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For example menopause 60 years old buy discount fertomid 50 mg on-line, intravenous hydration has not been proven superior to oral hydration womens health hotline purchase line fertomid. The hydration protocol is not as important as the fact that some form of hydration is administered. It is suggested that the resulting urine alkalinization reduces the generation of free radicals and may also increase urine flow. Several clinical trials and metaanalyses suggest that sodium bicarbonate provides equal or superior protection to isotonic saline. Studies have recommended that optimal hydration with intravenous normal saline is 1 to 1. Although these protocols are impractical in the outpatient setting, they should be implemented for inpatients after discussion with the referring clinician, with particular attention to volume load and cardiac function. A proposed intravenous volume expansion protocol (using either isotonic saline or sodium bicarbonate) is 3 mL/kg/hr for 1 hour or 1 mL/kg/hr for 6 hours before the procedure followed by 1 mL/kg/hr for 6 hours after the procedure. Additional studies are required to assess whether a single bolus of sodium bicarbonate administered just before contrast medium administration is effective, as Tamura and coworkers suggested, because this protocol would be extremely useful in daily practice. If the patient can tolerate a hydration bolus, a total intravenous bolus of 500 to 1000 mL of isotonic saline should be administered before and after the examination. For example, it has been recommended that patients should not receive more than 300 mL of contrast media within 24 hours unless the benefits clearly outweigh the risks. It is controversial whether it is truly nephroprotective or simply lowers the serum creatinine level without preventing renal damage. Images of the patient are obtained through a multistep process of energy transfer and signal transmission. When a patient is placed in the magnet, the mobile protons associated with fat and water molecules align longitudinal to the external magnetic field. No signal is obtained unless a resonant radiofrequency pulse is applied to the patient. The radiofrequency pulse causes the mobile protons within the patient to move from a lower, stable energy state to a higher, unstable energy state (excitation). When the radiofrequency pulse is removed, the protons return to the lower-energy steady state while emitting frequency transmissions or signals (relaxation). In radiologic terms, an external radiofrequency pulse "excites" the protons, causing them to "flip" to a higher energy state. When the radiofrequency pulse is removed, the protons "relax" with emission of a "radio signal. The emitted signals are captured by a receiving coil and reconstructed into images through a complex computerized algorithm: the Fourier transform. The greater the number of mobile protons, the greater the signal produced by the tissue. For example, a volume of urine has more mobile protons than does the same volume of renal tissue; therefore urine produces more signal than do the kidneys. Stones have far fewer mobile protons per unit volume and therefore produce little signal. The T2 time is how quickly the proton signal decays as a result of non-uniformity of the magnetic field. A pulse sequence is a set of defined radiofrequency pulses and timing parameters used to obtain image data. These sequences include, but are not limited to , spin echo, gradient echo, inversion recovery, and steady-state free precession. The data are obtained in volumes (voxels), reconstructed as two-dimensional pixels, and displayed in relation to variations in tissue signal intensity (tissue contrast). Tissue contrast, like signal intensity, is determined by proton density and relaxation times. These include, but are not limited to , choice of pulse sequence, coil types and gradients, slice orientation and thickness, field of view and matrix, gating to reduce motion, and use of intravenous contrast material. These fast sequences can be obtained in less than 30 seconds while the patients hold their breath. The benefits of rapid acquisition include improvement in image quality, as a result of reduction of motion artifact; reduction of total scan time; and the ability to perform dynamic imaging. Not all implants or devices cause problems, but knowledge of the type of device is crucial for determining whether the patient can safely enter the magnet. Unlike iodinated contrast agents, the dose response to Gd-C is nonlinear; the signal intensity increases at low concentrations and then decreases at higher concentrations. Hence the collecting systems, ureters, and bladder first brighten and then darken on T1-weighted sequences as the gadolinium concentration within the urine increases. Gd-C agents have been approved for parenteral use since the 1980s and are generally well tolerated with a good safety profile. Although most Gd-C agents are clinically interchangeable, they can be differentiated on the basis of molecular stability, viscosity, and osmolality. Risk factors for adverse reactions include a history of prior reaction to Gd-C and/or iodinated contrast agents, where rates are at an eight-fold higher risk; and asthma, as well as other allergies, where rates are reported as high as 3. Because adverse reactions may occur more frequently with ionic Gd-C agents, the use of a non-ionic agent should be considered, if available. As with iodinated contrast material, hemodialysis filters Gd-C effectively, and dialysis is therefore recommended immediately after use of contrast material in patients already on hemodialysis. Burning, itching, or severe pain in involved areas or "deep bone pain" in hips and ribs has been described, as has rapid, new-onset fluctuating hypertension. Patients who may be at high risk include those over 60 years of age and those with a history of renal disease, diabetes treated with prescribed medications, and/or hypertension. Physician discretion should be used to determine the risk of Gd-C use in this patient population.

