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Note the engorged vasa recta supplying the more distal segment of inflamed bowel arrhythmia medscape purchase 12.5mg lopressor with visa. The diagnosis of Crohn disease was confirmed on colonoscopy with biopsy of the terminal ileum pulse pressure range lopressor 12.5mg on line. Fistulas are a key feature of the transmural inflammation caused by Crohn disease arrhythmia vs dysrhythmia buy genuine lopressor on line. Also note the disproportionate dilation of the duodenum arrhythmia qt prolongation purchase 25mg lopressor mastercard, another common feature of scleroderma. Balbir-Gurman A et al: Pneumatosis cystoides intestinalis in scleroderma – Dysphagia, regurgitation related conditions. Ohkubo H et al: An epidemiologic survey of chronic intestinal pseudo – Epigastric fullness and burning pain obstruction and evaluation of the newly proposed diagnostic criteria. Forbes A et al: Gastrointestinal complications: the most frequent internal complications of systemic sclerosis. Parodi A et al: Small intestinal bacterial overgrowth in patients suffering 0 Rectum and anus from scleroderma: clinical effectiveness of its eradication. Gregersen H et al: A new method for evaluation of intestinal muscle – Fecal impaction; stercoral ulceration contraction properties: studies in normal subjects and in patients with systemic sclerosis. These reflect the muscle atrophy within the bowel wall and its replacement by collagen and fibrosis. Mutnuri S et al: Visceral angioedema: an under-recognized complication of bradykinin angiotensin-converting enzyme inhibitors. There was no history of prior abdominal surgery, making adhesive bowel obstruction a less likely etiology. Wen Z et al: the lymphoscintigraphic manifestation of (99m)Tc-dextran lymphatic imaging in primary intestinal lymphangiectasia. Ersoy O et al: Evaluation of primary intestinal lymphangiectasia by capsule endoscopy. Urganci N et al: Evaluation of paediatric patients with protein losing 0 Secondary form enteropathy a single centre experience. A rare diagnosis chylomicrons and fat-soluble vitamins, excessive leakage of protein-losing enteropathy. Moss G: the etiology and prevention of feeding intolerance paralytic ileus • Small bowel feces sign found just proximal to point of revisiting an old concept. Mesenteric vessels to these segments are engorged and crowded with blurred margins. Bowel distention and ascites help to confirm that the pneumatosis is likely on the basis of bowel ischemia, rather than one of the "benign" (nonischemic) causes of pneumatosis. Milone M et al: Computed tomography findings of pneumatosis and portomesenteric venous gas in acute bowel ischemia. Zorgdrager M et al: Pneumatosis intestinalis associated with enteral tube cough (depending on etiology) feeding. Romano S et al: Multidetector row computed tomography findings from • Prognosis ischemia to infarction of the large bowel. The patient remained relatively asymptomatic, confirming this as "benign" (nonischemic) pneumatosis, likely due to medications. This combination of findings is essentially diagnostic of transmural bowel infarction. It is critical to recognize the submucosal presence of gas density, which is diagnostic for pneumatosis. Despite the interpretation of benign pneumatosis coli, this patient was taken to surgery. Mitchell A et al: Coeliac disease in an adult presenting as intussusception • 3 layers seen without a lead point. Lianos G et al: Adult bowel intussusception: presentation, location, etiology, 0 Intussuscipiens: Sheath or outer tube diagnosis and treatment. El Fortia M et al: Tetra-layered sign of adult intussusception (new ultrasound Microscopic Features approach). Long-segment, obstructing intussusceptions such as this often have a lead mass when seen in adults. The high-density obstructing gallstone is seen, as a laminated calcification, at the site of transition from the dilated to the decompressed bowel. The track is outside the internal sphincter, but does not cross the external sphincter, compatible with an intersphincteric perianal fistula. Enhancement along fistulous tracts suggests that the fistula is active, rather than chronic and healed. Seton catheters, often utilized to keep fistulous tracts open and facilitate drainage, appear low signal on all pulse sequences. Note the fistulous track arising from the rectum above the levator muscle complex. Notice that the fistula is contiguous with a large T2 hyperintense "horseshoe" type abscess in the intersphincteric space. Crohn disease is a common cause of spontaneous enteric fistulas, as it is a chronic, transmural inflammatory disease. There is a tract of gas and fluid leading to the anterior abdominal wall defect. Yikilmaz A et al: Value of multislice computed tomography in the diagnosis • Epidemiology of acute mesenteric ischemia. Romano S et al: Small bowel vascular disorders from