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Stereotaxic surgery, also called stereotactic surgery or stereotaxy, a three-dimensional surgical technique that enables lesions deep within tissues to be located and treated using cold, heat, or chemicals. This device, named the Horsley-Clarke apparatus, facilitated the study of the cerebellum in animals by enabling accurate electrolytic lesioning to be made in the brain. Since then, a number of modifications and refinements have been made to stereotaxic devices, procedures, and atlases, and these advances have significantly improved the utility of stereotaxy. Stereotaxic surgery is often used to locate lesions in the brain and to deliver radiation therapy. In procedures that involve the brain, such as ablation therapy in Parkinson disease, the head is held motionless in a head ring, and the lesion or area to be treated is located using three-dimensional coordinates based on information from X-rays, computerized axial tomography, magnetic resonance imaging, or electrodes. In radiation therapy, stereotaxis is used to focus high-intensity radiation on localized areas to shrink tumours or to obliterate arteriovenous malformations. Stereotaxic technique also is highly effective for guiding fine-needle aspiration biopsies of brain lesions; it requires that only one burr hole be made in the skull with the patient under local anesthesia. Stereotaxic fine-needle biopsy also is used to evaluate breast lesions that are not palpable but are detected by mammography.

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Emphysema, also called pulmonary emphysema, condition characterized by widespread destruction of the gas-exchanging tissues of the lungs, resulting in abnormally large air spaces. Lungs affected by emphysema show loss of alveolar walls and destruction of alveolar capillaries. As a result, the surface available for the exchange of oxygen and carbon dioxide between inhaled air and blood traversing the lungs is reduced. In addition, loss of elastic tissue from the walls of the destroyed alveoli causes the lungs to expand within the chest cage. The expanded lungs compress the small bronchi and thus increase resistance to airflow. This is especially evident during expiration, when contraction of the muscles of the chest wall and abdomen increase intrathoracic pressure and further reduce the passage of air through the small bronchi.

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Disease may be defined as an injurious deviation from a normal physiological state of an organism sufficient to produce overt signs, or symptoms. The deviation may be either an obvious organic change in the tissue composing an organ or a functional disturbance whose organic changes are not obvious. The severity of the changes that occur in cells and tissues subjected to injurious agents is dependent upon both the sensitivity of the tissue concerned and the nature and time course of the agent. A mildly injurious agent that is present for short periods of time may either have little effect or stimulate cells to increased activity. Strongly injurious agents in prolonged contact with cells cause characteristic changes in them by interfering with normal cell processes. Most causative agents of disease fall into the latter category.

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The main criteria for judging relationships between domestic or cultivated organisms and wild ancestors were similarities of structure and function, but cytogenetical examinations, particularly comparisons of chromosomes and chromosome sets, also are adding to the knowledge of the origins of domesticated organisms. With animals, morphological and biochemical studies are made. During the 11,000 or 12,000 years that have passed since the beginning of domestication, the animals and plants that humans have selected as useful to them have undergone profound changes. The consequences of domestication are so great that the differences between breeds of animals or varieties of plants of the same species often exceed those between different species under natural conditions. The most important consequence of domestication of animals consists of a sharp change in their seasonal biology. The wild ancestors of domesticated animals are characterized by strict seasonal reproduction and molting rhythms. Most domesticated species, on the contrary, can reproduce themselves at almost any season of the year and molt little or not at all. No less characteristic are the changes that occur in plants as a result of domestication. Their structure and general appearance may be drastically changed.

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The specific economic application of domesticated animals did not appear at once. Dogs probably accompanied hunters and helped them hunt wild animals; they probably also guarded human settlements and warned the inhabitants of possible danger. At the same time, they were eaten by humans, which was probably their main importance during the first stages of domestication. Sheep and goats were also eaten in the initial stages of domestication but later became valuable for producing the commodities of milk and wool. The principal aim of cattle breeding in ancient times was to obtain meat and skin and to produce work animals, which greatly contributed to the development of agriculture. Cattle, at the initial stages of domestication, produced a small amount of milk, sufficient only to rear their calves. The development of high milk yield in cows with their breeding especially for milk production is a later event in the history of domestication.

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Inborn errors of metabolism are caused by genetic defects in intermediary metabolic pathways. Although long considered to be the domain of human paediatric medicine, they are also recognised with increasing frequency in companion animals. The diagnosis of diseased animals can be achieved by searching for abnormal metabolites in body fluids, although such screening programmes have, until now, not been widely available to the small animal clinician. A comprehensive battery of analytical tools exists for screening for inborn metabolic diseases in humans which can be applied to animals and serve not only for the diagnosis of affected patients but also to detect asymptomatic carriers and further our understanding of metabolic pathways in dogs and cats. Moreover, naturally occurring animal models of inherited metabolic diseases provide a unique opportunity to study the biochemical and molecular pathogenesis of these disorders and to investigate possible therapeutic options.