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The anticipated cure rate for recommended first-line empirical regimens is 80% to 95% menstruation 10 days late discount 50 mg fertomid amex. These drugs do not induce cross-resistance with other classes of antimicrobial agents and to date teva women's health birth control guide order fertomid 50 mg fast delivery, limited resistance has been observed in community uropathogens. The fluoroquinolones-norfloxacin, ciprofloxacin, and levofloxacin-are not generally recommended as first-line therapy because of concerns that their widespread use will lead to the emergence of resistance. Fluoroquinolones with limited urinary excretion, such as moxifloxacin, are not indicated for treatment of urinary tract infection. Fosfomycin is given as a single dose; multiple doses of this antimicrobial are associated with rapid emergence of resistance. Single-dose therapy is not recommended for other agents because a single dose is generally 5% to 10% less effective than the recommended longer regimens. Nitrofurantoin, fosfomycin trometanol, and pivmecillinam currently remain effective for many of these strains. However, investigation may be appropriate to rule out alternative pathologic processes when the diagnosis is uncertain or clinical presentation is atypical. Effective control can be achieved with low-dose prophylactic antimicrobial therapy given either daily or every other day at bedtime or after intercourse (see Table 37. This strategy is recommended for women who experience more than two episodes in 6 months. Antimicrobial prophylactic therapy decreases recurrent symptomatic episodes by about 95% while the agent is being taken, but it does not alter the frequency of recurrent infection once prophylaxis is discontinued. About 50% of women experience reinfection within 3 months of discontinuing prophylaxis. Reinstitution of prophylaxis for as long as 2 years is appropriate for these women. Self-treatment is another effective strategy for managing recurrent infections; this approach is often preferred by women who are traveling or who experience less frequent recurrences. The only feasible behavioral intervention to prevent recurrent urinary tract infection is to avoid spermicide use. Other proposed nonantimicrobial approaches for prevention include daily intake of cranberry products, oral or vaginal probiotics to reestablish normal vaginal flora, and estrogen replacement for postmenopausal women. Several other potential nonantimicrobial approaches for prevention of recurrent urinary tract infection are under investigation. The ratio of pyelonephritis to cystitis episodes is reported to be between 18: 1 and 29: 1 in women with recurrent infection. Pyelonephritis is associated with substantial morbidity; hospitalization is required for as many as 20% of affected nonpregnant women. When this complication occurs at the end of the second trimester or early in the third trimester, preterm labor and delivery may occur and lead to poor fetal outcomes, as with any febrile illness in later pregnancy. However, the renal scars were not associated with hypertension or renal impairment. However, this condition is now recognized as an end stage of many chronic inflammatory conditions of the kidney, and it is attributable to infection in only a few patients in whom there is a clear history of renal infection. This surface protein appears to have a direct role in the pathogenesis of pyelo- nephritis through induction of mucosal inflammation. Young diabetic women are 15 times more likely to be hospitalized for pyelonephritis than age-matched nondiabetic women. Behavioral risk factors associated with pyelonephritis in postmenopausal women have not yet been described. There is a wide spectrum of severity, however, from mild irritative symptoms with minimal costovertebral angle tenderness to severe symptoms that may include high fever, nausea and vomiting, and severe pain. Acute cholecystitis, renal colic, and pelvic inflammatory disease are occasionally confused with pyelonephritis. When patients present with severe symptoms, underlying complicating factors such as obstruction and abscess must be excluded. A urine specimen for culture should be obtained before initiation of antimicrobial therapy in every case of suspected pyelonephritis. The culture will confirm the diagnosis of urinary tract infection and identify the specific infecting organism and susceptibilities so that antimicrobial therapy can be optimized. Bacteremia is identified in 10% to 25% of women presenting with acute pyelonephritis if blood culture specimens are collected routinely. However, the clinical utility of routine blood cultures is limited because bacteremia does not alter therapy, nor is it predictive of outcome. Growth of the same organism from both blood and urine usually confirms a urinary source for the infection. However, bacteria isolated from the urine are occasionally attributable to bacteremia from a source outside the urinary tract. This finding may reflect hematogenous seeding with development of renal microabscesses, which is well described for Staphylococcus aureus in particular. The leukocyte count is usually elevated and may be useful as a parameter to monitor the response to therapy. C-reactive protein and procalcitonin values are elevated in most women with acute pyelonephritis and tend to correlate with severity of presentation. Ultrasonography is often the initial imaging modality because it is safe and widely accessible. Obstruction of the renal tubules by inflammatory debris or impaired function with tubular ischemia may result in a "striated nephrogram. Acute focal pyelonephritis (or acute lobar nephronia) is infection confined to a single lobe and may be more common in women who have diabetes or are immunocompromised. The response to treatment is similar, however, for patients with or without this imaging finding.

