Ah, but this would require an acknowledgment that their top-down system has failed. Richard Amerling, MD is an Associate Professor of Clinical Medicine and a renowned academic nephrologist at the Beth Israel Medical Center in New York City. Dr. Amerling studied medicine at the Catholic University of Louvain in Belgium, graduating cum laude in 1981. He completed a medical residency at the New York Hospital Queens and a nephrology fellowship at the Hospital of the University of Pennsylvania. He has written and lectured extensively on health care issues and is President-elect of the Association of American Physicians and Surgeons. Dr. Amerling is the author of the Physicians' Declaration of Independence.

SWISS MEDICAL WEEKLY : VACCINE ADJUVANTS

Vaccine adjuvants Aluminium was the first commercial vaccine adjuvant, used to improve the immunogenicity of diphtheria vaccine. Until recently, oil-in-water emulsions were the only other compounds added to the list of adjuvants. In recent years, many potential new classes of adjuvants have been discovered and have undergone testing for efficacy and safety in humans. This review discusses the different mechanisms of action of the available adjuvants and appraises new approaches using “vaccine-omics” to discover novel types of adjuvants. Abstract The purpose of vaccination is to prime a naïve immune system and establish a pathogen-specific protective immunological memory. Essentially, vaccination induces two important immune phenotypes: (i.) a virus-specific B-cell response with production of neutralising anti­bodies with the help of a T helper cell type 2 (Th2) memory and/or (ii.) a virus-specific cytotoxic T cell and T helper cell type 1 (Th1) memory. Currently, most commercially available vaccines target the induction of neutralising antibodies. The vaccine-induced immune response is influenced by: (i.) vaccine factors, i.e., type and composition of the antigen(s), (ii.) host factors i.e., genetic differences in immune-signalling or senescence, and (iii.) external factors such as immunosuppressive drugs or diseases. Adjuvanted vaccines ­offer the potential to compensate for a lack of stimulation and improve pathogen-specific protection. A large amount of data regarding adjuvanted vaccines concerns their safety and tolerability. Prevention of ­infection compared with nonadjuvanted vaccines is rarely examined. The best immune biomarker indicative of protection and prevention of infection is debated: most research has considered antibody titres, which are easy to measure, but T-cell responses, especially Th2 ­cytokine release and measurement B-cell activation directly might correlate better with protection. The adjuvant potential of aluminium salts was discovered in 1926, but their mechanism of action is complex and still not fully understood. In the last decade, new data on their mechanism of action have emerged, but most studies on vaccine efficacy have been performed in mice. MF59 and AS03 are squalene-based oil-in-water emulsions. Experiments with nanoparticle adjuvants suggest that the particle size may be a key factor for their activity: microspheres with diameters of <10 nm seem to ­activate antigen presenting cells, whereas particles with diameters of 30–100 nm show a slow release of antigen. MF59 has a droplet size of approximately 130 nm. ­Although the immunogenicity of MF59- and AS03-adjuvanted vaccines has been demonstrated in terms of antibody responses, the increased protective effect has only been shown in two studies and one study, respectively. New small molecules may help to significantly increase vaccine responses. Emerging technology such as in-­silico modelling of adjuvant receptor interactions using super-computers; combined with RNA sequencing and microarray single nucleotide polymorphisma discovery, uncovering critical steps in vaccine responses, will bring about the design of novel classes of adjuvants. Read the article This is a summary of a paper that was published on www.smw.ch. Must be cited as: Egli A, Santer D, Barakat K, Zand M, Levin A, Vollmer M, Weisser M, Khanna N, Kumar D, Tyrrell L, Houghton M, Battegay M, O’Shea D. Vaccine adjuvants – understanding molecular mechanisms to improve vaccines. Swiss Med Wkly. 2014;144:w13940.

GERMANY: HAMBURG-EPPENDORF Univ Hosp STEM CELL TRANSPLANT

1460 bed Univ.Hosp HAMBURG-EPPENDORF: Auto.Stem Cell Transplant approx. Euro 50,000.