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Sickle cell anemia is an inherited form of anemia a condition in which there isn’t enough healthy red blood cells to carry adequate oxygen throughout your body. Normally, your red blood cells are flexible and round, moving easily through your blood vessels. In sickle cell anemia, the red blood cells become rigid and sticky and are shaped like sickles or crescent moons. These irregularly shaped cells can get stuck in small blood vessels, which can slow or block blood flow and oxygen to parts of the body. There’s no cure for most people with sickle cell anemia. But treatments can relieve pain and help prevent problems associated with the disease. Sickle cell anemia is caused by a mutation in the gene that tells body to make the red, iron-rich compound that gives blood its red color. Hemoglobin allows red blood cells to carry oxygen from your lungs to all parts of body. In sickle cell anemia, the abnormal hemoglobin causes red blood cells to become rigid, sticky and misshapen.

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Pleural effusion is the abnormal accumulation of fluid within the chest cavity . This occurs either because too little fluid is being absorbed in the pleural cavity, or because too much fluid is being produced in the pleural cavity. Alterations in the dog’s blood pressure and protein content in the blood, or the penetrability of blood vessels and lymphatic function, may contribute to fluid accumulation. Pleural effusion can affect both dogs and cats. If you would like to learn more about how this disease affects cats. It causes High hydrostatic pressure; Low Oncotic Pressure: inability of blood plasma proteins to pull water into the circulatory system, resulting in excess fluid build-up; Vascular or lymphatic abnormality: disorders of the vessels and/or ducts that convey fluids; Chest filled with lymph fluid mixed with lipids ; Lymphangiectasia; Diaphragmatic hernia: passage of a loop of intestine through an abnormal hole in the diaphragm muscle; Blockage of the venacava; Congestive heart failure; Cancer in the chest cavity; Blood in the chest cavity; Trauma to the chest; Lung lobe torsion; Blood clot of the lungs; Infection: bacterial, viral, or fungal; Heartworms; Hypoalbuminemia: abnormally low levels of blood protein albumin; Protein-losing enteropathy; Protein-losing nephropathy; Liver disease; Inflammation of the pancreas; Overhydration; Bleeding disorder.

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Anticipating the future use of arginine to enhance fetal and neonatal growth as well as to treat diabetes and obesity, we performed studies in pigs, rats, and sheep to determine the pharmacokinetics of orally or i.v. administered arginine and the safety of its chronic supplementation. Our results indicate that all 3 species rapidly catabolized the supplemental arginine. The elevated circulating concentrations of arginine generally returned to baseline levels within 4–5 h after administration, with the rates varying with the age and physiological status of the animals. The clearance of arginine was greater in pregnant than in nonpregnant animals, in young than in adult animals, in lean than in obese animals, and in type-1 diabetic than in nondiabetic animals. I.v. administration of arginine-HCl to pregnant ewes did not result in any undesirable treatment-related effect. Neonatal pigs, growing-finishing pigs, pregnant pigs, and adult rats tolerated large amounts of chronic supplemental arginine administered via enteral diets without the appearance of any adverse effect. On the basis of the comparative studies and a consideration of species differences in food intake per kilogram body weight, we estimate that a 70-kg human subject should be able to tolerate long-term parenteral and enteral supplemental doses of 6 and 15 g/d arginine, respectively, in addition to a basal amount of arginine from regular diets.

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Canine Cystinuria is an autosomal recessive disorder that affects a dog’s ability to filter cystine out of urine. Normally, tubules in the kidney are responsible for re-absorption of cystine, filtering it out of the urine. In dogs with Canine Cystinuria, the tubules are unable to transport the cystine, allowing it to accumulate in the urine. Cystine is generally insoluble in the acidic conditions of canine urine, allowing it to crystallize and form caliculi, also known as stones. The cause of Cystinuria is a single nucleotide polymorphism that occurs in the SLC3A1 gene which causes a premature stop codon. Cystinuria is a recessive disorder, meaning that the dog must have two copies of the defective gene to suffer from the disease. Because Cystinuria is a recessive disorder, a dog can also be a carrier of this disease, meaning it carries one copy of the mutation but does not display any symptoms. If two carriers are bred together, there is a 25% chance per puppy born that it will develop symptoms of Cystinuria. Animal Genetics accepts Buccal Swab, Blood, Dewclaw. Collection kits are available and can be ordered at test now.

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