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It is also important to separate hematuria caused by glomerular abnormalities from bleeding due to other pathologic kidney conditions menstruation kidney pain cheap fertomid 50 mg buy. Rajiv Agarwal women's health center queens blvd buy fertomid 50 mg on line, Nephrology Division, Indiana University School of Medicine, Indianapolis. Another indication that bleeding is more likely of glomerular origin is coexistent significant proteinuria (>0. The presence of pyuria together with hematuria suggests inflammation or infection and warrants a urine culture. Urine cytologic analysis is indicated when otherwise unexplained hematuria is documented. If the explanation for hematuria is not evident on the initial study, the next diagnostic imaging test to perform is cystoscopy. If no abnormality is noted and there is any suspicion of upper tract disease, retrograde pyelography may be performed. There is controversy about the specific age to be used for diagnostic stratification. However, high-grade proteinuria and even full-blown nephrotic syndrome can coexist with nephritic syndrome in some patients. The character of the glomerular hematuria does not always predict the underlying cause of the disorder, nor does it predict the long-term renal outcome of the process. Nephritic syndrome can occur as an isolated renal process or as a feature of a systemic disease or a hereditary disorder. The features that help differentiate these classes of hematuria have been discussed earlier (see "Hematuria") and are listed in Table 25. Glomerular hematuria, when visible, is often described as dark brown, tea- or cola-colored, or smoky as opposed to the overtly red color often seen with urologic pathology. The patient may also note that the urine has become foamy as a result of the excretion of albumin, which has a soaplike action and reduces the surface tension of urine. Back, flank, or abdominal pain does not distinguish glomerular hematuria from urothelial hematuria. There may be a history of an antecedent upper respiratory tract or skin infection in patients with poststreptococcal glomerulonephritis. In other patients with an underlying form of chronic glomerulonephritis, such as IgA nephropathy, gross hematuria may occur simultaneously with, or immediately after, an episode of pharyngitis (synpharyngitic hematuria). A history of hypertension, fluid retention, and/or edema formation suggests glomerular hematuria, particularly if renal function is reduced. Fever, skin rash, and joint symptoms raise the possibility of a systemic disease causing glomerular hematuria. Joint findings may suggest a rheumatologiccollagen vascular disease or vasculitis. Examination of the suprapubic area, back, and the flanks is generally unrevealing. Proteinuria is a frequent accompaniment to hematuria in patients with nephritic syndrome but is usually absent in patients with urothelial hematuria. The proteinuria can range from low-grade (<500 to 1000 mg/ day) to overt nephrotic levels (>3000 mg/day). Alternatively, a spot urine protein/creatinine ratio can be determined, which gives a reasonable estimate of the magnitude of proteinuria. Examination of the urine sediment with phasecontrast microscopy can be especially helpful. Sedimentation rate and C-reactive protein level are often elevated, regardless of the cause of nephritic syndrome. Usually, this is accomplished with a quantitative urine collection for the measurement of creatinine clearance. However, all methods that rely on a single serum creatinine measurement will give erroneous results when renal function is rapidly changing, and the serum creatinine concentration is not relatively stable. A low C3 with normal C4 levels suggests poststreptococcal glomerulonephritis or membranoproliferative glomerulonephritis, whereas low C3 and C4 levels are more consistent with postinfectious glomerulonephritis, systemic lupus erythematosus, hepatitis C­associated membranoproliferative glomerulonephritis (type I), or mixed cryoglobulinemia. Complement levels are extremely variable in poststaphylococcal IgA glomerulonephritis. Other serologic studies, mainly to measure various autoantibodies, are ordered when specific underlying systemic diseases are considered the possible cause. Other infectious diseases that must always be considered are infectious endocarditis or another persistent bacterial infection, such as an abscess or infected vascular access. Blood cultures must be ordered for all patients with otherwise unexplained fever, heart murmurs, or leukocytosis. The commonly ordered laboratory studies for patients with nephritic syndrome are shown in Table 25. High-grade, albumin-dominant proteinuria (generally >3000 mg/day or spot urine protein/creatinine ratio of >3000 mg of protein/gm of creatinine) 2. Lipiduria However, milder and earlier forms of many clinical disorders that can generate the full nephrotic syndrome may produce lower degrees of albuminuria in the range from 30 to 3000 mg/day, with or without the other features. Also, the full spectrum of nephrotic syndrome may not develop in some patients, despite high-grade albuminuria. The principal underlying abnormality responsible for all the clinical features of nephrotic syndrome is increased permeability of the glomerular capillaries. Nephrotic syndrome may occur as an idiopathic and isolated condition, may be an inherited disorder, or may be a complication of an underlying systemic disease or allergic or immunologic disorder. It is always imperative to identify any underlying cause, when one exists Table 25. This is accomplished by recognizing clues from the history and physical examination, reviewing a routine set of laboratory studies, and performing more specific tests suggested by the initial findings.

