which gland produces thyroxine?
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That would be the THYROID GLAND, it is a hormone secretion used for the body ; ) hope that helps...
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Endocrine Pituitary Gland \nThe pituitary gland, or hypophysis, is an endocrine gland about the size of a pea that sits in the small, bony cavity (sella turcica) at the base of the brain. Its posterior lobe is connected to a part of the brain called the hypothalamus via the infundibulum (or stalk), giving rise to the tuberoinfundibular pathway. The posterior lobe is thus derived from neural ectoderm while the anterior lobe is derived from oral ectoderm. The anterior pituitary lobe receives releasing hormones from the hypothalamus via a portal vein system. The pituitary gland secretes hormones regulating a wide variety of bodily activities, including trophic hormones that stimulate other endocrine glands. For a while, this led scientists to call it the master gland, but now we know that it is in fact regulated by hormones released from the hypothalamus. It is physically attached to the brain by the pituitary, or hypophyseal stalk connected with the median eminence.\nThe pituitary gland is divided into two sections: the anterior lobe (adenohypophysis) and the posterior lobe (neurohypophysis). The posterior pituitary is, in effect, a projection of the hypothalamus. It does not produce its own hormones, but only stores and releases the hormones oxytocin and antidiuretic hormone (ADH - also known as vasopressin).\nThe anterior pituitary secretes growth hormone, prolactin, follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, adrenocorticotropic hormone, endorphins and other hormones. It does this in response to a variety of chemical signals from the hypothalamus, including TRH (thyrotropin-releasing hormone), CRH (corticotropin-releasing hormone), DA (dopamine, "prolactin inhibiting factor"/PIF), GnRH (gonadotropin-releasing hormone), and GHRH (growth hormone releasing hormone), which travel to the anterior lobe by way of a special capillary system from the hypothalamus, down the median eminence, to the anterior lobe. These hormones from the hypothalamus cause release of the respective hormone from the pituitary, i.e. TRH releases TSH, CRH releases ACTH, GnRH releases FSH and LH and GHRH causes the release of GH except for DA, which constantly inhibits the release of prolactin normally. There is also an interaction between the hormones from the hypothalamus, i.e. TRH induces the release of prolactin. The control of release of hormones from the pituitary is in a negative feedback loop. Their release is inhibited by increasing levels of hormones from the target gland on which they act.\nThere is also an intermediate lobe in many animals. In adult humans it is just a thin layer of cells between the anterior and posterior pituitary, nearly indistinguishable from the anterior lobe. The intermediate lobe produces melanocyte-stimulating hormone (MSH), although this function is often (imprecisely) attributed to the anterior pituitary.\nFunctions of the pituitary are:\nThe pituitary gland helps control the following body processes of the pituitary gland are:\nGrowth \nBlood pressure \nSome aspects of pregnancy and childbirth \nBreast milk production \nSex organ functions in both women and men \nThyroid gland function \nThe conversion of food into energy (metabolism) \nWater and osmolarity regulation in the body
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endocrine and digestive
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Hypothyroidism Symptoms \n\n   1.  Insufficient production of thyroid hormones.\n   2. A pathological condition resulting from severe thyroid insufficiency, which may lead to cretinism or myxedema.\n\n\nHypothyroidism\n\nA disorder in which the thyroid gland produces too little thyroid hormone causing a decrease in the rate of metabolism with associated effects on the reproductive system. Symptoms include fatigue, difficulty swallowing, mood swings, hoarse voice, sensitivity to cold, forgetfulness, and dry/coarse skin and hair. \n\nHypothyroidism FAQS :\n\nWhat are thyroid hormones?\nThyroid hormones are produced by the thyroid gland. This gland is located in the lower part of the neck, below the Adam's apple. The gland wraps around the windpipe (trachea) and has a shape that is similar to a butterfly - formed by two wings (lobes) and attached by a middle part (isthmus).\n\nThe thyroid gland uses iodine (mostly available from the diet in foods such as seafood, bread, and salt) to produce thyroid hormones. The two most important thyroid hormones are thyroxine (T4) and triiodothyronine (T3), which account for 99.9% and 0.1% of thyroid hormones present in the blood respectively. However, the hormone with the most biological activity is T3. Once released from the thyroid gland into the blood, a large amount of T4 is converted into T3 - the active hormone that affects the metabolism of cells.\n\nThyroid hormone regulation- the chain of command\nThe thyroid itself is regulated by another gland that is located in the brain, called the pituitary. In turn, the pituitary is regulated in part by the thyroid (via a "feedback" effect of thyroid hormone on the pituitary gland) and by another gland called the hypothalamus.\n\nThe hypothalamus releases a hormone called thyrotropin releasing hormone (TRH), which sends a signal to the pituitary to release thyroid stimulating hormone (TSH). In turn, TSH sends a signal to the thyroid to release thyroid hormones. If a disruption occurs at any of these levels, a defect in thyroid hormone production may result in a deficiency of thyroid hormone (hypothyroidism).
