Edward Christian Healy, M.B.A., M.D.

https://www.hopkinsmedicine.org/profiles/results/directory/profile/2290046/edward-healy

As discussed later medicine for constipation buy cheap cyclophosphamide 50 mg, the high incidence of stenosis certainly is a rationale for monitoring graft flow in hopes of preventing eventual thrombosis treatment effect cyclophosphamide 50 mg lowest price. The documented inflammatory response and hyperplasia within grafts have focused attention on devices and drugs that may prevent or reduce the eventual stenosis 911 treatment center buy cyclophosphamide mastercard. Despite this theoretic gain with monitoring medications requiring prior authorization buy cyclophosphamide on line, the impact of aggressive surveillance programs on maintenance of vascular access is controversial medications management cheap generic cyclophosphamide canada. There may be no difference in eventual access survival whether the approach is preemptive intervention or responding to a thrombosis event when it occurs. With support of the specialty from the creation of the American Society of Diagnostic and Interventional Nephrology, reports have documented the quality and safety of the care delivered by interventional nephrologists. Strategies to prevent both of these pathologic processes have been used with the goal of prolonging access survival, so far with no clear prevention regimen established. Thrombosis may be the final pathway to access failure, but so far, agents well known to prevent thrombosis in other vascular diseases have not affected access survival consistently. In fact, a large, multicenter trial in the Veterans Administration Heath System with the newer agent clopidogrel plus aspirin had to be discontinued because of bleeding problems in the treatment group. Finally, personalized medicine may eventually become part of vascular access protocols as genetic studies uncover possible predictors of higher risk for access loss. One such study has suggested that polymorphism in the methylenetetrahydrofolate reductase gene (C677T) may be a predictor of access thrombosis, presumably through the impact on homocysteine. Further advances resulted in catheters made of softer material, and the development of the cuff provided catheters that could be used for markedly longer durations. Some patients would face death from kidney failure without the availability of this catheter technology. However, the data suggest an inappropriately high utilization of catheters as a means of vascular access. Catheters are routinely "locked" with installation of high-dose heparin solutions injected into both lumens, but this procedure does not completely prevent the problem. The use of heparin for locking may occasionally result in bleeding through an error in dose or failure to remove the heparin solution before use. Even the addition of systemic therapy with low-dose warfarin did not prevent thrombosis in a clinical trial setting and led to an increase in complications. These catheter-related infections can result in more complex infections, such as osteomyelitis, endocarditis, and septic arthritis, despite antibiotic therapy. Careful management of catheter-related infection is critical, including an adequate duration of antibiotic treatment (3-week minimum) and an aggressive approach to catheter removal and replacement, with replacement delayed until the patient is symptom free (so-called line holiday). Attempting to treat infected catheters with antibiotics alone usually results in failure, although infection with some organisms. The combined use of antibiotic installation into catheters and systemic antibiotics may increase success in preserving the existing catheter. Several approaches to prevention of infection with catheters have demonstrated potential promise. The use of mupirocin ointment at the exit site may reduce the incidence of infection. Most of the soluble large molecules found in the blood are the products of complex intracellular synthetic energy-requiring processes. Most continue to be active, serving to signal and regulate processes in distant organs. Loss is first prevented by the bilipid cell membrane barrier, which keeps many of the most precious molecules in a sequestered intracellular location. Those that are secreted or leak out of the cell are often bound to serum macromolecules, most notably serum albumin, a well-known transport protein. Although the glomerular membrane is highly permeable in comparison with cell membranes in general, albumin and its bound ligands as well as other macromolecules are poorly filtered and thus are protected from loss. Small proteins and peptides that leak through the filter are efficiently reabsorbed by the proximal tubule, where they are broken down and their subunits reutilized. Smaller molecules are often end products of metabolism or ingested intruders that the kidney effectively eliminates by filtration without reabsorption. Precious small molecules are reclaimed after filtration by selective reabsorptive mechanisms in the renal tubules. Dialyzers lack the latter vital functions, so losses are prevented by including some of these measurable small solutes in the dialysate, effectively eliminating the gradient for diffusive loss. Fortunately, most of these small solutes are abundant and can be relatively inexpensively added to the dialysate. Although both the native or natural kidney and the artificial kidney are excretory "organs" and both use semipermeable membranes to separate small from large particles, they operate on different principles. The natural kidney is a selective filtration or convection device driven by blood pressure generated by the heart with highly selective reabsorption and secretion