arterial etiology and 0 60-70% of acute ischemia due to arterial occlusion, 5 impaired venous drainage. Romano S et al: Ischemia and infarction of the small bowel and colon: • Complications: Stricture, infarction, necrosis, perforation spectrum of imaging findings. The wall is thickened and ascites is present, findings worrisome for transmural ischemic injury. This patient was subsequently diagnosed with a hypercoagulable state and responded to anticoagulation. Note the aberrant position of the superior mesenteric vessels and focal ascites. The mesenteric injury was surgically repaired and a segment of small intestine was resected. Honaker D et al: Blunt traumatic abdominal wall hernias: Associated injuries and optimal timing and method of repair. Linsenmaier U et al: Diagnosis and classification of pancreatic and duodenal • Complications injuries in emergency radiology. The active mesenteric bleeding alone would have warranted surgical intervention in this case. Also seen is an abdominal wall hematoma from the seat belt impact and diffuse mesenteric infiltration. At surgery, serosal avulsion and transmural laceration of the small bowel were confirmed. This and the seat belt contusion are highly associated with bowel and mesenteric injuries. The balloon tip of the catheter used to inject the contrast medium is just above the ileoanal anastomosis. The sharp angulation and tethered appearance of a segment of small bowel are typical of an adhesive small bowel obstruction. The afferent limb (duodenum) is dilated due to a stricture that caused partial bowel obstruction. The elevated intraluminal pressure within the duodenum contributed to the biliary obstruction. Farinella E et al: Modified H-pouch as an alternative to the J-pouch for anorectal reconstruction. Pfefferkorn U et al: Recurrent pancreatitis as only presenting symptom of Ileoanal pouch "failure" (need for permanent end intermittent small bowel obstruction after biliopancreatic diversion with duodenal switch. Sandrasegaran K et al: Small-bowel complications of major gastrointestinal Usually perform "pouchogram" (fluoroscopic tract surgery.

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Encephaloceles are cranial defects blood pressure normal 50mg lopressor with mastercard, usually occipital heart attack pain discount lopressor online visa, with herniated fluid-filled or brain-filled cysts hypertension zoloft discount lopressor 50mg. Diagnosis the diagnosis of anencephaly during the second trimester of pregnancy is based on the demonstration of absent cranial vault and cerebral hemispheres blood pressure bottom number over 100 purchase lopressor us. However, the facial bones, brain stem and portions of the occipital bones and mid-brain are usually present. Ultrasound reports have demonstrated that there is progression from acrania to exencephaly and finally anencephaly. These abnormalities are secondary to the Arnold-Chiari malformation and include frontal bone scalloping (lemon sign), and obliteration of the cisterna magna with either an "absent" cerebellum or abnormal anterior curvature of the cerebellar hemispheres (banana sign). In encephalocele the prognosis is inversely related to the amount of herniated cerebral tissue; overall the neonatal mortality is about 40% and more that 80% of survivors are intellectually and neurologically handicapped. Certainly before 24 weeks and particularly in cases of associated spina bifida, the head circumference may be small rather than large for gestation. Prognosis Fetal or perinatal death and neurodevelopment in survivors are strongly related to the presence of other malformations and chromosomal defects. The first two types are often accompanied by microcephaly and facial abnormalities. Experience with apparently isolated partial agenesis of the vermis or enlarged cisterna magna is limited and the prognosis for these conditions is uncertain. Diagnosis the diagnosis is made by the demonstration of brain abnormalities, such as holoprosencephaly. The brain is small, with the cerebral hemispheres affected to a greater extent than the midbrain and posterior fossa. Unilateral megalencephaly is associated with severe mental retardation and untreatable seizures. In hydranencephaly there is absence of the cerebral hemispheres with preservation of the mid-brain and cerebellum. Etiology Hydranencephaly is a sporadic abnormality that may result from widespread vascular occlusion in the distribution of the internal carotid arteries, prolonged severe hydrocephalus, or an overwhelming infection such as toxoplasmosis or cytomegalovirus. In porencephaly there is one or more cystic areas in the cerebral cortex, which usually communicates with the ventricle; the differential diagnosis is from intracranial cysts (arachnoid, glioependymal), that are usually found either within the scissurae or in the mid-line and compress the brain. They occur most