on 13-Jul-2017 (Thu)

I think it is very important to make the link between the muf.zdathun and the Arabic modernist project, to bring Abbasid poets such as Abu Tammiim, Ibn al-R1lmi, al-Bul).turi, and certainly the later al-Mutanabbi into the discussion of Arabic poetry and its directions today.

Periodic bond yields for both straight and zero-coupon bonds are conventionally computed based on semi-annual periods, as U.S. bonds typically make two coupon payments per year. For example, a zero-coupon bond with a maturity of five years will mature in 10 6-month periods. The periodic yield for that bond, r, is indicated by the equation Price = Maturity value x (1 + r)^-10. This yield is an internal rate of return with semi-annual compounding. How do we annualize it?

The convention is to double it and call the result the bond's yield to maturity. This method ignores the effect of compounding semi-annual YTM, and the YTM calculated in this way is called a bond-equivalent yield (BEY).

However, yields of a semi-annual-pay and an annual-pay bond cannot be compared directly without conversion. This conversion can be done in one of the two ways:

• Convert the bond-equivalent yield of a semi-annual-pay bond to an annual-pay bond.
  

• Convert the equivalent annual yield of an annual-pay bond to a bond-equivalent yield.
  

Example

• A Eurobond pays coupon annually. It has an annual-pay YTM of 8%.
• A U.S. corporate bond pays coupon semi-annually. It has a bond equivalent YTM of 7.8%.
• Which bond is more attractive, if all other factors are equal?

Solution 1

• Convert the U.S. corporate bond's bond equivalent yield to an annual-pay yield:
• Annual-pay yield = [1 + 0.078/2]² - 1 = 7.95% < 8%
• The Eurobond is more attractive since it offers a higher annual-pay yield.

Solution 2

• Convert the Eurobond's annual-pay yield to a bond equivalent yield (BEY):
• BEY = 2 x [(1 + 0.08)^0.5 - 1] = 7.85% > 7.8%
• The Eurobond is more attractive since it offers a higher bond equivalent yield.

A zero-coupon bond is a debt security that doesn't pay interest (a coupon) but is traded at a deep discount, rendering profit at maturity when the bond is redeemed for its full face value.

prehypertension as a systolic blood pressure of 120-139 mm Hg or a diastolic blood pressure of 80-89 mm Hg in the absence of preexisting end-organ disease (for example, diabetes mellitus, chronic kidney disease, or cardiovascular disease)

prehypertension as a systolic blood pressure of 120-139 mm Hg or a diastolic blood pressure of 80-89 mm Hg in the absence of preexisting end-organ disease (for example, diabetes mellitus, chronic kidney disease, or cardiovascular disease).

prehypertension as a systolic blood pressure of 120-139 mm Hg or a diastolic blood pressure of 80-89 mm Hg in the absence of preexisting end-organ disease (for example, diabetes mellitus, chronic kidney disease, or cardiovascular disease)

Appropriate follow-up for those with prehypertension occurs at annual visits.

If blood pressures measuring 140/90 mm Hg or greater were documented, this would require repeat measurements for at least three visits over the period of at least 1 week of more to establish a diagnosis of hypertension

Ambulatory blood pressure monitoring records blood pressures periodically during normal activities. It is indicated primarily for diagnosis of suspected white coat hypertension (persistently elevated blood pressure readings in the office without evidence of end-organ damage) or to confirm a poor response to antihypertensive medication. It may also be useful in assessing for masked hypertension (evidence of end-organ damage without apparent elevated blood pressures) or for evaluating episodic or resistant hypertension.

This patient has risk factors for CIN (older age, elevated serum creatinine, diabetes mellitus)

The use of gadolinium in MRI studies is relatively contraindicated in patients with an estimated glomerular filtration rate of less than 30 mL/min/1.73 m2due to the increased risk of NSF.

Znajdź ludzi, którzy będą wspierać twoją zdolność do stawiania oporu, posiadania własnej opinii, podejmowania ryzyka i stawania się sobą. Od tego „bezpiecznego horyzontu wspierających cię przyjaciół” możesz rozpocząć proces dorastania.

aby być napraw- dę dorosłym, stanąć na równi z mamą, musisz mieć własne sądy o świecie.

r many of us, as for Dikmen's Turkish narrator, the culture that we are teaching is also foreign;

literary pragmatics, an inter- disciplinary area of literary linguistic study that ap- proaches literary works as social acts of interactive communication, can be used in the intermediate to advanced language classroom in order to promote critical linguistic awareness.1

Balkan endemic nephropathy (BEN) and is at increased risk for transitional cell carcinoma.

BEN is a slowly progressive tubulointerstitial disease that has recently been linked to aristolochic acid.

Free hemoglobin is partially bound by haptoglobin but may also be filtered into the urine, producing a red color. Heme reacts with peroxidase in the urine dipstick, causing a false-positive result for blood. Hemoglobinuria is distinguished from true hematuria by the absence of erythrocytes on urine microscopy. Similar findings on urinalysis will also occur with the release of myoglobin into the circulation, usually from muscle injury (rhabdomyolysis). Myoglobin is a small molecule relative to hemoglobin, is not bound within the circulation by haptoglobin, and is readily filtered through the kidneys, resulting in red-colored urine. It also reacts with peroxidase in the urine dipstick indicating blood, although microscopic examination will also be negative for erythrocytes.

MKSAP17 MCQ 1646 .Mustafa M. A Bladder cancer is a concern in a patient with a significant smoking history presenting with a finding of red urine. However, the urine color change in bladder cancer is due to bleeding into the urinary tract, and erythrocytes would be seen on urinalysis.

