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Estradiol

Susan B Bressler, M.D.

  • Professor of Ophthalmology

https://www.hopkinsmedicine.org/profiles/results/directory/profile/0000206/susan-bressler

The radiation dose depends on the location of the source with regard to those exposed pregnancy 8th week generic 2 mg estradiol otc. Furthermore menstruation for a month buy estradiol 1mg line, the radiation dose depends upon the type of radiation menopause onset discount estradiol 1mg without prescription, such as whether it is a- women's health issues-night sweats estradiol 1 mg visa, b or g-rays and the energy of the radiation women's health clinic quivira discount 1 mg estradiol free shipping. Although people can neither see nor feel radiation women's health clinic queensland buy estradiol 1 mg without a prescription, it is known that radiation deposits energy to the molecules of the body. The energy is transferred in small quantities for each interaction between the radiation and a molecule and there are usually many such interactions. The temperature increase occurs because the radiation energy is transformed into heat. Even though it is generally very diffcult to detect the rise in temperature, the realization that heat is gener ated by radiation is a key element in understanding the concept of radiation dose. Radiation dose is measured in units of gray (Gy) 1 Gy = 1 joule absorbed energy per kg 56 L. He obtained his PhD in 1930 at the Cavendish Laboratory under Rutherford at a time when the laboratory was a world centre for fundamental research in atomic physics. Gray worked as a physicist at Mount Vernon Hospital, and became interested in the effect of oxygen on radiosensitivity. Cells with a low content of oxygen (hypoxic cells) are less sensitive to radiation compared to normal cells. This behavior has caused problems for the treatment of cancer, because most tumors contain regions with hypoxic cells. Gray Conferences and Workshops have become established as prestigious meetings at which a high level of presentation and discussion take place. Here we are outside Grays institute at Mont Vernon hos pial from left; John Boag, Malfrid Henriksen (wife of the author) and Hal Gray. It is useful, therefore, to consider some of these units and to see the relations between the old units and the gray unit (Gy). This unit was quite uncertain since the reddening of the skin varied from one person to another. In the case of ultraviolet radiation, this dose unit (along with the attending uncertainties) is still in use. This unit can not be used for the dose itself since it is actually a measure of radiation exposure, i. To calculate the radiation dose (in Gy) from an exposure of 1 R depends on the energy of the x or g-radiation and the composition of the irradiated material. For example, if soft tissue is exposed to g-radiation of 1 R, the radiation dose will be approximately 9. This is an abbreviation for radiation absorbed dose and is defned as: the amount of radiation which yields an energy absorption of 100 erg per gram. From this you can easily see that both gray and rad are defned as energy absorbed the relation between the two are: 1 gray = 100 rad In this book, the gray is used most of the time. But use of the rad is diffcult to avoid due to its perva sive use in the older literature. This is a puzzle, since the primary products, ions and excited molecules, are the same. The answer to this puzzle is connected to the spatial distribution of the primary products. Thus, for x and g-rays the primary products are evenly distributed, whereas in the case of protons, a-particles and heavy ions, the primary products are found along the track of the particle. The distribution of ions and excited molecules vary with the type of radiation Track of an Electrons, a-particle x-rays and g-rays In the illustration above the ions and excited molecules are indicated by dots i. To the left is presented the situation for x-rays, b-particles and g-rays, whereas to the right is given the situation for an a-particle. In this case the ions are formed along a track with smaller tracks branching off from the main track (they are called d-tracks). The number of dots within the two circles is the same, indicating the same radiation dose measured in Gy. For the most simple biological end point, such as cell killing, we can do straight forward experiments. In the case of humans, most interest has been concerned on; a) genetic effects and b) cancer. We do not know the particular type of damages and it is of course not possible to do experiments. Similarly, experiments have been carried out for radiation induced cancer in mice, rats and rabbits. The radiation organizations discussed already in 1945 just after the second world war, that it would be useful to introduce a new unit. This unit was in 1950 defned as: that dose of any ionizing radiation which produces a relevant biological effect equal to that produced by one roentgen of high voltage x-radiation. Consequently, the radiation dose was given in Gy (gray) and the rem-unit was changed to Sv (sievert). The use of Sv It should be remembered that Sv is not a physical dose unit that can be measured with dosimeters. In this system are given dose units such as; equiva lent dose, effective dose and collective dose. It is very diffcult to estimate the equivalent dose for a mixture of neutron energies as found for the cosmic radiation. He served for several years as director of the Swedish National Institute of Radiation Protection. Sievert constructed an ionization chamber for depth dose measurements (called Sievert chamber). Sievert is honored for his work in dosimetry (the measure ment of absorbed dose) by naming the unit for equivalent dose sievert (abbreviated Sv). Sievert (1896 1966) 62 Effective Equivalent Dose In some cases, only a part of the body is irradiated. For example, mainly the bronchi and lungs are involved in the case of radon and radon decay products. Different organs and types of tissue have dif ferent sensitivities with regard to what is termed the late effects of radiation. Late effects are biological responses that are only observed after a substantial amount of time has passed, often years. In order to compare the risk for late effects of different types of radiation, the so-called effective dose is used. This calculated dose is called the effective dose (often shortened to simply the dose) and is desig nated E. Here w1 represents a weighting factor for organ 1 and H1is the equivalent dose (given in Sv) for organ number 1, and so on. The body has been divided into 15 different organs each with a weighting factor w. The notion is used for the combined contribution from 14 different tissues 13 for each sex and in addition prostate (for men) and uterus/cervix (for women). In the following we shall give a brief overview of the concepts used when working