CDC:(Carlos) CHAGAS' DISEASE

promed@promedmail.org to promed-post, promed-edr-post, promed-ahead-p. TRYPANOSOMIASIS (CHAGAS DISEASE) - USA ************************************** A ProMED-mail post ProMED-mail is a program of the International Society for Infectious Diseases Date: Tue 20 May 2014 Source: PawNation [edited] Chagas disease, a condition caused by infection with the protozoal parasite _Trypanosoma cruzi_, has always been a big problem for our neighbors to the south. The US Centers for Disease Control (CDC) says that it is "endemic throughout much of Mexico, Central America, and South America where an estimated 8 million people are infected." The United States has not been immune to Chagas disease, however. CDC "estimates that more than 300 000 persons with _Trypanosoma cruzi_ infection live in the United States" but says that most of these people "acquired their infections in endemic countries". Chagas disease is becoming increasingly important in [the US] right now for 2 reasons: 1. The range of the disease appears to be moving farther northward into the United States (can anybody say "climate change?") 2. The disease affects many different species -- most notably dogs and people. The parasite that causes Chagas disease is transmitted by triatomine bugs, more commonly called kissing bugs. Unlike many other types of vector-borne diseases, the bite of a kissing bug is not responsible by itself for transmission. The true story is a bit grosser. When a kissing bug bites a person, dog, or other mammal, it tends to defecate (poop) more or less at the same time. The bite causes the victim to scratch, and that activity is likely to push the nearby feces and the parasites it contains into the small wound caused by the bite. Dogs can also become infected with _T. cruzi_ by eating infected bugs or prey, or the disease can be passed congenitally from a mother to her offspring. The signs of Chagas disease in dogs vary with the duration of infection: - Acutely infected dogs typically have a fever, loss of appetite, lethargy, swollen lymph nodes, and an enlarged liver and/or spleen. This phase may go unnoticed by owners, particularly since the clinical signs tend to resolve with time. - Dogs have no symptoms at all in the latent phase, which may last for several years. - With chronic infection, however, dogs can develop a type of heart disease called dilated cardiomyopathy. This may result in congestive heart failure or more shockingly, affected dogs may drop dead before developing any symptoms of heart disease. Unfortunately, no medications have been found that effectively treats Chagas disease in dogs. Symptomatic treatment for dilated cardiomyopathy and congestive heart failure can help dogs feel better and live longer than they would otherwise, but the underlying problem remains. A vaccine is also not available, so prevention is limited to practices that limit a dog's exposure to kissing bugs and other sources of infection with _T. cruzi_. The Veterinary Medicine and Biomedical Sciences program at Texas A&M (Texas is a Chagas disease hotspot) makes the following recommendations: - Prevent dogs from eating bugs - House dogs indoors at night - Prevent dogs from eating potentially infected animals (mice, rats, etc.) - Test breeding females to prevent congenital transmission They also state that "although direct transmission from dogs to humans has not been reported, infection in dogs indicates the local presence of infected vectors, which may present an increased risk of vector borne transmission to humans." See CDC's website () for more information on Chagas disease in people and for photos of the bug, as well as the agent itself.

USA MAYO CLINIC (ROCHESTER) Prof. Stephen RUSSELL MBChB(Edin.) FRCP(Lond.) PhD (Lond.)FRCPath(UK) uses gene virotherapy in Plasma cell cancer.