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Info on the Endocrine system:
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The basic definition of endocrine glands that I was taught in college was that they are ductless glands.  However, we were also taught that they release hormones directly into the bloodstream.  Both "B" and "C" are correct answers but "B" is the more "classical" answer.
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No.  A goiter is a thickening/enlargement of the tyroid gland located in the front of the troat, just under your "adams apple".  A goiter can get quite large and very obvious.  A large neck can be a hereditary trait.  If you are really concerned, talk to your physician about having tyroid studies done, specifically TSH( tyroid stimulating hormone), TS1, TS2, and TS3, which are the thyroid stimilating hormones.
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Most of the hormones produced in our bodies are excreted by the endoctrine system, the main contributor being the anterior and posterior pituitary.\n\nPosterior pituitary secretes 2 hormones: oxytocin (released during labor in women) and ADH (anti-diuretic hormone- released to increase sodium reabsorption when the body is dehydrated, low blood pressure, or in other cases when the body needs more water.)\n\nAnterior pituitary secretes many more hormones throughout your body, but the main ones are:\n\nFSH (follicle-stimulating hormone)\nLH (luteinizing hormone)\nACH (adrenocorticotropic hormone)\nTSH (thyroid-stimulating hormone)\nProlactin\nEndorphins (which make you happy)\n& GH (growth hormone)\n\nHope this helps.
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Here is a very detailed write up :\n\nhttp://www.nicholsdiag.com/products/thyroid/di-calcit.pdf
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Try http://thyroid.about.com/blthyroid.htm \nThis site has a ton of good information about thyroid disease.
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The hormone is synthesized and secreted from alpha cells (α-cells) of the islet of Langerhans, which are located in the endocrine portion of the pancreas. The alpha cells are located in the outer rim of the islet.
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The pituitary gland (which is part of the endocrine system) secretes HGH {human growth hormone} which promotes bone growth.This is how the endocrine system works with the skeletal system.
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My Spanish isn't good, but I think you mean THYROID. \n\nTry this address for info in Spanish:\nhttp://www.tiroides.net/
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Understanding Thyroid Problems -- Treatment\n\nWebMD Medical Reference \n\nThe Basics | Symptoms | Detection & Treatment\n\nHow Do I Know If I Have Them?\n\nA doctor can diagnose hyperthyroidism and hypothyroidism by testing the levels of thyroid hormones in your blood.  Doctors measure hormones secreted by the thyroid itself, as well as thyroid-stimulating hormone (TSH), a chemical released by the pituitary gland that triggers hormone production in the thyroid.\n\nWhen you are hypothyroid, higher quantities of TSH are circulating in your blood as your body attempts to foster increased production of thyroid hormones.  The reverse is true with hyperthyroidism, in which TSH levels are below normal and circulating thyroid-hormone levels are high.\n\nTo determine the cause of hyperthyroidism, doctors often use radioactive iodide uptake tests, which track the amount of iodide absorbed by the thyroid gland. Iodide, obtained from the foods we eat, is a key ingredient in the manufacture of thyroid hormone, so the amount of iodide the thyroid absorbs is a reliable indicator of how much hormone the gland is producing.  For this test, you must swallow a small amount of radioactive iodide in liquid or capsule form.  After a predetermined wait, the doctor places an instrument over your neck to measure how much of the radioactive iodide has gathered in your thyroid.\n\nIf the results of this test suggest that the gland is collecting excessive amounts of iodide, the doctor may then conduct a radioactive iodide uptake scan.  In this test, the doctor uses a special film to create a picture that shows the exact location of the radioactive iodide in your thyroid gland.  The scan will reveal, for example, if the iodide is collecting in adenomas, indicating that the nodules are responsible for the excess hormone.  If the scan shows that the iodide is spread equally throughout the tissue, the whole thyroid is involved in the excess production.\n\nSome doctors believe that blood tests may not be sensitive enough to detect milder forms of hypothyroidism.  Instead, they advocate monitoring your body's basal (resting) temperature.  To track your basal temperature accurately, you must closely follow certain guidelines:  Shake the thermometer below 95° F at night and place it where you can reach it without getting out of bed.  The following morning, before you get out of bed, take your temperature via your armpit for 10 minutes while staying as still as possible.  Keep records of your temperature for at least three days.  (Women should do this during the first two weeks of the menstrual cycle, as their basal temperature may rise during the latter half.)  Normal basal body temperatures fall between 97.4° F and 97.8° F.  If your basal temperature is consistently low, you could be mildly hypothyroid.\n\nIf you have one or more adenomas, your doctor will want to keep careful records of when they were first found and how they develop, since not all adenomas produce excess thyroid hormone. In fact, most of these nodules are not malignant, especially if they remain the same size over long intervals.  (Cancerous tissue, by contrast, will undergo noticeable growth.)  Nodules that appear suddenly are typically fluid-filled cysts and are often benign.  They can be evaluated with a noninvasive ultrasound exam.  If blood tests indicate that the nodules are producing excess thyroid hormone, and if you have other symptoms, your doctor will treat you for hyperthyroidism.\n\nIn any case, you should receive periodic checkups if you have a nodule on your thyroid gland, since you may become hyperthyroid in the future.  If your blood tests show elevated hormone levels, your doctor may recommend other tests, including radioactive iodide uptake tests and scans that indicate whether the nodules are "hot" or "cold."  Hot nodules, or those that are actively trapping iodide and producing too much thyroid hormone, are rarely cancerous.  But cold nodules -