in radiation pro tection. It can be obtained by the product of the average individual dose with the number of people in the group. For example in com bination with mammography to a large group, the collective dose is calculated as the product of the single dose and number of women. The unit used for the collective dose is person-sievert (person-Sv) or sometimes man-sievert. Committed equivalent dose When a radioactive compound enters the body, the activity will decrease with time, due both to physical decay and to biological clearance, as noted earlier. Accumulated dose over a certain period of time, usually 50 years, is called the committed equivalent dose. It can not be used in biological experiments on animals, fsh, plants, insects, etc. A large number of articles and opinions have been published where the dose is given in Sv. Consequently, the present author would like to use the Gy (rad) units throughout the book. Radiobiological work during the last 20 years have revealed that biological systems have a number of defense mechanisms such as repair, apoptosis and adaptive response. Fur thermore it appears that these processes may be stimulated by radiation particulary small doses given at a low doserate. May be that we should be happy with the radiation around us and may be we would proft on a higher background level. Founded 1927 Barrel type chambers as secondary transfer standards in 1922, the company is located in Freiburg on the western side of Kustner Dosimeter the famous Black Forest mountains in southwestern Germany. The development and production of mechanical, 1936 Waterproof sealed chambers for brachytherapy electronic and software components are all done in house. The com 2005 Dedicated proton chamber Bragg Peak Chamber pany has grown continuously. All technical data published in this catalog are typical data for the various detector types. Certain data of individual detectors may vary slightly within the ranges of tolerance. The electrical signal of a detector when irradiated is measured by an electrometer connected to the detector. Further correction factors depending on the detector characteristics and the beam quality may be used. A variety of detector types with different design for intensity measurements of ionizing radiation is available. The radiation detection for dosime tric purposes in the medical field of diagnostic radiology, radiotherapy and nuclear medicine is mainly based on three principles of measurement, realized by three different detector types: the ionization chamber, the semicon ductor detector and the diamond detector. Ionization Chamber An ionization chamber basically consists of a gas volume between two electrodes connected to a high voltage supply of typically 100 V to 1000 V. These, being positive and negative charge carriers, are attrac ted by the electrodes thus creating a current which can be measured by an electrometer. Semiconductor Detector In silicon semiconductors a layer of n-type silicon is brought into contact with a layer of p-type silicon, allowing electrons to drift from the n to the p region of the detector thus creating an insulating intrinsic zone. Incident radiation frees electrons in the intrinsic zone (sensitive layer of the detector) which move to the posi tively charged p region, generating a current. Diamond Detector A high purity diamond can operate as a solid state ionization detector. Ionizing radiation can push elec trons from the valence band to higher energy levels thereby first filling electron traps caused by impurities and then bringing electrons to the conductivity band. An external bias is needed to produce an ionization current very much like in an ionization chamber. A sta ble current can only be measured though after suffi cient pre-irradiation to fill the traps. A guard on central electrode potenti al leading up to the sensitive volume limits dark cur rents and stem effects. Plane-Parallel Ionization Chamber A plane-parallel chamber (also known as flat chamber) consists of a high voltage electrode plate and a mea suring electrode plate confining the sensitive volume. A guard on central electrode potential around the measuring electrode plate limits dark current and per turbation effect. Spherical Ionization Chamber A spherical chamber consists of two concentric balls representing the central measuring electrode and the chamber wall and confining the sensitive volume. A guard on central electrode potential around the mea suring electrode stem limits the dark current. Well-Type Ionization Chamber A well-type chamber consists of an outer housing with an inset cylindrical cavity representing the chamber wall to receive the measuring object. A guard on central electrode potential around the measuring electrode stem limits the dark current. Semiconductor Detector A silicon semiconductor detector consists of a layered silicon disk with contact wires to the measuring instru ment. This is embedded horizontally or vertically in protective and / or build-up material depending on the intended application to form a useful probe. Diamond Detector A diamond detector consists of a diamond disk with contact wires to the measuring instrument. This is embedded vertically in water-equivalent protective material to produce a probe with the highest possible spatial resolution in axial direction for use in therapy beam analysis. Internal traceability is proudly extended to on laboratory for dosimetric measuring quantities. Early photographs of the calibration laboratory show Hammer and Kustner dosi meters and their ionization chambers facing X-ray tubes supplied by open high-voltage leads. Original and the building with the calibration laboratory (with solar panels) seen from above (Photo: Bavaria Luftbild Verlags GmbH) ments) and calibration calculation for the department office writing the calibration certificates. Besides the dose and dose rate ranges the laboratory maintains facilities for the calibration of non-invasive kV-meters and nuclear medicine isotope calibrators. This inclu shows very successful re des complete electrical recalibration of the modern sults. Joint deve 300 kV X-ray installation with filter wheel lopment has lead to such successful results as the Bohm extrapolation chamber and the Roos electron Comparison measurements chamber. Specification Useful ranges: Type of product vented cylindrical Chamber voltage (100. Correction factors needed to determine absorbed dose to water or air kerma are published in the Ion collection efficiency at nominal voltage: pertinent dosimetry protocols. This makes the 31010 chamber to one of the most com monly used chambers in scanning water phantom sys Ion collection efficiency at nominal voltage: tems. The chamber is designed for the use in solid state phantoms and is therefore not waterproof. The thin entrance window allows meas urements in solid state phantoms up to the surface.