downstream. In contrast, the dialyzer separates molecular species primarily by simple diffusion without the need for pressure generation or reabsorption. Urea, for example, is highly reabsorbed after filtration by the glomerulus, but selective reabsorption plays no role within hemodialyzers. As a consequence, native kidney clearance rates of creatinine are higher and dialyzer clearance rates are lower than their clearances of urea. The artificial hollow-fiber kidney contains 8000 to 10,000 fibers, each approximately 200 µm in diameter and 250 mm in length, providing a surface area for exchange of about 1. Each of the 1 to 2 million functioning nephrons in the two native kidneys has a proximal tubule diameter of about 40 µm and a length of about 14 mm, providing a minimum surface area for proximal reabsorption of approximately 3 m2 (if one ignores microvilli). The native kidneys also perform several known and probably other unknown synthetic functions such as the regulated synthesis of erythropoietin and activation of vitamin D. For endogenous solutes, the first pathway on the route to elimination is diffusion through intracellular and extracellular pathways, including passive or facilitated diffusion across membranes. Thus, diffusion is a vital transport mechanism for the function of both native and artificial kidneys. Because removal of small solutes appears to be the major function of both excretory methods, dialyzer clearance of small solutes can be compared with similar clearances by the native kidney as a reasonable first step toward assessing hemodialyzer adequacy. However, the levels of retained toxic solutes are not used as performance measures for dialysis because their identities are unknown and because their generation rates probably vary from patient to patient and from time to time (see later). Instead, performance of dialysis is judged from the clearance of representative solutes. Small solute clearance can be used to measure the most important dialyzer function, which is to lower the concentration of small toxic solutes in the patient. This is an inescapable conclusion based on the observation that dialysis works extremely well to rapidly reverse life-threatening uremia. The mechanism for this life-giving property of dialysis is not mysterious; it is simply the result of solute removal by diffusion across the semipermeable dialysis membrane. Although effective in reversing uremia, earlier cellulose-based dialyzer membranes removed solutes with molecular weights above 3000 Da very poorly, so small solutes are the obvious main culprits accounting for the uremic syndrome and the primary targets for dialyzer clearance. It is therefore reasonable to use the clearance of a representative small solute as a measure of this fundamental dialysis function. Clearance is recognized as the best measure of first-order processes such as diffusion and filtration. A zero-order process such as urea generation by the liver is uninfluenced by the solute concentration, but first-order removal processes use the concentration as the driving force for diffusion, rendering the removal rate directly proportional to the concentration. Clearance (K) is the proportionality constant: K = Removal rate Concentration (1) K has value as an expression of first-order processes that is independent of either the solute removal rate or its concentration. For intermittent dialysis, the main advantage of the clearance expression is that it tends to remain constant despite rapid changes in both the solute concentration and the removal rate during the procedure. From equation 1, clearance can also be expressed as the extraction ratio (E) multiplied by flow: E = (C in - Cout) C in K = Q E (2) (3) For a constant-flow system, the extraction ratio is also constant over time despite marked changes in concentration. E is the fraction of total inflow (Q), and K is the absolute flow that is completely cleared of the solute; both tend to remain constant during dialysis. Clearance is affected by the flow of both blood and dialysate as well as other variables such as the convective filtration rate (see later) but is independent of concentration. Although clearance is independent of solute concentration, the converse is not true. During a period of steady-state kinetics, in which generation equals removal, if the generation rate of a solute is fixed, its concentration is inversely proportional to its clearance. Because dialysis is simpler than native kidney function and removes solutes primarily by diffusion, the calculation of clearance is nearly the same for all easily dialyzed substances if one assumes that these solutes are distributed in a single mixed pool within the patient. Generation rates of various solutes differ, but if each is relatively constant from week to week. Furthermore, the dose requirement or need for dialysis does not seem to vary from time to time in the same (anuric) patient, provided that a minimum threshold clearance is delivered during each treatment. Native kidneys appear to clear small solutes at a rate far above the minimum required to sustain life. For example, removal of a kidney for transplantation can be done without adverse consequences in the donor. In practical terms, it is impossible to compare dialyzers by measuring removal rates alone because removal depends on the solute concentration. Measurement of clearance eliminates this requirement, allowing use of a single term to make valid comparisons among purgative instruments. Similarly, finding a lower concentration of a solute within a patient does not indicate that the clearance is higher; it may simply reflect a lower generation rate. If a steady state exists in which input equals output, the