MKSAP17 MCQ 1646 .Mustafa M. A Bladder cancer is a concern in a patient with a significant smoking history presenting with a finding of red urine. However, the urine color change in bladder cancer is due to bleeding into the urinary tract, and erythrocytes would be seen on urinalysis. Glomerulonephritis may be associated with bleeding into the urine and would be suspected if erythrocytes, particularly acanthocytes (dysmorphic erythrocytes), were found on urine microscopic examination. Proteinuria may also be found in glomerulonephritis,

Glomerulonephritis may be associated with bleeding into the urine and would be suspected if erythrocytes, particularly acanthocytes (dysmorphic erythrocytes), were found on urine microscopic examination. Proteinuria may also be found in glomerulonephritis,

definition of resistant hypertension, which is defined by blood pressure readings not at target despite three agents, one of which must be a diuretic.

Chlorthalidone is often preferred over other thiazide-type diuretics primarily due to its higher potency and longer duration of action.

minoxidil promotes sodium retention and is almost always given with a diuretic.

In amyloidosis involving the kidney, glomerular lesions tend to be prominent and present with proteinuria, often in the nephrotic range.

amyloid resulting from monoclonal lambda or kappa light chains is termed AL amyloid

AL amyloid may present with nonspecific systemic symptoms such as fatigue or weight loss, but most commonly presents with symptoms associated with infiltration of different organ systems. These may include restrictive cardiomyopathy, peripheral neuropathy, hepatosplenomegaly, and, less commonly, cutaneous purpura and macroglossia

Findings on biopsy show deposits that stain apple green on Congo red staining under a polarizing microscope; these deposits are also visible on electron microscopy.

Type 4 (hyperkalemic distal) RTA is caused by aldosterone deficiency or resistance. Primary aldosterone deficiency is seen in primary adrenal deficiency (Addison disease),

Type 4 (hyperkalemic distal) RTA is caused by aldosterone deficiency or resistance. Primary aldosterone deficiency is seen in primary adrenal deficiency (Addison disease)

of hyporeninemic hypoaldosteronism in which there is diminished renin release by the kidney.

occurs most commonly in patients with mild to moderate kidney disease due to diabetic nephropathy (such as this patient) or chronic interstitial nephritis (such as in systemic lupus erythematosus or AIDS). It may also be associated with acute glomerulonephritis, specific drugs that impair renin release (NSAIDs and calcineurin inhibitors), tubulointerstitial disease, and drugs that reduce aldosterone production (ACE inhibitors, cyclooxygenase inhibitors, and heparin).

type 4 (hyperkalemic distal) RTA typically present with hyperkalemia, a normal anion gap metabolic acidosis, and impaired urine acidification, but with the ability to maintain the urine pH to <5.5. The specific cause can be differentiated by measurement of plasma renin activity, serum aldosterone, and serum cortisol. Initial treatment includes correction of the underlying cause if possible, with discontinuation of offending medications. Replacement of mineralocorticoids with fludrocortisone is indicated for patients with documented deficiency and should be considered for those with hyporeninemic hypoaldosteronism unless hypertension or heart failure is present.

Type 1 (hypokalemic distal) RTA results from a defect in urine acidification in the distal tubule with impaired excretion of hydrogen ions and a normal anion gap metabolic acidosis.

Type 2 (proximal) RTA involves a defect in regenerating bicarbonate in the proximal tubule and is characterized by hypokalemia, glycosuria (in the setting of normal plasma glucose), low-molecular-weight proteinuria, and renal phosphate wasting

Glomerular hematuria is typically characterized by brown- or tea- colored urine with dysmorphic erythrocytes (or acanthocytes) and/or erythrocyte casts on urine sediment examination, although some glomerular disorders may cause gross hematuria. Other findings suggestive of a glomerular source include proteinuria.

Diagnosis of thin glomerular basement membrane disease is usually based on the history of persistent hematuria, normal kidney function, and positive family history of hematuria without kidney failure.

thin glomerular basement membrane (GBM) disease, an inherited type IV collagen abnormality that causes thinning of the GBM and results in hematuria. The disorder may affect up to 5% of the population, and 30% to 50% of patients report a family history of hematuria. The disease is characterized by microscopic or macroscopic hematuria that may be first discovered in young adults. Diagnosis is usually based on the history of persistent hematuria, normal kidney function, and positive family history of hematuria without kidney failure; biopsy is not typically required. Long-term prognosis for kidney function is excellent, with rare progression to chronic kidney disease (CKD).

Fabry disease is a rare X-linked inherited disorder in which there is deficiency of α-galactosidase A (an enzyme in the glycosphingolipid pathway) that leads to progressive deposit of globotriaosylceramide (Gb3) in lysosomes. This disorder may present as CKD in young adulthood. Other associated clinical features include premature coronary artery disease, severe neuropathic pain, telangiectasias, and angiokeratomas.

Hereditary nephritis (also known as Alport syndrome), also a heritable disorder of type IV collagen, is a rare cause of end-stage kidney disease with a prevalence of 0.4% among adult U.S. patients. Most cases are X- linked (80%) and are associated with sensorineural hearing loss and lenticonus (conical deformation of the lens), with proteinuria, hypertension, and kidney failure developing over time. The remaining cases are autosomal recessive (15%) or autosomal dominant (5%) and may also be associated with hearing loss. Female carriers variably develop kidney disease depending on activity of the X chromosome in somatic renal cells.