frequently in the area of the cerebral fissure and in the midline. Diagnosis the diagnosis is made by the demonstration of a supratentorial mid-line translucent elongated cyst. Prognosis In the neonatal period about 50% of the infants present with heart failure and the rest are asymptomatic. The most common syndromes with hypertelorism are the median cleft syndrome (hypertelorism, median cleft lip with or without a median cleft of the hard palate and nose, and cranium bifidum occultum), craniosynostoses (including Apert, Crouzon, and Carpenter syndromes), agenesis of the corpus callosum and anterior encephaloceles. For severe cases, a number of operative procedures, such as canthoplasty, orbitoplasty, surgical positioning of the eyebrows, and rhinoplasty, have been proposed. The median cleft face syndrome is usually associated with normal intelligence and life span. The severity of the cosmetic disturbance should not be underestimated, because this syndrome may be associated with extremely grotesque features. Prenatal diagnosis is based on the demonstration of decreased ocular diameter and careful examination of the intraorbital anatomy is indicated to identify lens, pupil, and optic nerve. Facial clefts encompass a broad spectrum of severity, ranging from minimal defects, such as a bifid uvula, linear indentation of the lip, or submucous cleft of the soft palate, to large deep defects of the facial bones and soft tissues. The typical cleft lip will appear as a linear defect extending from one side of the lip into the nostril. The diagnosis of isolated cleft palate is difficult and in cases at risk for Mendelian syndromes fetoscopy may be necessary. Otocephaly is a rare, lethal, sporadic abnormality characterized by severe hypoplasia of the mandible (agnathia) and severe midline defects, including holoprosencephaly, anterior encephalocele, cyclopia, aglossia, microstomia, and mid-facial location of the ears (‘ear-head’). Specific mutant gene defects and chromosomal abnormalities account for less than 5% of the patients. The left and right sides are assessed by determining the relative position of the head and spine. The examination of the fetal heart begins with the assessment of the disposition of abdominal and thoracic organs, as an abnormal disposition is frequently associated with complex cardiac anomalies. A transverse section of the thorax reveals the four-chamber view of the fetal heart. The thickness of the interventricular septum and of the free ventricular walls is the same. In M-mode ultrasound, one line of information only is continuously displayed: instead of a two dimensional scan of the heart, a recording of the variations of echoes along a single line is produced. Color Doppler is useful to assess normal anatomy and physiology, valvular regurgitation or stenosis, shunting and the orientation of flows. Analysis of atrioventricular inflows, hepatic veins and inferior vena cava can also be used to assess cardiac rhythm. The trabecular defects occur in the muscular portion of the septum, and the outlet defects are in the infundibular portion of the right ventricle. Prevalence Ventricular septal defects, which represent 30% of all congenital heart defects, are found in about 2 per 1, 000 births. Prognosis Ventricular septal defects are not associated with hemodynamic compromise in utero because the right and left ventricular pressures are very similar and the degree of shunting should be minimal. Rarely very large defects, associated with massive left to right shunt, can be associated with congestive heart failure soon after birth. Abnormal development of these structures is commonly referred to as endocardial cushion defects, atrioventricular canal or atrioventricular septal defects. In the complete form, persistent common atrioventricular canal, the tricuspid and mitral valve are fused in a large single atrioventricular valve that opens above and bridges the two ventricles. The atrial septal defect is of the ostium primum type (since the septum secundum is not affected) and thus is close to the crest of the interventricular septum. In mitral / tricuspid atresia, there is only one atrioventricular valve connected to a main ventricular chamber. The subaortic forms include a fixed type, representing the consequence of a fibrous or fibromuscular obstruction, and a dynamic type, which is due to a thickened ventricular septum obstructing the outflow tract of the left ventricle. Prevalence Aortic stenosis, which represents 3% of all congenital heart defects, is found in about 1 per 7, 000 births. Severe aortic stenosis may result in atrioventricular valve insufficiency and intrauterine heart failure. Conversely, the valvar type can be a cause of congestive heart failure in the newborn and fetus as well. If the left ventricular function is adequate balloon valvuloplasty is carried out in the neonatal period and in about 50% of cases surgery