removal rate of a substance is simply a measure of its generation rate, revealing little about the effectiveness of the dialyzer. Whereas urea clearance by the dialyzer should correlate with the clearance of other small (dialyzable) solutes that are presumably responsible for uremic toxicity, the generation of urea as an end product of protein catabolism correlates poorly with uremic toxicity. In fact, patients with higher urea generation rates have better outcomes, probably as a reflection of better appetite and higher protein intake. For purposes of measuring the dose of dialysis and dialysis adequacy, only the relative change in urea concentration during dialysis is used to model clearance; the absolute concentrations are ignored. The change in urea concentration during dialysis, which reflects its clearance, is used as a surrogate for the clearance of other small easily dialyzed solutes, some of which must be toxic or dialysis would not reverse the life-threatening component of uremia. This logic justifies use of urea clearance as an index of dialysis adequacy while acknowledging that isolated urea concentrations cannot be used for this purpose. The biomaterials used to make the hollow-fiber dialyzer, together with the pore size and thickness of the membrane, determine its clearance, or the membrane permeability constant (K0), for a given solute. K0A is expressed in milliliters per minute and, like clearance, is independent of solute concentration. Simultaneous filtration across the same membrane used for dialysis removes additional solute, but the amount removed is inversely related to the efficiency of the dialysis. For example, if the dialyzer removes solute very efficiently by diffusion, with an extraction ratio approaching 100%, addition of ultrafiltration adds very little or nothing to the removal rate, which cannot exceed 100% of the inflow. The effect of ultrafiltration on clearance is expressed as follows143: K d = Q b(C in - Cout) C in + Q f (Cout C in) (6) where Qb is the blood inflow rate, Cin is the inflow concentration, Cout is the outflow concentration, and Qf is the ultrafiltration rate in millimeters per minute. As Cout approaches zero, the dialysis component of clearance maximizes, and the Qf component extinguishes. Analogous to clearance, which expresses the dialyzer removal rate normalized to the inflow solute concentration, K0A is an expression of dialyzer performance normalized to blood and dialysate flow rates (Qb and Qd, respectively). K0A, which is sometimes called the "intrinsic clearance" of a dialyzer, can be viewed as the maximum clearance possible for a particular solute and dialyzer at infinite Qb and Qd. It is the best parameter for comparing dialyzers, with higher values indicating more efficient solute removal. As the level increases, the concentration gradient from blood to dialysate decreases, causing the removal rate and the clearance to decrease, both eventually falling to zero as equilibrium is reached. Solute-related variables include the physical and chemical properties of the substance to be removed and its distribution in the body. Treatment-related variables include the permeability of the membrane to solutes of various sizes, dialysis treatment time, membrane surface area, and flow rates of blood and dialysate (see preceding equations). Molecular size and membrane permeability together limit the rate of movement for individual molecular species. In flowing systems, the concentrations of larger molecules tend to remain constant along the length of the dialyzer, uninfluenced by blood and dialysate flow. The molecular activity of a solute determines its capacity for movement across the dialysis membrane. Because watersoluble solutes are active only in the water phase of the blood, only the water component (90% of normal blood volume) participates in the dialysis process. Blood flow through the dialyzer for water-soluble solutes (nearly all) should be expressed as blood water flow or about 90% of whole blood flow. Similarly, blood concentrations should be expressed as blood water concentrations, which are about 7% higher than whole serum concentrations. For charged molecules, the Donnan effect acts in the opposite direction, reducing the effective blood activity. The Donnan effect for blood equilibrated with dialysate is attributable to nondialyzable plasma proteins, mostly albumin, which has a net negative charge (17 mEq/mmol albumin). The asymmetric charge distribution across the membrane effectively "captures" a small fraction of the positively charged sodium ions on the plasma side, reducing their potential for diffusion. In general, the rate of movement or flux (J) of smaller molecules is higher than the flux of larger molecules. Dialyzer clearance is an expression of solute removal as a fraction of the blood concentration (adjusted for blood water content) at the dialyzer inflow port. In contrast, whole-body clearance is an expression of removal as a fraction of average concentrations throughout the body. The average "whole-body concentration" is substituted for dialyzer inflow concentration in the denominator of the standard clearance formula (Equation 1). Wholebody concentrations are higher than serum concentrations during dialysis because of solute disequilibrium, so whole-body clearances are always lower than dialyzer clearances. Typical solutes that exhibit disequilibrium distribute preferentially in the intracellular compartment and diffuse slowly across the cell membrane to the extracellular compartment. Removal in vivo, however, is limited by sequestration in remote tissue compartments. Solutes such as digoxin have an apparent large distribution, often larger than total body water volume.