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As damage spreads women's health group lafayette co order estradiol line, cells lose their ability to do their jobs and pregnancy week 6 buy on line estradiol, eventually menstruation 2 months buy 2mg estradiol amex, die pregnancy 30 weeks order estradiol with a mastercard. Plaques are deposits of a protein fragment called beta-amyloid that build up in the spaces between nerve cells womens health twitter 2 mg estradiol amex. Tangles are twisted fibers of another protein called tau that build up inside cells women's health magazine old issues cheap estradiol 2 mg overnight delivery. Most 5 experts believe that they disable or block communication among nerve cells and disrupt processes the cells need to survive. However, they have identified certain risk factors that increase the likelihood of developing Alzheimer?s. One in nine people in this age group and nearly one-third of people age 85 and older have Alzheimer?s. Risk genes increase the likelihood of developing a disease but do not guarantee it will happen. Deterministic genes directly cause a disease, guaranteeing that anyone who inherits one will develop a disorder. The reason for these differences is not well understood, but researchers believe that higher rates of vascular disease in these groups may also put them at greater risk for developing Alzheimer?s. Other risk factors Age, family history and genetics are all risk factors we can?t change. However, research is beginning to reveal clues about other risk factors that we may be able to influence. There appears to be a strong link between serious head injury and future risk of Alzheimer?s. One promising line of research suggests that strategies for overall healthy aging may help keep the brain healthy and may even reduce the risk of developing Alzheimer?s. These measures include eating a healthy diet, staying socially active, avoiding tobacco and excess alcohol, and exercising both the body and mind. These include heart disease, diabetes, stroke, high blood pressure and high cholesterol. Work with your doctor to monitor your heart health and treat any problems that arise. Studies of donated brain tissue provide additional evidence for the heart-head connection. The first step in following up on symptoms is finding a doctor with whom a person feels comfortable. In some cases, the doctor may refer the individual to a specialist, such as a: Neurologist, who specializes in diseases of the brain and nervous system. The workup is designed to evaluate overall health and identify any conditions that could affect how well the mind is working. Physicians can almost always determine that a person has dementia, but it may sometimes be difficult to determine the exact cause. Evaluating mood and mental status Mental status testing evaluates memory, the ability to solve simple problems and other thinking skills. The doctor may ask the person his or her address, what year it is or who is serving as president. The individual may also be asked to spell a word backward, draw a clock or copy a design. The doctor will also assess mood and sense of well-being to detect depression or other illnesses that can cause memory loss and confusion. Physical exam and diagnostic tests A physician will: Evaluate diet and nutrition. Information from these tests can help identify disorders such as anemia, infection, diabetes, kidney or liver disease, certain vitamin deficiencies, thyroid abnormalities, and problems with the heart, blood vessels or lungs. All of these conditions may cause confused thinking, trouble focusing attention, memory problems or other symptoms similar to dementia. Neurological exam A doctor will closely evaluate the person for problems that may signal brain disorders other than Alzheimer?s. Researchers are studying other imaging techniques so they can better diagnose and track the progress of Alzheimer?s. Find out if the doctor will manage care going forward and, if not, who will be the primary doctor. While there is currently no cure, treatments are available that may help relieve some symptoms. Research has shown that taking full advantage of available treatment, care and support options can improve quality of life. A timely diagnosis often allows the person with dementia to participate in this planning. The person can also decide who will make medical and financial decisions on his or her behalf in later stages of the disease. This interactive tool evaluates needs, outlines action steps and links the user to local services and Association programs. The following stages provide an overall idea of how abilities change once symptoms appear and should be used as a general guide. Despite this, the person may feel as if he or she is having memory lapses, such as forgetting familiar words or the location of everyday objects. During a detailed medical interview, doctors may be able to detect problems in memory or concentration. Damage to nerve cells in the brain can make it difficult to express thoughts and perform routine tasks. People can wander or become confused about their location at any stage of the disease. If not found within 24 hours, up to half of those who get lost risk serious injury or death. As memory and cognitive skills worsen, significant personality changes may occur and extensive help with daily activities may be required. At this stage, individuals may: Need round-the-clock assistance with daily activities and personal care. But drugs and non-drug treatments may help with both cognitive and behavioral symptoms. By keeping levels of acetylcholine high, these drugs support communication among nerve cells. The second type of drug works by regulating the activity of glutamate, a different messenger chemical involved in information processing: Memantine (Namenda?), approved in 2003 for moderate-to-severe stages, is the only drug in this class currently available. The third type is a combination of cholinesterase inhibitor and a glutamate regulator: Donepezil and memantine (Namzaric?), approved in 2014 for moderate-to-severe stages. Other possible causes of behavioral symptoms include: Drug side effects Side effects from prescription medications may be at work. Drug interactions may occur when taking multiple medications for several conditions. There are two types of treatments for behavioral symptoms: non-drug treatments and prescription medications. Non-drug treatments Steps to developing non-drug treatments include: Identifying the symptom. Prescription medications Medications can be effective in managing some behavioral symptoms, but they must be used carefully and are most effective when combined with non-drug treatments. Medications should target specific symptoms so that response to treatment can be monitored. Use of drugs for behavioral and psychiatric symptoms should be closely supervised. Some medications, called psychotropic medications (antipsychotics, antidepressants, anti-convulsants and others), are associated with an increased risk of serious side effects. These drugs should only be considered when non-pharmacological approaches are unsuccessful in reducing dementia-related behaviors that are causing physical harm to the person with dementia or his or her caregivers. Behavioral: A group of additional symptoms that occur at least to some degree in many individuals with Alzheimer?s. Early on, people may experience personality