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A goiter is an enlargement of the thyroid gland. Persons with enlarged thyroids may have normal function of the gland (euthyroidism), thyroid deficiency (hypothyroidism), or overproduction of the hormones (hyperthyroidism). Goiter may be congenital or acquired, endemic or sporadic.\nThe goiter often results from increased pituitary secretion of thyrotropic hormone in response to decreased circulating levels of thyroid hormones. Thyroid enlargement may also result from infiltrative processes that may be inflammatory or neoplastic. Goiter in patients with thyrotoxicosis is caused by thyrotropin receptor-stimulating antibodies.\n\n\n Figure 561-1 Congenital goiter in infancy. A, Large congenital goiter in an infant born to a mother with thyrotoxicosis who had been treated with iodides and methimazole during pregnancy. B, A 6-wk-old infant with increasing respiratory distress and cervical mass since birth. The operation revealed a large goiter that almost completely encircled the trachea. Notice the anterior deviation and posterior compression of the trachea. Partial thyroidectomy completely relieved the symptoms. It is apparent why a tracheostomy is not adequate treatment for these infants. The cause for the goiter was not found.\n561.1 Congenital Goiter\nCongenital goiter is usually sporadic and may result from a fetal thyroxine (T4 ) synthetic defect or the administration of antithyroid drugs or iodides during pregnancy for the treatment of thyrotoxicosis. Goitrogenic drugs and iodides cross the placenta and at high doses may interfere with synthesis of thyroid hormone, resulting in goiter and hypothyroidism in the fetus. The concomitant administration of thyroid hormone with the goitrogen does not prevent this effect, because insufficient amounts of T4 cross the placenta. Iodides are included in many proprietary preparations used to treat asthma; these preparations must be avoided during pregnancy because they have often been a cause of unexpected congenital goiter. Amiodarone, an antiarrhythmic drug with a 37% iodine content, has also caused congenital goiter with hypothyroidism. Even when the infant is clinically euthyroid, there may be retardation of osseous maturation, low levels of T4 , and elevated levels of thyroid-stimulating hormone (TSH). In women with Graves disease on antithyroid drugs, these effects can occur when the mother takes only 100–200?mg of propylthiouracil/24?hr; all such infants should undergo thyroid studies at birth. Administration of thyroid hormone to affected infants may be indicated to treat clinical hypothyroidism, to hasten the disappearance of the goiter, and to prevent brain damage. Because the condition is rarely permanent, thyroid hormone may be safely discontinued after the antithyroid drug has been excreted by the neonate, usually after a week.\nEnlargement of the thyroid at birth may occasionally be sufficient to cause respiratory distress that interferes with nursing and may even cause death. The head may be maintained in extreme hyperextension. When respiratory obstruction is severe, partial thyroidectomy rather than tracheostomy is indicated ( Fig. 561–1 ).\nGoiter is almost always present in the congenitally hyperthyroid infant. These goiters usually are not large; the infant manifests\n\n1882\nclinical symptoms of hyperthyroidism, and the mother often has a history of Graves disease (see Chapter 562.1 ). TSH receptor-activating mutations are also a recognized cause of congenital goiter. \nWhen no causative factor is identifiable, a defect in synthesis of thyroid hormone should be suspected. Neonatal screening programs find congenital hypothyroidism caused by such a defect in 1/30,000–50,000 live births. If the infant is hypothyroid, it is advisable to treat immediately with thyroid hormone and to postpone more detailed studies for later in life. Because these defects are transmitted by recessive genes, a precise diagnosis is helpful for genetic counseling. Monitoring subsequent
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Iodine does not block the formation of T3 and T4, but the key element. During the process of transformation, iodine binds with other polymers and become ionized, a state called iodide. Only when ionized, can iodine be active and interact with other elements. \n\nThe cause of goiter is iodine deficiency, and the body tries to compensate the deficiency with enlarged thryroid gland. T3 and T4 both are beneficial to goiter. The difference is T4 is usually converted to T3 by deiodinases, so T3 is considered as the major thryroid hormone, altough the plasma concentration of T4 is much higher.
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it was called hormone.\nin animal the thyroid glands will secreted the thyroid hormone that promotes growth and maturation of central nervous system.in plant there were the auksin and gibberelin.