Syndromes

• Examine fracturs and pattern of fractures
• Are there muscle contractions that may be causing the abnormal posture?
• Fever
• Tension in the voice or sounds
• Acute bilateral obstructive uropathy - sudden blockage of the kidneys
• People who have chronic lung or heart disease
• The spray can irritate the nose, eyes, and throat. These side effects often go away in a few days.
• Repair any damaged tissues. To do this, your surgeon will make 1 - 3 more small incisions and insert other instruments through them. A tear in a muscle, tendon, or cartilage will be fixed. Damaged tissue may need to be removed.
• You are often stressed or anxious
• Lack of interactive play

For many of these entities menstruation vs miscarriage fertomid 50 mg purchase on line, biopsies are infrequently performed menopause insomnia treatment fertomid 50 mg with amex, which limits clinicopathologic correlations. The incidence of analgesic nephropathy varies among different countries and among different U. These two populations differed in the degree of regular analgesic use, consistent with previous suggestions that variations in the frequency of analgesic nephropathy track with patterns of analgesic use. In the 1990s, there was a clear decrease in the prevalence and incidence of analgesic nephropathy among patients undergoing dialysis in several European countries and Australia. Most authors associated this decrease with the removal of phenacetin from analgesic mixtures. The development of analgesic nephropathy requires prolonged regular ingestion of combination analgesics (at least six tablets daily for >3 years). Most of the clinical features displayed by patients with analgesic nephropathy are consistent with the general features outlined previously. This entity is recognized far more frequently in women than in men (five to seven times). These features include atrophy of tubular cells with flattened epithelial cells and tubule dilation, interstitial fibrosis, and areas of mononuclear cell infiltration within the interstitial compartment and between tubules. The cellular infiltrate in chronic interstitial disease is composed of lymphocytes, macrophages, and B cells, with only occasional neutrophils, plasma cells, and eosinophils. If immunofluorescent studies are performed on biopsy specimens, they might occasionally reveal immunoglobulin or C3 along the tubular basement membranes. In chronic interstitial disease, the glomeruli may remain remarkably normal by light microscopy, even when marked functional impairment is present. As chronic interstitial injury progresses, glomerular abnormalities are more evident and consist of periglomerular fibrosis, segmental sclerosis and, ultimately, global sclerosis. Small arteries and arterioles show fibrointimal thickening of variable severity, but vasculitis is not a feature of chronic interstitial disease. These nonspecific symptoms depend on the severity of the renal insufficiency but may include nocturia, lassitude, weakness, nausea, and sleep disturbances. In a series of patients with biopsydocumented chronic interstitial disease, the creatinine clearance at presentation was below 50 mL/min in 75% of cases and below 15 mL/min in about 33% of cases. Flank pain with or without associated hematuria may indicate a sloughed and potentially obstructing papilla. It is thought that the caffeine component of combination analgesics contributes to dependence on the drugs. At that point, renal functional abnormalities attributable to chronic interstitial nephritis are nonspecific, including nocturia, sterile pyuria, and azotemia. Discontinuation of heavy analgesic use can slow or arrest progression of the renal disease. The major presenting symptom of this complication is microscopic or gross hematuria. New-onset hematuria should be evaluated with urinary cytology and, if indicated, cystoscopy with retrograde pyelography. The pathogenesis of these uroepithelial malignancies presumably relates to the concentration and accumulation of phenacetin metabolites with alkylating capabilities within the renal medulla and lower urinary tract. This has also been observed by others; that is, classic analgesic nephropathy can occur in the absence of phenacetin, which was withdrawn from analgesic mixtures in the United States, Australia, and Western Europe in the early 1980s. Phenacetin and its metabolites, including acetaminophen, can injure cells through lipid peroxidation. If cellular glutathione is depleted, there is the possibility of potentiation of the renal toxicity of phenacetin, acetaminophen, and