changes such as irritability, anxiety or depression. In later stages, individuals may develop sleep disturbances; agitation (physical or verbal aggression, general emotional distress, restlessness, pacing, shredding paper or tissues, yelling); delusions (firmly held belief in things that are not real); or hallucinations (seeing, hearing or feeling things that are not there). Since 1982, we have awarded over $350 million to more than 2,300 research investigations worldwide. Alois Alzheimer first described the disease in 1906, a person in the United States lived an average of about 50 years. As a result, the disease was considered rare and attracted little scientific interest. The Centers for Disease Control and Prevention recently estimated the average life expectancy to be 78. Clinical studies drive progress Scientists are constantly working to advance our understanding of Alzheimer?s. But without clinical research and the help of human volunteers, we cannot treat, prevent or cure Alzheimer?s. Clinical trials test new interventions or drugs to prevent, detect or treat disease for safety and effectiveness. Clinical studies are any type of clinical research involving people and those that look at other aspects of care, such as improving quality of life. Every clinical trial or study contributes valuable knowledge, regardless if favorable results are achieved. Researchers have developed several ways to clear beta-amyloid from the brain or prevent it from clumping together into plaques. We don?t yet know which of these strategies may work, but scientists say that with the necessary funding, the outlook is good for developing treatments that slow or stop Alzheimer?s. Eating a diet low in saturated fats and rich in fruits and vegetables, exercising regularly, and staying mentally and socially active may all help protect the brain. Staff are available to answer questions regarding the report, including utilization and limitations of the data. Historical data back to 1990 are available for most datasets using this tool, which is also accessible at. The Pennsylvania Department of Health is an equal opportunity provider of grants, contracts, services, and employment. There are many problems inherent with county-level data, primarily the small numbers of events. This report used a statistical approach that is commonly accepted and used for small area analysis and can also be rather easily understood by the general population. Even with five-year summary figures, there are many counties with primary cancer sites that have very few cases. Therefore, in the interest of reliability, statistical analysis is not shown for any primary site in a county with fewer than 10 cases reported during the five-year period of 2008-2012. This report tabulates the number of observed and expected cancer cases and standardized incidence ratios for 23 primary cancer sites, as well as all cancer sites combined, by county and by sex. A Technical Notes section appears at the beginning of this report to emphasize the importance of understanding and appropriately using the data shown here. This section fully explains all the steps used in the presentation and analysis of the data for this report. A selected series of county outline maps that graphically depict the results of the analysis are presented. Along with all primary sites combined, maps were created for the five leading sites for males and the five leading sites for females. At the bottom of each county outline map is a rate depicting the completeness of case ascertainment for Pennsylvania. Following this are graphs which show the counties with the five lowest and five highest age-adjusted rates for this selected series of sites. If you use any of the statistics presented in this report, we highly recommend that you read the Technical Notes section carefully and thoroughly. Please note all the qualifications listed in this report and review as many of the cited references as possible before you proceed any further. This section explains how the figures that appear in this 18 pnrn report were computed, followed by a discussion of the E? If a resident of the n = age groups (five-year groups up to 85+) state was diagnosed as having more than one primary tumor, each tumor is required to be reported and is It requires the application of the average annual (2008 counted separately by site. By adding together the the Pennsylvania Department of Health (Department) also estimated Pennsylvania male population ages 0-4 for each exclude in situ cases (except for bladder cancers). Prior to of the years from 2008 to 2012, one would obtain the figure 1999 data, most cancer reports released by the of 1,857,093. The number of expected cases this figure represents the total number of primary, that appear in this report are rounded figures, obtained after malignant tumors that would have been reported to the all the age group calculations have been completed. If the lower number in the confidence interval is cases equals the expected number of cases. A ratio above above 100, there is a 95 percent probability that 100 indicates that there were more cases observed than a significantly higher number of cases were expected. Therefore, a ratio of 85 is interpreted as less than 100, there is a 95 percent probability 15 percent fewer observed cases occurring than that significantly fewer cases were observed expected. Pennsylvania has many rural counties with small n populations, and, with a small number of events, there is a higher probability of chance variation in an observed where n = number of observed cases. However, it should be noted that there is no the ?true ratio 95 percent of the time.

Benign tumours in certain areas of the brain can still be life-threatening and may require urgent treatment women's health center fort worth tx cheap 2mg estradiol amex. They may spread within the brain and spinal cord women's health issues journal impact factor buy genuine estradiol online, or come back soon afer treatment women's health issues examples cheap 2 mg estradiol mastercard. It rarely spreads to other parts of the body menstruation related headaches buy genuine estradiol on line, but may spread to other parts of the brain women's health clinic lawrenceburg tn 1 mg estradiol free shipping. Sometimes cancer starts in another part of the body and then travels through the bloodstream to the brain menstrual smell generic estradiol 2 mg fast delivery. For example, bowel cancer that has spread to the brain is still called metastatic bowel cancer, even though the person may be having symptoms caused by how the cancer is afecting the brain. How cancer starts Abnormal cells Abnormal cells multiply Malignant cancer Grows own Invades blood vessels surrounding (angiogenesis) tissue What is a tumour? The brain The brain interprets information received via the nerves from the senses (taste, smell, touch, hearing and sight). It is made up of nerve cells and nerve bundles that connect the brain to all parts of the body through a network of nerves called the peripheral nervous system. The spinal cord lies in the spinal canal, protected by a series of bony vertebrae called the spinal column. Meninges Both the brain and spinal cord are surrounded by thin layers of protective tissue (membranes) called the meninges. Pituitary gland At the base of the brain is the pituitary gland, which is about the size of a pea. Tese