is necessary within the first 10 years of life because of aortic insufficiency or residual stenosis. Non-cardiac anomalies include diaphragmatic hernia, Turner syndrome but not Noonan syndrome. Isolated interruption of the aortic arch is often encountered with enlargement of the right ventricle (right ventricle to left ventricle ratio of more than 1. The definitive diagnosis of the syndrome depends on the demonstration of hypoplasia of the ascending aorta and atresia of the aortic valve. Intrauterine growth may be normal, and the onset of symptoms most frequently occurs after birth. Fetuses with pulmonary atresia and an enlarged right heart have a very high degree of perinatal mortality. This probably reflects that the prenatal variety is more severe than the one detected in children or adults. Diagnosis Complete transposition is probably one of the most difficult cardiac lesions to recognize in utero. Corrected transposition is characterized by a double discordance, at the atrio-ventricular and ventriculo-arterial level. Conversely, the right atrium is connected with the right ventricle, which is in turn connected to the ascending aorta.

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Additionally blood pressure medication reduce anxiety purchase lopressor 50mg amex, analyses of treatment effect will be performed using the Cox proportional hazard model with the four stratification factors included as fixed covariates prehypertension 120-139 over 80-89 discount 100mg lopressor, as well as any factors that show an imbalance between the arms) pulse pressure different in each arm purchase 50mg lopressor with mastercard. Where feasible arrhythmia 4279 discount lopressor 25mg without a prescription, treatment comparisons with respect to the primary endpoint (overall survival) will be compared within ethnic and racial categories. To inspect the missing data mechanism for each tool, we will use at least a graphical method. Specimen submission is a requirement; taking into account a 90% submission rate (accounting for some inability to obtain specimens and for some specimens to be inadequate to obtain marker data), we will have approximately 770 specimens available for these correlative studies. Traditional descriptive statistics and summary tables will be generated for all data from this study. Because the treatment trial is powered for an overall hazard ratio (under the proportional hazards assumption) of at least 1. It should also be noted that these calculations assume independence between these markers, when in fact there may be some correlation between them. This is due to the fact that the distributions of these continuous measures often do not lend themselves to a linear term in the Cox model. It should be emphasized that there is no single ‘best’ way to dichotomize gene expression for a single marker, and thus we will need to be cautious in the way we generalize these data. Assuming no differences between the ethnicities, or among the races, the statistical power for detecting the hypothesized treatment difference is 0. The statistical power for non-whites, and Hispanic/Latino is too low for any meaningful treatment comparisons. Journal of Clinical Oncology 2008; 25, 18s Part I: page 203 s (abstract 4523) Baselga J, Rosen N. Loss of homotypic cell adhesion by epithelial-mesenchymal transition or mutation limits sensitivity to epidermal growth factor receptor inhibition. Patterns of failure after curative resection of pancreatic carcinoma cancer 1990;66:56-61. A randomized trial of chemoradiotherapy and chemotherapy after resection of pancreatic cancer. Epithelial to mesenchymal transition is a determinant of sensitivity of non-small cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition. Six Hundred Fifty Consecutive Pancreaticoduodenectomies in the 1990s, Pathology, Complications, and Outcomes. You are being asked to take part in this study because you have pancreatic cancer that was removed by surgery. You are eligible for this study because there was no visible cancer left behind and not more than 8 weeks have passed since your operation. The standard treatment for patients with pancreatic cancer that was removed by surgery is to receive the chemotherapy drug gemcitabine. In this study, you will get either gemcitabine alone or gemcitabine combined with erlotinib. This study will compare the effects, good and/or bad, of the drug erlotinib in combination with gemcitabine to gemcitabine alone for patients with pancreatic cancer that was removed by surgery to find out which is better. We expect that most patients will not have signs of progression although a few patients may show signs of progression at this point. The other half will get one additional month of gemcitabine (with or without erlotinib) and then will get radiation treatments with a fluoropyrimidine for about 5 weeks. Therefore, this study will also determine