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greater than the interest that can be achieved from other high credit-rated investments Long bonds with higher interest-rate coupons that were auctioned during periods of higher interest rates will trade at a substantial premium to the par value during periods when current interest rates are low As an example a 6 percent 30-year T-bond that has, say, 15 years left, may trade at 120 percent of par value when interest rates are lower In contrast, as interest rates rise, the secondary market value of long bonds will fall Treasury in ation-protected securities (TIPS) TIPS are in ation-indexed bonds issued by the US Treasury The rate of return is adjusted to the consumer price index (CPI) as a measure of current in ation The coupon rate is determined at auction like other Treasury securities, but have a yeild generally lower than T-Bonds or notes The advantage to TIPS is that you are generating a real rate of return because the coupon rate is adjusted to account for in ation This protects the bond holder against the negative effects of in ation over the term of the bond TIPS are currently offered in 5-year, 10-year, and 20-year maturities TIPS have an active secondary market as well, and in periods of low interest rates and/or expectations for increasing in ation, these bonds can be very popular

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endocrine and radiologic studies periodically In some cases of idiopathic DI, there are serum antibodies that react with the supraoptic neurons, raising the question of an autoimmune disorder In a few such instances, postmortem examination has disclosed a decreased number of neurons in the supraoptic and paraventricular nuclei Also, anorexia nervosa is often associated with mild DI Finally, it should be mentioned that certain drugs used in neurologic practice for example, carbamazepine may be the cause of reversible DI (excessive secretion of ADH is more common in relation to this drug), and as mentioned, lithium regularly causes DI, even at times at the upper range of its therapeutic serum concentration In all these conditions, the severity and permanence of the DI are determined by the nature of the lesion In cases of acute onset, three phases have been delineated: rst, a severe DI lasting days; then, as the neurohypophysis degenerates, a reduction in severity of DI due to release of stored ADH; and nally a persistent pattern, usually lifelong The neurohypophysial axons can regenerate, allowing for some degree of recovery even after years Diagnosis of DI This is always suggested by the passage of large quantities of dilute urine accompanied by polydipsia and polyuria lasting throughout the night The last two signs are, of course, obscured in an unresponsive patient, in which case careful measurement of uid output and input are needed to expose the disorder The thirst mechanism and drinking usually prevent dehydration and hypovolemia, but if the patient is stuporous or the thirst mechanism is inoperative, severe dehydration and hypernatremia can occur, leading to coma, seizures, and death A low urine osmolality and speci c gravity are found in DI, in conjunction with high serum osmolality and sodium values Osmotic dehydration as a cause of the polydipsia-polyuria syndrome, such as occurs with the glycosuria of diabetes mellitus, must, of course, be excluded A period of 6 to 8 h of dehydration increases urinary osmolality in a person with normal kidneys and neurohypophysis; it is this change in urine concentration that is most useful in the differential diagnosis of polyuria, particularly in distinguishing compulsive water drinkers from those with DI; in the latter group, urinary volume and serum electrolytes normalize with dehydration Proof that the patient has a central cause of DI and not nephrogenic unresponsiveness to vasopressin is obtained by injecting 5 U of vasopressin (Pitressin) subcutaneously; this will diminish urine output and increase osmolality when there is a central cause of DI Diagnosis is aided by the radioimmunoassay for plasma ADH; ADH is usually reduced to less than 10 pg/mL in patients with central DI (normal, 14 to 27 pg/mL) Treatment of DI Vasopressin tannate in oil, synthetic vasopressin nasal spray, and a long-acting analogue of arginine vasopressin (desmopressin, DDAVP) administered by nasal insuf ation (10 to 20 mg or 01 to 02 mL) are used to control chronic DI The nasal form is generally preferred because of its long antidiuretic action and few side effects In unconscious patients, aqueous vasopressin, 5 to 10 U given subcutaneously, is effective for 3 to 6 h; DDAVP, 1 to 4 mg subcutaneously, is effective for 12 to 24 h These drugs must be given repeatedly, guided by urine output and osmolality (we have given these drugs intravenously in critical situations) The brief duration of action of the medication is advantageous in postoperative states and after head injury, for it allows the recognition of recovery of neurohypophyseal function and the avoidance of water intoxication If a longer duration of treatment is anticipated, one uses vasopressin tannate in oil (25 U), the action of which persists for 24 to 72 h In the unconscious patient, great care must.

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Java implementations of barcode reader in ABBYY Cloud OCR SDK is very simple and takes only few lines of code. See the codesample to find out the ...
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It really depends on the hardware you are using (i.e. The Barcode scanner ) most scanners simulate keyboard input and will for example write a ...

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