hormones control many body functions, including growth and development, and also tell other glands to start or stop releasing hormones. Glial cells support the neurons by holding them in place, supplying nutrients and clearing away dead neurons, waste products and germs. It controls things you do voluntarily, such as speaking or making decisions, as well as those you do automatically, such as blood circulation and heart rate. The cerebral hemispheres The cerebrum is divided into two halves called hemispheres. The right hemisphere controls muscles on the lef side of the body, and the lef hemisphere controls muscles on the right side as well as speech. Corpus callosum The two hemispheres are connected by a band of nerve fbres called the corpus callosum (see diagram, previous page), which transfers information between them. A: A brain or spinal cord tumour occurs when abnormal cells grow and form a mass or a lump. The tumour may be called benign (not cancerous) or malignant (cancerous), but both types can be serious and may need urgent treatment (see pages 28?44). A: Every year an estimated 2000 malignant brain tumours are diagnosed in Australia. About 55 people are diagnosed with malignant spinal cord or other central nervous system tumours each year. Data is not collected Australia wide, but in 2013, there were more than 1000 benign brain and spinal cord tumours in Victoria, Queensland and Western Australia combined. They are classifed based on the type of cell (as seen under a microscope) and how the cells are likely to behave (based on their genetic make-up). The most common cancers to spread to the brain are melanoma, lung, breast, kidney and bowel. Family history In rare cases, a fault in the genes, usually passed down from one parent, can increase the risk of developing a brain tumour. For example, some people have a genetic condition called neurofbromatosis, which can lead to tumours of the neurons. Mobile phones and microwave ovens Many people are concerned limit the time you spend on that electromagnetic radiation your mobile phone or consider from mobile phones or texting rather than calling. Evidence to date Microwave ovens have been does not show that mobile in widespread use since the phone use causes cancer. There is no evidence However, if you are concerned that ovens in good working about potential harm from order release electromagnetic mobile phones, you may radiation at levels harmful choose to use a headset, to humans. A: In some cases, a brain tumour grows slowly and symptoms develop gradually, so you may not be aware that anything is wrong at frst. However, any new, persistent or worsening symptoms should be reported to your doctor. General symptoms Brain tumour symptoms may be caused by increased pressure in the skull (intracranial pressure). Pressure can build up because the tumour itself is taking up too much space or because it is blocking the fow of cerebrospinal fuid around the brain (see page 33). Symptoms caused by tumour position Other symptoms relate to where in the brain or spinal cord the tumour is located see the diagram on the next two pages. Key questions 13 Common tumour symptoms Some brain tumour symptoms depend on where the tumour is located. You will then be referred to a neurosurgeon, neurologist or neuro-oncologist, who will examine you and may do more tests. During and afer treatment, you will see a range of health professionals who specialise in diferent aspects of your care. The hospital social worker can provide practical In general, children diagnosed and emotional support. In many children, Quality, CanTeen and Redkite treatment will cause all signs (see page 62) offer support of the cancer to disappear for families, young adults and (remission). Call 13 11 20 or visit your Some hospitals have staff, local Cancer Council website. Occasionally a brain tumour will be found during a scan for something unrelated, such as a head injury. The doctor will ask you about your symptoms and medical history, and will do a physical examination. You may be referred to have more tests and scans to confrm a diagnosis of a brain or spinal cord tumour. Physical examination Your doctor will assess your nervous system to check how diferent parts of your brain and body are working, including your speech, hearing, vision and movement. The doctor may also test eye and pupil movements, and may look into your eyes using an instrument called an ophthalmoscope. This allows the doctor to see your optic nerve, which sends visual information from the eyes to the brain. Diagnosis 19 Blood tests You are likely to have blood tests to check your overall health. Blood tests can also be used to check whether the tumour is producing unusual levels of hormones, which could indicate that the pituitary gland is afected (see page 6). A contrast dye may be injected into a vein to help make the scan pictures clearer. It may take about 30 minutes to prepare for the scan, but the actual test is painless and takes about 10 minutes. If you have had an allergic reaction to iodine or dyes during a previous scan, tell your medical team beforehand. You should also let them know if you are diabetic, have kidney disease or are pregnant. You will then lie on an examination table inside a large metal tube that is open at both ends. The test is painless, but the machine can be noisy and some people feel anxious or claustrophobic in the tube. If you think you may become distressed, mention it beforehand to your medical team. You may be given medicine to help you relax or you might be able to bring someone into the room with you for support. Diagnosis 21 Further tests You may also have some of the tests below to estimate how quickly the tumour is growing (the grade, see facing page) and whether it has spread into nearby tissue. You will be injected with a small amount of radioactive fuid and then your body will be scanned with a special camera. Cancer cells absorb the solution at a faster rate than normal cells do and show up brighter on the scan. Surgical biopsy If scans show an abnormality that looks like a tumour, some or all of the tissue may be removed for examination under a microscope. In some cases, the neurosurgeon makes a small opening in the skull and inserts a needle to take a sample. In other cases, a larger part of the skull has to be removed (craniotomy, see page 30) to get to the tumour. Every kind of cancer, including brain cancer, changes the genes of the afected cells. A pathologist may run special tests on cells from the tumour to look for these gene changes. Grading tumours The grade of a tumour describes how quickly it is growing and how it is likely to behave. A specialist doctor called a pathologist examines a sample of tumour tissue under a microscope and looks for several features to work out the grade. With other types of cancer, doctors give the cancer a stage to describe the extent of the cancer in the body. Primary brain and spinal cord tumours are not staged in this way as most don?t spread to other parts of the body. You may wish to discuss your prognosis and treatment options with your doctor, but it is not possible for anyone to predict the exact course of the disease. Tese include the tumour type, location, grade and genetic make up; your age, general health and family history; and how well the tumour responds to treatment. Both low-grade and high-grade tumours can be