the effects, good and/or bad, of radiation for patients who remain disease-free after gemcitabine chemotherapy. Scientists will study your tumor tissue and blood to try to learn more about pancreatic cancer and determine what characteristics of pancreatic cancer cells predict cancer growth. If, after 5 months of chemotherapy your cancer has not grown back you will be randomized again to one of two treatments. You will be treated with one of the following: If you are in group 3 (Arm 3): One additional cycle of the same chemotherapy you received in the first 5 months of this study (either gemcitabine alone or gemcitabine with erlotinib). Radiation will be given to the area where your tumor was once a day, Monday through Friday for 5 weeks (28 radiation treatments). This pump weighs about seven ounces and would be worn by you throughout the 5 weeks. If you are in group 1 (Arm 1) or 2 (Arm 2), you will have follow-up exams every six months for two years and then every year for your lifetime to record whether your cancer grows back. It is important to tell the study doctor if you are thinking about stopping so any risks from the drugs or radiation can be evaluated. You should talk to your study doctor about any side effects that you have while taking part in the study. The interaction between warfarin and capecitabine is very large and could result in severe bleeding. It is important you understand that you need to use birth control while on this study. It has been proven that gemcitabine will reduce the chance that this cancer will come back and that this will increase your lifespan. You and/or your health plan/ insurance company will need to pay for some or all of the costs of treating your cancer in this study. Check with your health plan or insurance company to find out what they will pay for. If this would occur, other possible options are: • You might be able to get the erlotinib from the manufacturer or your pharmacy but you or your insurance company may have to pay for it. You can print a copy of the “Clinical Trials and Insurance Coverage” information from this Web site. You will get medical treatment if you are injured as a result of taking part in this study. No matter what decision you make, there will be no penalty to you and you will not lose any of your regular benefits. We will tell you about new information or changes in the study that may affect your health or your willingness to continue in the study. The Committee members may receive confidential patient information, but they will not receive your name or other information that would allow them to identify you by name. You can talk to your study doctor about any questions or concerns you have about this study. Contact your study doctor [name(s)] at [telephone number]. For questions about your rights while taking part in this study, call the [name of center] Institutional Review Board (a group of people who review the research to protect your rights) at (telephone number). You can still be a part of the main study even if you say ‘no’ to taking part in this additional research. Consent Form for Quality of Life Study We want to know your view of how your life has been affected by cancer and its treatment. In the future, this information may help patients and doctors as they decide which medicines to use to treat cancer. Just like in the main study, we will do our best to make sure that your personal information will be kept private. To participate in the main part of this study, you must agree to have your tumor tissue and blood sample sent to the tissue bank to be used for studies that are essential components of this clinical trial. Therefore, permission to use the tissue block and blood sample is mandatory for your participation in the main study. Please read the information sheet called "How is Tissue Used for Research" to learn more about tissue research. If you agree, the urine will be kept and may be used in research to learn more about cancer and other diseases. The research that may be done with your tissue, blood, urine is not designed specifically to help you. Reports about research done with your tissue, blood, urine will not be given to you or your doctor. Things to Think About the choice to let us keep the left over tissue and blood and urine for future research is up to you. Then any tissue that remains will no longer be used for research and will be returned to the institution that submitted it and leftover blood and urine will be destroyed. However, tissue, blood, and urine already used and data obtained from it will remain part of the study data. While your doctor/institution may give them reports about your health, they will not give them your name, address, phone number, or any other information that will let the researchers know who you are. Sometimes tissue, blood, and urine are used for genetic research (about diseases that are passed on in families).