sjr@mayo.edu Research goal is to demonstrate the value of oncolytic virotherapy as a new modality for the treatment of cancer. Long-Term Research Aims To develop genetically engineered oncolytic viruses that are selectively destructive to a variety of disseminated cancers, to elucidate the molecular targeting mechanisms that govern their cancer specificity, and to advance them to clinical testing. Mid-Term Research Aims Generate, study and translate novel oncolytic rhabdoviruses (VSV) and picornaviruses (EMCV). Advance imaging strategies to noninvasively monitor in vivo spread of oncolytic viruses. Develop clinically viable approaches for transient suppression or evasion of antiviral immunity to oncolytic viruses. Develop strategies to enhance extravasation of oncolytic viruses in tumors. Identify and exploit synergistic interactions between anticancer drugs and oncolytic viruses. Continue to advance the clinical development of oncolytic measles viruses (MV-NIS). Approach Viruses from several families are engineered in our laboratory. We currently have oncolytic projects focusing on Measles, Vesicular Stomatitis Virus, Coxsackievirus A21, and Mengovirus. Nonreplicative AAV, lentivirus and adenovirus vectors are also used extensively. Virus tropisms are engineered by the display of single chain antibodies and other targeting proteins on viral surface glycoproteins (measles, lentiviruses), or by incorporating microRNA target sequences at strategic sites in the viral genome (CVA21, VSV, Mengovirus). These targeting approaches were developed in our laboratory (Nat. Biotec. 2004, 22: 331-6; Nat. Biotec. 2005, 23: 209-14; Nat. Med. 2008, 14: 1278-83; J. Virol. 2010, 84: 1550-62) In vivo, virus propagation is noninvasively monitored by engineering the oncolytic virus genomes to encode secretable marker peptides, like carcinoembryonic antigen, or the thyroidal sodium iodide symporter (NIS) which concentrates radioactive iodine into virus infected tissues. These oncolytic monitoring approaches were also developed in our laboratory (Nat. Med. 2002, 8: 527-531, Blood 2004,103: 1641-6) and the technology has been advanced to clinical testing in phase I clinical trials here at Mayo Clinic. Immune elimination of intravenously administered oncolytic viruses is being addressed in several ways. For example, virus-infected cells are being used as vehicles to carry viruses via the bloodstream to sites of tumor growth, thereby avoiding antibody neutralization (Am J Hematol. 2009, 84: 401-7; Mol Ther. 2010, 18: 1155-64). Also, immunosuppressive drugs are being used in conjunction with oncolytic virotherapy to suppress the adaptive antiviral immune response, thereby facilitating repeat virus administration (Clin. Pharmacol. Ther. 2007, 82: 700-10). Clinical translation is our goal (Cancer Res. 2010, 70: 875-82) and we are fortunate at Mayo Clinic to have a GMP manufacturing facility for pilot-scale production of clinical-grade oncolytic viruses to support phase I clinical trials. We also have a group of scientists at Mayo Clinic who are dedicated the performance of FDA-mandated pharmacology and toxicology testing in support of our translational efforts. My research lab comprises approximately 10 scientists (3 technologists, 4 or 5 postdoctoral scientists and 1 or 2 graduate students). Additional students participate in lab. activities during the summer months. While the overarching goals of the projects undertaken in the laboratory are highly connected, individual lab members typically work relatively independently of each other, and are expected to play a major role in the development of their own project directions. UK DAILY MAIL Mayo Clinic researchers say the result demonstrated that virotherapy, destroying cancer with a virus that infects and kills cancer cells but spares normal tissues, can be effective against the deadly cancer multiple myeloma.. Viruses naturally come into the body and they destroy tissue.' He hopes the idea could eventually lead to a new treatment, and the team are also testing the measles virus’s effectiveness at fighting ovarian, brain, head and neck cancers and mesothelioma. 'We recently have begun to think about the idea of a single shot cure for cancer and that’s our goal with this therapy. 'These patients were not responsive to other therapies and had experienced several recurrences of their disease.' The findings appear in the journal Mayo Clinic Proceedings. Read more: http://www.dailymail.co.uk/sciencetech/article-2628617/Could-measles-cure-cancer-First-trial-experimental-treatment-leaves-49-year-old-woman-complete-remission.html#ixzz31yT3jKHm FULL TEXT http://www.mayoclinicproceedings.org/article/S0025-6196%2814%2900332-2/fulltext

Roy.Soc.Med "Int Journal of STD & AIDS"