life-threatening, but the prognosis may be better if the tumour is low-grade, or if the surgeon is able to remove the entire tumour. Some brain or spinal cord tumours, particularly gliomas, can come back (recur) and may change to a higher grade (progress). In this case, treatments such as surgery, radiation therapy or chemotherapy may be used to control the growth of the tumour for as long as possible, relieve symptoms and maintain quality of life. The grade checks how different parts indicates how quickly the of your brain are working. You may be the likely outcome of their injected with a dye before disease (prognosis). Check with your doctor how soon your treatment should start, and take as much time as you can before making a decision. Some people with more advanced cancer choose treatment even if it only ofers a small beneft for a short period of time. Others want to make sure the benefts outweigh the side efects so that they have the best possible quality of life. Talking with doctors When your doctor frst tells you that you have cancer, you may not remember the details about what you are told. Many people like to have a family member or friend go with them to take part in the discussion, take notes or simply listen. If you are confused or want more explanation, you can ask questions see page 63 for a list of suggested questions. If you have several questions, you may want to talk to a nurse or ask the ofce manager if it is possible to book a longer appointment. Your doctor can refer you to another specialist and send your initial results to that person. You can get a second opinion even if you have started treatment or still want to be treated by your frst doctor. You might decide you would prefer to be treated by the doctor who provided the second opinion. Taking part in a clinical trial Your doctor or nurse may suggest you take part in a clinical trial. Doctors run clinical trials to test new or modifed treatments and ways of diagnosing disease to see if they are better than current methods. For example, if you join a randomised trial for a new treatment, you will be chosen at random to receive either the best existing treatment or the modifed new treatment. Over the years, clinical trials have improved treatments and led to better outcomes for people diagnosed with cancer. It may be helpful to talk to your specialist or clinical trials nurse, or get a second opinion. For more information, call Cancer Council 13 11 20 for a free copy of Understanding Clinical Trials and Research, or visit australiancancertrials. Making treatment decisions 27 Tr e a t m e n t The main treatments for brain or spinal cord tumours are surgery, radiation therapy and chemotherapy. Medicines, such as steroids or anticonvulsants (anti-seizure medicines), may be given to reduce symptoms. Tere also could be new, experimental treatments or improvements in existing treatments. Tese are given in clinical trials your doctor will tell you if you are eligible to join (see previous page). The aim of treatment may be to remove the tumour completely, slow its growth, or relieve symptoms by shrinking the tumour and reducing swelling. Removing all or part of the tumour may allow you to return to leading an active life. Sometimes the entire tumour can be removed in an operation called a total resection. Partial removal may be chosen because the tumour is widespread, or near major blood vessels or other important parts of the brain or spinal cord.

Diseases

  • Bacterial pneumonia
  • Pseudo-Turner syndrome
  • Sinus cancer
  • Floaters
  • Pterygium colli
  • Verloes Gillerot Fryns syndrome
  • Ceramidase deficiency
  • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
  • Periventricular laminar heterotopia
  • Malonic aciduria

Angiographic control was performed by the dissection and retrograde puncture of the femoral arteries womens health questions buy estradiol with a mastercard. From a microscopic point of view women's health center hattiesburg ms cheapest estradiol, all of the aneurysms exhibited intact endothelium premier women's health boca raton generic estradiol 2 mg overnight delivery, the absence of an inflammatory response menstrual cycle 8 days apart order estradiol on line amex, moderately damaged elastic lamina inside of the aneurysm (but undamaged at the neck) menstruation forecast estradiol 1 mg discount, and Main Models of Experimental Saccular Aneurysm in Animals 53 apical thrombus 6teen menstrual cycle buy 1 mg estradiol otc. No animal exhibited neurological sequelae (due to the intracranial collateral vessels network) or showed systemic signs of elastase intoxication[59]. Further modification of this model consisted of reducing the time of enzymatic digestion to 20 minutes (figure 4). Graphic representation of the endovascular elastase-induced aneurysm construction technique. These technical modifications resulted in experimental aneurysms similar to those observed in humans with regard to the arterial origin, shape, hemodynamics, and patency. The high hemodynamic tension caused by the long curvature of the brachiocephalic artery makes these experimental aneurysms similar to those occurring in the ophthalmic segment of the human internal carotid artery[40]. Two weeks later, the elastic lamina ruptured and aneurysms were formed (average dimensions of 4. The cells present in the organized thrombus exhibited features of smooth muscle cells and fibroblasts. The execution of this technique required less than one hour, and although it included surgical procedures. From a technical perspective, it is noteworthy that the concentration of elastase and the time of incubation exert a partial effect on the size of the aneurysms. One study compared animals that were not subjected to elastase to animals that were subjected to low, medium, and high concentrations of this drug, under variable durations. The rabbits that were not subjected to elastase exhibited complete thrombosis of the arterial stump and did not form 54 Aneurysm aneurysms, whereas the rabbits that were given elastase in progressive concentrations formed aneurysms. The increase of the elastase dose above a given value did not influence the size of the aneurysms; however, high concentrations of elastase induced the dilation of the parent artery and resulted in a more complex geometry of the aneurysm neck, which is closer to that observed in human aneurysms. Low concentration (25%) of elastase induced aneurysms without dilation of the adjacent artery[61]. The second simplification was achieved using an accurate neurological assessment of the rabbits using a four-point scale to rate the observed movements of the rabbits on a flat surface to verify whether paresis of the legs or abnormal gait occurred (movements in a circle or difficulty to walk). Although the studies performed to date have not reported any loss of animals, Moller Hartmann et al. The first potential cause depends on how elastase is injected through the introducer. Thus, instead of elastase, the blood column of the introducer dead space is pushed into the arterial lumen. Furthermore, the authors observed that doses of 100U of elastase were usually lethal. If the contrast material remained, without washing out or dilution for two minutes, the test was deemed to be negative, i. When these procedures were applied, none of the animals died, and all developed aneurysms. The problem posed by the blood