their reactive metabolites. Given the high prevalence of analgesic nephropathy in Western Europe during the 1980s, attempts have been made to develop diagnostic criteria for the entity. Ifacetaminophen is present alone,sufficientglutathioneis generatedin the papillae todetoxify the reactive intermediate. Renal biopsies from these patients revealed findings consistent with those of chronic interstitial nephritis. With growing numbers of case reports came the recognition that the spectrum and severity of the disease were heterogeneous and more common but not consistently as severe as the initial reports had suggested. Typically, these patients present clinically because of mild-to-moderate renal insufficiency. As in many case of chronic interstitial nephritis, hypertension is not a prominent finding. The urine sediment is typically bland, although evidence of tubular dysfunction may be present on chemical analysis, including low-grade, nonnephrotic proteinuria (including albumin and low-molecularweight filtered proteins) and occasionally glycosuria. Although there is no guarantee that discontinuation of ingestion of the herbal medication will arrest disease progression, it is the prudent recommendation. Other than the ingestion history, the clinical and laboratory findings are nonspecific. No specific therapies have been described to arrest the progression of this disease process reliably. The susceptibility of some but not all individuals exposed to the same herbal preparations is not well understood, although gender, toxin dose, and toxin metabolism may all play a role. In genetically manipulated mice, the absence of the Smad3 signaling system abrogates the expression of aristolochic acid nephropathy. Renal and urinary abnormalities first appear after residing in an endemic area for at least 15 years.

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Twenty-year follow-up of orthostatic proteinuria suggests a benign long-term course geriatric women's health issues cost of fertomid. It is present in 50% of patients after 10 years and only 17% of patients after 20 years womens health ri fertomid 50 mg order line. Thus, it is important to reassess patients after an interval of about 1 year to be certain that the degree or pattern of proteinuria has not changed. The proteinuria disappears in some patients, whereas others will have a more ominous glomerular lesion that portends an adverse long-term outcome. These patients must be evaluated periodically for as long as proteinuria persists. Hematuria can result from injury to the kidney or to another site in the urinary tract. Healthy individuals may excrete as many as 105 red cells in the urine in a 12-hour period. An acceptable definition of hematuria is more than two red cells per high-power field in centrifuged urine. The urine dipstick test detects one or two red cells per highpower field and is a very sensitive test. The incidence of malignancy, especially of the bladder, ranges from 5% in individuals with persistent microscopic hematuria to over 20% in individuals with gross hematuria. In children with asymptomatic hematuria, hypercalciuria is the cause in 15% of cases, and 10% to 15% have IgA nephropathy. In up to 80% of children and 15% to 20% of adults with hematuria, no cause can be identified. In patients with isolated asymptomatic hematuria without proteinuria or renal insufficiency, the hematuria resolves in 20% of cases; however, some of these patients will develop hypertension and proteinuria. Glomerular hematuria, in contrast to hematuria caused by injury elsewhere in the urinary tract, is characterized by misshapen red cells that have been distorted by osmotic and chemical stress as red blood cells pass through the nephron. Hematuria with dysmorphic cells, especially cells that have membrane blebs producing the picture of acanthocyturia, is strong evidence for glomerular bleeding. Although brown or cola-colored urine is most commonly associated with glomerular hematuria, its absence does not exclude glomerular disease. The differential pathologic diagnosis of glomerular hematuria without proteinuria, renal insufficiency, or red blood cell casts includes IgA nephropathy, thin basement membrane nephropathy, hereditary nephritis, and histologically normal glomeruli. Approximately 30% of these patients had IgA nephropathy, 20% had thin basement membrane nephropathy, and 30% had no discernible lesion. The remaining patients had mesangioproliferative glomerulonephritis, interstitial nephritis, or focal glomerulosclerosis. In contrast, 