2013 European Guideline on the management of proctitis, proctocolitis and enteritis caused by sexually transmissible pathogens Henry JC de Vries1,2,3,4⇑ Adele Zingoni5 John A White6 Jonathan DC Ross7 Alexander Kreuter8 1STI outpatient clinic, Cluster Infectious Diseases, Health Service Amsterdam, Amsterdam, The Netherlands 2Department of Dermatology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands 3Centre for Infectious Diseases and Immunology Amsterdam (CINIMA), Amsterdam, The Netherlands 4Centre for Infectious Disease Control, National Institute of Public Health and the Environment, Bilthoven, The Netherlands 5Department of Biomedical Sciences and Human Oncology, Dermatologic Clinic, University of Turin, Turin, Italy 6Department of Genitourinary Medicine, Guy's and St Thomas' NHS Foundation Trust, London, UK 7Sexual Health Clinic – University Hospitals Birmingham NHS Foundation Trust, Whittall Street Clinic, Birmingham, UK 8Department of Dermatology, Venereology, and Allergology, HELIOS St. Elisabeth Hospital Oberhausen, Germany HJC de Vries, STI Outpatient Clinic, Cluster Infectious Diseases, Health Service Amsterdam, Amsterdam, The Netherlands. Email: h.j.devries@amc.uva.nl Abstract Proctitis is defined as an inflammatory syndrome of the distal 10–12 cm of the anal canal, also called the rectum. Infectious proctitis can be sexually transmitted via genital-anal mucosal contact, but some also via mutual masturbation. N. gonorrhoeae, C. trachomatis (including lymphogranuloma venereum), Herpes Simplex Virus and T. pallidum are the most common sexually transmitted anorectal pathogens. Shigellosis can be transferred via oral-anal contact and may lead to proctocolitis or enteritis. Although most studies on these infections have concentrated on men who have sex with men (MSM), a significant proportion of women have anal intercourse and therefore may also be at risk. A presumptive clinical diagnosis of proctitis can be made when there are symptoms and signs, and a definitive diagnosis when the results of laboratory tests are available. The symptoms of proctitis include anorectal itching, pain, cramps (tenesmus) and discharge in and around the anal canal. Asymptomatic proctitis occurs frequently and can only be detected by laboratory tests. The majority of rectal chlamydia and gonococcal infections are asymptomatic. Therefore when there is a history of receptive anal contact, exclusion of anorectal infections is generally indicated as part of standard screening for sexually transmitted infections (STIs). Condom use does not guarantee protection from bacterial and protozoan STIs, which are often spread without penile penetration.

ONTARIO: Plasma Cell Cancer declared by Liberal Govt an "OCCUPATIONAL DISEASE".

Ontario adds multiple myeloma to list of job-related cancers for firefighters The Ontario government is extending health care protection for firefighters - all the way back to 1960. On April 30, Premier Kathleen Wynne announced the province will increase cancer coverage for firefighters by adding six cancers to the list of those presumed to be related to their jobs. "We want to ensure that firefighters can get the support that they need and the care they need," Wynne said at a news conference in a Toronto-area fire station. "Firefighters face incredible risks every day - not only in the blazes they battle, but in the smoke they breathe in and all that is in that smoke." Breast cancer, multiple myeloma and testicular cancer will be added to the list immediately. Prostate cancer, lung cancer and skin cancer will be phased in by 2017. The addition of all six will be retroactive to Jan. 1, 1960. Wynne said the changes will make it easier for firefighters to qualify for benefits under the Workplace Safety and Insurance Act. Cancers already on the list include brain, bladder and kidney cancer, non-Hodgkin's lymphoma and certain types of leukemia. Source: CBC News