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They are amply present in purple grape juice and blood pressure levels variation buy lopressor canada, to blood pressure medication zapril 12.5mg lopressor visa a lesser extent blood pressure 58 over 38 purchase 100mg lopressor, also in red wine arteria lusoria buy lopressor 12.5 mg low cost. Purple grape juice might even be more potent than aspirin, which is widely recommended as a way of warding off heart attacks. The study found that both aspirin and red wine slow the activity of blood platelets by about 45 percent, while purple grape juice dampens them by 75 percent. It is not clear, 411 Timeless Secrets of Health and Rejuvenation however, whether the thinning of blood after drinking red wine is caused by flavonoids or by the diuretic effects of the alcohol contained in the wine. To have the benefits advocated for red wine and more, it is better to drink the fresh juice of purple grapes. Eating a diet rich in fruits and vegetables is one of the best ways to maintain a healthy circulatory system, while alcohol is not. Although the flavonoids contained in red wine may have some beneficial effects on the blood, the alcohol that goes with it, after initially thinning the blood due the alcohol’s diuretic effects, makes it thicker than it was before. If you need proof, ask a friend to apply the muscle test from chapter 1 on you while you hold a bottle of red wine or another alcoholic beverage in your hand. If your arm muscle tests weak, it shows that any benefit that may be been left in the red wine from the grape juice has been voided. The alcohol in the wine actually causes the shutdown of energy flow to the muscles. Dirty Business with our Food—Genetically Modified Genetic engineering of food is rapidly becoming an extremely lucrative business that is likely to place man’s global food production in the hands of a few powerful people or governments. In the name of progress and improvement of food production, the plan is to make every nation dependent on using the genetically engineered seeds that the world’s leading food industries have produced and for which they own the patent rights. In January 2005, Monsanto announced it will buy the commercial fruit and vegetable seed company Seminis. Once the majority of the world is using gene-manipulated seeds to grow their crops, the man-made Frankenstein foods will take their toll on human life. The aim of the wealthiest and most influential group of people in the world is to drastically reduce the size of the world’s population. Because a smaller population and the world’s natural resources would be a lot easier to control than 8 billion people. Genetically engineered foods play a decisive role in this plan, and unless the rest of humanity wakes up to its responsibility as caretakers of Mother Earth, it is most likely going to succeed. Monsanto, which also produced the poisonous sweetener aspartame, is inserting genes from plants of unrelated species into the soybean plant to make it resistant to the potent herbicide Roundup (glyphosate). The unsuspecting farmers would only welcome such a miracle plant, unless of course they see the risk involved. The Roundup resistant soybean seed can now be heavily sprayed with Roundup to kill weeds, but without causing damage to the soybean. No more problems with weeds suffocating the soybean plants, but bigger problems for the consumer! Today, these genetically modified soybean products, which comprise about 80 percent of the beans available, have been found in most baby formulas including Carnation, Similac, Enfamil, Isomil, and Neocare as well as Doritos, Fritos, vegetable oils, soybean oil, margarine, and much more. With soy now being an ingredient of thousands of common food products, the masses are systematically poisoned with harmful herbicides. One of the genes used in the new soybean is derived from the petunia plant, which is a nightshade variety. Suddenly, by inadvertently eating something that contains a soy product, they may end up becoming crippled with arthritis. They may have no problem with soy as such, but soy isn’t just soy anymore; it is now also a nightshade, at least on the genetic level. When Monsanto inserted the Brazil nut gene into soy, people allergic to Brazil nuts suffered anaphylaxis from ingesting a soy product. Anaphylaxis is a serious, life threatening reaction where one is not able to breathe. Monsanto was ordered to remove the gene to avoid further complications of that nature. The process of genetic engineering of food often involves the use of a live virus, small enough to enter cell nuclei and, thereby, infect other genetic material. The chicken cancer virus is used as a carrier to implant the growth hormone gene into farmed fish so they will grow faster. Once the virus has infected the fish, it will likely end up on your dinner plate and also infect you. With