216 Chinese adults with isolated hematuria who underwent a kidney biopsy were much more likely to have IgA nephropathy than any other lesion. The data showed that patients with a relatively normal serum creatinine level, hematuria, and proteinuria of less than 1 g protein per day were most likely to have thin basement membrane nephropathy, IgA nephropathy, or no identifiable renal lesion. When hematuria is accompanied by 1 to 3 g protein per day of proteinuria but no significant renal insufficiency, IgA nephropathy was the most likely cause. Patients with hematuria and a serum creatinine of more than 3 mg/dL most often had aggressive glomerulonephritis with crescents. Specimens from patients with systemic lupus erythematosus were excluded from the analysis. Proliferative or necrotizing glomerulonephritis other than immunoglobulin A nephropathy or lupus nephritis. Includes causes of nephrotic syndrome such as membranous nephropathy and focal segmental glomerulosclerosis. Certain rules generally apply to the clinical prediction of the most likely cause. Gross hematuria is most commonly found in IgA nephropathy or hereditary nephritis. Patients with thin basement membrane nephropathy typically do not have substantial proteinuria. The potential benefits of kidney biopsy in patients with isolated hematuria include reduction of patient and physician uncertainty by confirming a specific diagnosis. Nonetheless, the role of kidney biopsy in the evaluation of asymptomatic hematuria in patients without proteinuria, hypertension, or kidney insufficiency remains unclear. In biopsy series involving patients in whom asymptomatic hematuria is accompanied by low-grade proteinuria, specific glomerular diseases including IgA nephropathy and membranoproliferative glomerular disease may be discovered when there is no proteinuria, and IgA nephropathy and thin basement membrane disease or nondiagnostic minor changes remain the most common findings. However, isolated glomerular hematuria without proteinuria or renal insufficiency may not warrant a kidney biopsy, because the findings often will not affect management. In one study of patients with isolated hematuria, the biopsy results altered patient management in only 1 of 36 patients. Some diseases that cause proteinuria are underrepresented because they are not always evaluated by kidney biopsy. For example, in many patients steroid-responsive proteinuria is given a presumptive diagnosis of minimal change disease and patients do not undergo biopsy, and most patients with diabetes and proteinuria are presumed to have diabetic glomerulosclerosis and do not undergo biopsy. However, the extent of effacement appears to correlate more with the duration of active nephrotic syndrome than with the magnitude of proteinuria. Nephrotic syndrome not only may be caused by primary (idiopathic) glomerular diseases but also may be secondary to a large number of identifiable disease states Table 32. Despite the differences in these causes, the loss of substantial amounts of protein in the urine results in a shared set of abnormalities that comprise nephrotic syndrome Tables 32. Medications and other chemicals Organic, inorganic, elemental mercury* Organic gold Penicillamine, bucillamine Street heroin Probenecid Captopril Nonsteroidal antiinflammatory drugs Lithium Interferon- Chlorpropamide Rifampin Pamidronate Paramethadione (Paradione), trimethadione (Tridione) Mephenytoin (Mesantoin) Tolbutamide Phenindione Warfarin Clonidine Perchlorate Bismuth Trichloroethylene Silver Insect repellent Contrast media Anabolic steroids 2. Allergens, venoms, immunizing agents Bee sting Pollens Poison ivy and poison oak Antitoxins (serum sickness) Snake venom Diphtheria, pertussis, tetanus toxoid Vaccines 3.

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• Markova B, Albers C, Breitenbuecher F, et al. Novel pathway in Bcr-Abl signal transduction involves Aktindependent, PLC-gamma1-driven activation of mTOR/p70S6-kinase pathway. Oncogene 2010;29(5):739-751.
• Castellani JW, Sawk MN, Degroot DW, et al: Cold thermoregulatory responses following exertional fatigue. Front Biosci (School Ed) 2:854-865, 2010.
• Cheng JL, Bruno MJ, Bergman JJ, et al. Endoscopic palliation of patients with biliary obstruction caused by nonresectable hilar cholangiocarcinoma: efficacy of self-expandable metallic Wallstents. Gastrointest Endosc. 2002;56:33-39.
• Kuroda S, Houkin K, Kamiyama H, et al. Effects of surgical revascularization on peripheral aneurysms in moyamoya disease: Report of three cases. Neurosurgery 2001;49:463-8.