USA CDC: MERS-CoV

CDC HEALTH ADVISORY Distributed via the CDC Health Alert Network May 3, 2014, 16:30 ET (4:30 PM ET) CDCHAN-00361 Summary The first case of Middle East Respiratory Syndrome Coronavirus (MERS-CoV) infection in the United States, identified in a traveler, was reported to CDC by the Indiana State Department of Health (ISDH) on May 1, 2014, and confirmed by CDC on May 2. The patient is in a hospital in Indiana after having flown from Saudi Arabia to Chicago via London. The purpose of this HAN is to alert clinicians, health officials, and others to increase their index of suspicion to consider MERS-CoV infection in travelers from the Arabian Peninsula and neighboring countries. Please disseminate this information to infectious disease specialists, intensive care physicians, primary care physicians, and infection preventionists, as well as to emergency departments and microbiology laboratories. Background The first known cases of MERS-CoV occurred in Jordan in April 2012. The virus is associated with respiratory illness and high death rates, although mild and asymptomatic infections have been reported too. All reported cases to date have been linked to six countries in the Arabian Peninsula: Saudi Arabia, Qatar, Jordan, the United Arab Emirates (UAE), Oman, and Kuwait. Cases in the United Kingdom, France, Italy, Greece, Tunisia, Egypt, and Malaysia have also been reported in persons who traveled from the Arabian Peninsula. In addition, there have been a small number of cases in persons who were in close contact with those infected travelers. Since mid-March 2014, there has been an increase in cases reported from Saudi Arabia and UAE. Public health investigations are ongoing to determine the reason for the increased cases. There is no vaccine yet available and no specific treatment recommended for the virus. In some cases, the virus has spread from infected people to others through close contact. However, there is currently no evidence of sustained spread of MERS-CoV in community settings. Additional information is available at (http://www.cdc.gov/coronavirus/mers/index.html). Recommendations Healthcare providers should be alert for and evaluate patients for MERS-CoV infection who 1) develop severe acute lower respiratory illness within 14 days after traveling from countries in or near the Arabian Peninsula, excluding those who only transited at airports in the region; or 2) are close contacts of a symptomatic recent traveler from this area who has fever and acute respiratory illness; or 3) are close contacts of a confirmed case. For these patients, testing for MERS-CoV and other respiratory pathogens can be done simultaneously. Positive results for another respiratory pathogen (e.g H1N1 Influenza) should not necessarily preclude testing for MERS-CoV because co-infection can occur. Clusters of patients with severe acute respiratory illness (e.g., fever and pneumonia requiring hospitalization) without recognized links to cases of MERS-CoV or to travelers from countries in or near the Arabian peninsula should be evaluated for common respiratory pathogens. If the illnesses remain unexplained, providers should consider testing for MERS-CoV, in consultation with state and local health departments. Healthcare professionals should immediately report to their state or local health department any person being evaluated for MERS-CoV infection as a patient under investigation (PUI). Additional information, including criteria for PUI are at http://www.cdc.gov/coronavirus/mers/interim-guidance.html. Healthcare providers should contact their state or local health department if they have any questions. Persons at highest risk of developing infection are those with close contact to a case, defined as any person who provided care for a patient, including a healthcare provider or family member not adhering to recommended infection control precautions (i.e., not wearing recommended personal protective equipment), or had similarly close physical contact; or any person who stayed at the same place (e.g. lived with, visited) as the patient while the patient was ill. Healthcare professionals should carefully monitor for the appearance of fever (T> 100F) or respiratory symptoms in any person who has had close contact with a confirmed case, probable case, or a PUI while the person was ill. If fever or respiratory symptoms develop within the first 14 days following the contact, the individual should be evaluated for MERS-CoV infection. Ill people who are being evaluated for MERS-CoV infection and do not require hospitalization for medical reasons may be cared for and isolated in their home. (Isolation is defined as the separation or restriction of activities of an ill person with a contagious disease from those who are well.). Providers should contact their state or local health department to determine whether home isolation, home quarantine or additional guidance is indicated since recommendations may be modified as more data becomes available. Additional information on home care and isolation guidance is available at http://www.cdc.gov/coronavirus/mers/hcp/home-care.html. Healthcare providers should adhere to recommended infection-control measures, including standard, contact, and airborne precautions, while managing symptomatic contacts and patients who are persons under investigation or who have probable or confirmed MERS-CoV infections. For CDC guidance on MERS-CoV infection control in healthcare settings, see Interim Infection Prevention and Control Recommendations for Hospitalized Patients with MERS-CoV at http://www.cdc.gov/coronavirus/mers/infection-prevention-control.html. For suspected MERS-CoV cases, healthcare providers should collect the following specimens for submission to CDC or the appropriate state public health laboratory: nasopharyngeal swab, oropharyngeal swab (which can be placed in the same tube of viral transport medium), sputum, serum, and stool/rectal swab. Recommended infection control precautions should be utilized when collecting specimens. Specimens can be sent using category B shipping containers. Providers should notify their state or local health departments if they suspect MERS-CoV infection in a person. State or local health departments should notify CDC if MERS-CoV infection in a person is suspected. Additional information is available at http://www.cdc.gov/coronavirus/mers/guidelines-clinical-specimens.html. Additional or modified recommendations may be forthcoming as the investigation proceeds. For More Information For more information, for consultation, or to report possible cases, please contact the CDC Emergency Operations Center at (770) 488-7100.