the multitudes of genetically modified foods out there, our body will become a host for numerous viruses that normally would never be found in us. Likewise, Leukemia virus in chicken has been used as a carrier to insert human genes into developing poultry. A retrovirus was used to insert human fetal cells in pigs in order to grow aortas for transplantation into humans. When these viruses are used as part of genetic engineering, they combine with one another to create new plant and animal diseases. By eating these new foods, foreign genetic material from these viruses can be absorbed through our intestines and become incorporated into our cells. Thanks to genetic research and food production, we are now on the verge of creating new diseases against which we have no natural or unnatural way of defending ourselves. As more and more foods are grown that include foreign genes to make them resistant to certain pests, pesticides, herbicides or antibiotics, the more of these gene transporters or vectors will end up lodging in our intestinal tract, infecting the bacteria in our gut. The infected gut microbes will not only become antibiotic-resistant, but resistant to any kind of treatment. As for now, new genes have already been planted in potatoes, corn, sugar beets, tomatoes, and cotton (used to make junk food oil found on roasted nuts given out on airplanes) to make the plants resistant to pesticides. With increasing usage of genetically engineered plants, we will be faced with the following global scenario: 1. New viruses and diseases for which there won’t be a cure Already, 60 percent of processed foods now contain at least one genetically modified food item. Millions of people now consume chips with the firefly gene, potato chips with a chicken gene, or salsa with tomato containing a flounder gene. Cream of broccoli soup can have a bacteria gene in it, and salad dressing is most likely made with canola oil, vegetable oil or soybean oil (all genetically engineered). The tobacco gene is now used in lettuce and cucumbers and the petunia gene is used in soybeans and carrots. If you have celiac disease, you may need to avoid walnuts because they can have the barley gene in them. Even strawberries are not harmless anymore; they can now have “undisclosed genes” in them, so you will never know what else you are getting when you treat yourself to this delicious fruit. Many brands of apple juice contain the silkworm gene, and grapes can contain a virus gene. However, in spite of impressive nutritional content, soy products are biologically useless to the body, for reasons explained below. Today, soy is contained in thousands of different food products, which has led to a massive escalation of disease in both developed and underdeveloped countries. Given the fact that soybeans are grown on farms that use toxic pesticides and herbicides—and many are from genetically engineered plants—increasing evidence suggests soy is a major health hazard. With a few exceptions, such as miso, tempeh and other carefully fermented soy products, soy is not suitable for human consumption. Eating soy, soy milk, and regular tofu increases risks of serious health conditions. Numerous studies have found that soy products: • increase the risk of breast cancer in women, brain damage in both men and women, and abnormalities in infants • contribute to thyroid disorders, especially in women • promote kidney stones (because of excessively high levels of oxalates which combine with calcium in the kidneys) • weaken the immune system • cause severe, potentially fatal food allergies • accelerates brain weight loss in aging users Soy products contain: • Phytoestrogens (isoflavones) genistein and daidzein, which mimic and sometimes block the hormone estrogen • Phytic acids, which reduce the absorption of many vitamins and minerals, including calcium, magnesium, iron, and zinc, thereby causing mineral deficiencies • "Antinutrients" or enzyme inhibitors that inhibit enzymes needed for protein digestion and amino acid uptake 414 Timeless Secrets of Health and Rejuvenation • Haemaggluttin, which causes red blood cells to clump together and inhibits oxygen uptake and growth • Trypsin inhibitors that can cause pancreatic enlargement and, eventually, cancer Phytoestrogens are potent anti-thyroid agents which are present in vast quantities in soy. Infants exclusively fed on a soy-based formula have 13, 000 to 22, 000 times more estrogen compounds in their blood than babies fed a milk-based formula. This would be the estrogenic equivalent of at least five birth control pills per day. For this reason, premature development of girls (early puberty) has been linked to the use of soy formula, as has the underdevelopment of males. Infant soy formula and soy milk have been linked to autoimmune-thyroid disease, and now also to death.

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