column and contrast material inside of the introducer was resolved by performing continuous suction using a syringe[65]. Main Models of Experimental Saccular Aneurysm in Animals 55 Prospective studies on the morphology and viability of elastase-induced aneurysms in rabbits require serial high-quality angiographic control. Three routes are currently used: the femoral arteries, left external auricular vein, and left central auricular artery. In addition, retrograde femoral catheterization requires the dissection of the groin, arteriotomy, and subsequent ligation with permanent vascular occlusion, thus making subsequent angiography at this site impossible. Puncture of the left external auricular vein allows for repeated injections of contrast material, but the resulting images exhibit low spatial resolution and frequent motion-related artifacts. The anatomy of approximately 70% 80% of white New Zealand rabbits is favorable for retrograde injection in the left central auricular artery; therefore, pre-selection is important to exclude animals with unfavorable anatomy from studies[66]. Morphological and geometric features the elastase model efficiently reproduces aneurysms similar to ones that occur in the ophthalmic segment of the human internal carotid artery with regard to width, height, neck size, and diameter of the parent artery. The authors measured the width (points in the cavity exhibiting the maximal width), height (measurement of the aneurysmal dome to the mid-portion of a line connecting the proximal and distal portions of the aneurysm neck), neck (maximal diameter between the proximal and distal portions of the aneurysm orifice), the diameter of the parent artery (diameter of the artery just proximal to the aneurysm neck), and the dome/neck ratio (maximal dome width/neck width). Two weeks later, all of the animals had survived, none showed clinical evidences of neurological insult, and exhibited aneurysms at the apex of the long curve of the brachiocephalic artery, with an elongated shape, and a height greater than the width. A dome/neck ratio > 1 was observed in 50% of the aneurysms with an average value of 1. Although these measures were similar to those of human aneurysms, they did not reproduce all of the corresponding morphological characteristics, which are difficult to quantify for many reasons[44]. The average measurements of the dome width and length at days 3 and 28 after induction were (3. Conversely, the aneurysms that were not incubated with elastase progressively retracted and formed thrombi inside. Because a millimeter-scale was used and the differences found were small, the authors considered the low resolution of intravascular angiography, radiographic projections used, and variations of the cardiac cycle that promoted different intra-aneurysmal pressures to be potential sources of variation and the lack of histological correlation to be a limitation of the study[67]. The size of the neck has paramount importance when testing endovascular devices, as well as in the study of the physiopathology of aneurysms, and might be modified during the construction of experimental aneurysms. When the balloon is placed low, that is, exclusively inside of the subclavian and brachiocephalic arteries, the neck of the resulting aneurysms is wide (> 4 mm). The authors further observed that the position of the balloon did not influence the length of the aneurysms and that the balloons that were placed low did not always result in wide necks[69]. In addition to the low position of the balloon, the geometric relationship between the longest axis of the aneurysms and the axis of the parent artery played an important role in the determination of local hemodynamics and the final architecture of aneurysms. The authors found a positive correlation between the neck size and the dome height. In addition, the dome height was proportional to the angle formed by the brachiocephalic artery and the aneurysm neck. Therefore, the authors concluded that the larger the angle, the greater the hemodynamic stress caused by the blood flow on the distal neck and the aneurysm bottom[70]. The same authors applied the formula for the volume of cylinders to calculate the volume of aneurysms because the shape of the created aneurysms was cylindrical. In addition, the aneurysms with higher ligations exhibited Main Models of Experimental Saccular Aneurysm in Animals 57 larger dimensions such as the neck (3. The authors attributed these results to a larger cavity space of aneurysms with higher ligation, in addition to probable greater hemodynamic stress on the aneurysms. Finally, according to those authors, no animals died due to the accidental passage of elastase (through aberrant vessels) in the case of aneurysms with higher ligation[69]. Both experimental aneurysms were compared to human aneurysms with 5 10 mm of diameter (recently ruptured and obtained at autopsy), whose main characteristics included: 1) a complete absence of the internal elastic lamina in the aneurysms, and abrupt termination of the internal elastic lamina of the parent artery at the margins of the saccular orifice; 2) complete absence of the tunica media in the aneurysms and abrupt termination of the tunica media of the parent artery at the margins of the aneurysmal orifice; 3) absence of intramural inflammatory reaction in the aneurysms; 4) absence of neointimal fibromuscular proliferation; 5) a sac wall thickness of 51? In three out of the five studied aneurysms, one-third of the aneurysmal cavity was filled by a thrombus at different stages of organization and firmly adhered to the point of rupture. The elastase-induced aneurysms exhibited an abrupt termination of the internal elastic lamina at the margins of the saccular orifice, but the tunica medica was undamaged and continued into the interior of the saccular part of the aneurysms. The sac walls exhibited a mild to moderately inflammatory cellular (monocytes and neutrophils) response and a mild fibromuscular response. An unorganized thrombus filled one-third of the aneurysmal cavity in two out of the four investigated rabbits. The aneurysms constructed using a venous pouch exhibited a well-developed elastic lamina, and the tunica media extended into the sac wall. The wall of the venous pouch contained remarkable inflammatory infiltrate (monocytes and neutrophils) and extreme degrees of fibromuscular proliferation completely across the aneurysm wall, resulting in a remarkable neointimal thickening and luminal narrowing. Thus, the authors concluded that from a histological perspective, the elastase-induced aneurysms were the ones most similar to human aneurysms, in addition to exhibiting little spontaneous fibromuscular response compared to the surgical model with venous pouch grafting[71]. Accordingly, the elastase-induced model is currently used in tests for endovascular devices[39-42]. Papain-induced model Although the damage of elastic fibers induced by swine pancreatic elastase resulted in experimental aneurysms similar to those appearing in the ophthalmic segment of the human internal carotid artery, they are small (<5 mm), which is not completely consistent with the actual clinical characteristics of human aneurysms, where the aneurysms are larger than 5 mm. To overcome this limitation, Chinese researchers tested an association between elastase and collagenase in the in vitro pre-digestion of an arterial pouch grafted onto the aortic arch 58 Aneurysm of rabbits; however, that model exhibited a higher tendency to spontaneously rupture[72]. Mechanisms of action of papain Papain is a cysteine-proteinase type of endolytic enzyme extracted from the latex of green papaya (Carica papaya). It weighs 23,000 Da, and its molecules form a single peptide chain with 211 amino acid residues that fold into two distinct parts, which are divided by a cleft that represents its active site[74]. In addition to papain, the latex contains three additional enzymes (chymopapain, caricain, and glycil endopeptidase), which together with papain represent 80% of the enzymatic fraction, where papain corresponds to the smallest enzymatic fraction (5-8%). Although purification of papain is usually performed using precipitation techniques, it remains contaminated by other proteases[75]. With regard to its enzymatic activity, papain is activated by the addition of substances such as cyanide, reduced glutathione, and sulfate and is inactivated by oxidants. With regard to its specificity, in addition to hydrolyzing several substances, papain exhibits strong esterase activity, which makes its scope of action even wider to the point of acting on the very same substrates as pancreatic proteolytic enzymes with esterase activity[76]. Regarding its biological effects, papain exhibits remarkable elastolytic properties and has been successfully used in the production of experimental lung emphysema in animals[77, 78]. Junqueira (1980) studied the ability of papain to destroy the collagen fibers of several tissues (cartilage, bone, skin, and blood vessel) from several animal species, such as Gallus gallus (chicken), Canis familiaris (dog), Oryctolagus cuniculus (rabbit) and Sus scrofa (pig), and observed that the degree of collagen destruction varies according to the type of tissue[79]. Ionescu (1977) used papain to de-antigenize a venous heterograft to subsequently graft it onto the common carotid artery of dogs and observed that papain caused an excessive weakening of the graft with a tendency to form venous aneurysms. To overcome this problem, the author subjected the grafts to a previous treatment with formol to maintain their rigidity and flexibility and not form aneurysms[80]. With regard to commercial presentation, papain is found as raw latex (~ 12 U/mg), lyophilized powder (10 U/mg) and aqueous suspension (16-40 U/mg)[81]. Creation of papain-induced aneurysms the technique applied in the construction of papain-induced aneurysms uses the right common carotid artery of rabbits and is fully surgical, based on the study by Hoh et al. However, this technique does not use angiography during the puncture of the right common carotid artery and injection of the enzyme. This simplification proved to be safe and efficacious, and no animal exhibited complications due to the unduly passage of papain to an aberrant vascular branch that was accidentally present in the neck of the animals. Other innovations were the removal of the aortic arch and the supra-aortic trunks, direct measurement of the macroscopic dimensions of aneurysms and vessels using a caliper, and Main Models of Experimental Saccular Aneurysm in Animals 59 quantitative histological studies by means of histomorphometry in addition to a qualitative histological analysis[60,73]. Morphologic and geometric features Papain-induced aneurysms exhibited a size similar to the elastase-induced aneurysms described in previous studies. Nevertheless, it is noteworthy to stress that the papain induced aneurysms were measured directly on the right common carotid artery. This is an important point because most of the studies performed using elastase employed digital subtraction angiography to measure the aneurysms, which led to an overestimate of the aneurysm size. Thus, if papain-induced aneurysms were also measured by means of digital subtraction angiography, then their size would have most likely been overestimated. Independent from the method used, papain was efficacious in producing saccular aneurysms with an average diameter of 3. Histology From a histological perspective, papain caused the destruction of elastic fibers, endothelial damage, thrombosis, and intimal fibrosis. These alterations are similar to those found in elastase-induced aneurysms, in which the only difference is the degree of thrombosis, which was more remarkable in the papain-induced aneurysms[73]. Future of the enzymatic model Currently, there are no ideal animal models of experimental saccular aneurysms available. From a practical perspective, it is impossible for one single model to reproduce the full histological, geometric, and hemodynamic characteristics of the wide variety of aneurysms and human-related conditions. Nevertheless, the enzymatic model has been increasingly used in the production of saccular aneurysms due to its simplicity, easy execution, and lower cost, resulting from the use of small animals such as rabbits, in addition to allowing the control of height, width, and size of the aneurysm neck. Furthermore, the enzymatic model can be improved, as a wide variety of enzymes have not yet been tested. Despite the advantages of the enzymatic model, the use of both elastase and papain exhibits some limitations, such as an intramural inflammatory response, endothelial damage, and thrombosis. Indeed, thrombosis is the most important effect because it hinders the interpretation of the results of the embolization materials tested. However, even when they are present, the intra-aneurysmal thrombi do not invalidate this experimental model because under actual clinical conditions, most human aneurysms have thrombi present. Therefore, although they are not ideal for preclinical tests of embolization materials, enzymatic models most closely mimic the actual clinical conditions and thus exhibit a high potential to contribute to the study of the physiopathology of human intracranial aneurysms and testing of embolization materials and endovascular devices. Unruptured intracranial aneurysms and arteriovenous malformations: frequency of intracranial hemorrhage and relationship of lesions. Incidence of late hemorrhage and implications for treatment of incidental aneurysms. Modelo animal de doenca:criterios de escolha e especies de animais de uso corrente. Production of experimental aneurysms at a surgically created arterial bifurcation. Endovascular treatment of intracranial aneurysms: comparative evaluation in a terminal bifurcation aneurysm model in dogs. Flow dynamics of lateral carotid artery aneurysms and their effects on coils and balloons: an experimental study in dogs. Microsurgically produced bifurcation aneurysms in a rabbit model for endovascular coil embolization. Endovascular coil embolization of microsurgically produced experimental bifurcation aneurysms in rabbits. Lingual artery bifurcation aneurysms for training and evaluation of neurovascular devices. Histologic evaluation of platinum coil embolization in an aneurysm model in rabbits. Platinum coil-mediated implantation of growth factor-secreting endovascular tissue grafts: an in vivo study. Endovascular treatment of experimentally induced aneurysms in rabbits using stents: a feasibility study. Creation of saccular aneurysms in the rabbit: a model suitable for testing endovascular devices.

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