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Robert Abbe treatment 1st degree burns generic cyclophosphamide 50 mg on-line, a brachytherapy pioneer in the United States symptoms 0f pregnancy generic cyclophosphamide 50 mg with visa, is credited with the first successful interstitial implant medications bad for your liver buy cheap cyclophosphamide line, treating a 17-year-old boy with a destructive giant cell sarcoma of the lower jaw in 1904 (3) medicine quetiapine 50 mg cyclophosphamide purchase fast delivery. In 1958 medicine venlafaxine order cyclophosphamide 50 mg on-line, afterloading techniques using flexible iridium-192 (192Ir) wires were introduced, reducing radiation exposure to staff, and renewing interest in brachytherapy. This led to the development of new rules of implantation and dose calculation for interstitial brachytherapy using 192Ir wire sources, the Paris System, which formed the foundation for modern head and neck brachytherapy (4). Briefly, when uniform linear parallel sources are used, these rules result in a reference isodose that covers the treatment target volume. Patients with medical comorbidities who have contraindications for surgery may be poor candidates for brachytherapy. In addition, patients with alcohol dependence, major neurologic deficits, poor cardiopulmonary status, memory disorders, and hematologic disorders may also not be ideal candidates. Patients must be able to provide baseline self-care needs during the radiation delivery. This can include tracheostomy care, self-administered feeds through percutaneous endoscopic gastrostomy tube or a nasogastric tube, and a patient-controlled analgesic pump, as indicated. Patients with periods of confusion and disorientation would not be ideal candidates. The potential for alcohol or narcotic withdrawal should be addressed to avoid complications with the delivery of the implant. Patient-related factors associated with severe soft tissue and bone complications after an implant include severe diabetes, liver failure, and compromised arterial status (7). If dental extractions are required, complete healing must be ensured prior to brachytherapy to avoid the risk of osteoradionecrosis. Patient selection also includes an assessment of the appropriateness of a brachytherapy implant regarding the tumor location, size, extent of tumor volume, and organ function. The indications and contraindications by subsite are discussed in detail in the following pages. In general, brachytherapy is contraindicated for lesions that are abutting or invading into a bone because of a higher risk of osteonecrosis. The tumor needs to be accessible and should have a geometry that can be encompassed by a series of catheters or sources. Very large tumors for which it is difficult to assess the extent of infiltration are not ideal for brachytherapy implantation due to the risk of a geographic miss. In interstitial brachytherapy, the radioisotope is placed either temporarily or permanently into the tumor site or bed. A permanent interstitial implant may be advantageous when the target volume is irregular and complex, making temporary catheter placement impractical and avoiding situations that result in potential kinking of the catheters. In addition, a permanent implant allows for a higher total radiation dose to be delivered to the target volume. A commonly used radioisotope for permanent implants is iodine-125 (125I), which is characterized by a low average energy (28 keV), with rapid dose falloff to minimize dose to normal structures. This may be advantageous when critical normal structures, such as the spinal cord, are adjacent to the tumor implant. This involves loading sources (usually 192Ir) into catheters that have been implanted into the tumor volume. This allows for deliberate and accurate placement of the catheters, and optimization of the implant dosimetry using three-dimensional (3D) planning systems. Surface applicator techniques have been used successfully to deliver radiation intraoperatively to the exposed tumor bed after a gross total resection, and in the treatment of skin tumors and superficial soft tissue sarcomas of the head and neck region. Intracavitary brachytherapy techniques have been developed for the treatment of nasopharyngeal carcinoma, as well as for tumors of the paranasal sinuses and the nasal vestibule. Knowledge regarding the extent of tumor from palpation and inspection of the disease, prior radiologic examination, awareness of adjacent critical structures, prior radiation exposure, and relationship of the tumor to the surrounding structures are critical for optimal and safe placement of the radioactive sources. Currently, most interstitial head and neck implants are based on an afterloading system with computerized treatment planning. The guide materials are either twin or single guide gutters made of stainless steel. Once the iridium has been implanted, the gutter guides would then be removed, resulting in predictable implant geometry. Rigid metal hollow guide needles are implanted into the tumor volume, typically free hand, although templates are available. The placement and spacing can be verified by visualization, palpation, ultrasound guidance, or fluoroscopy. Plastic tubes are then threaded through the rigid hollow needles and left in place to cover the target volume, with subsequent removal of the metal needles. Radioactive sources are then afterloaded into the catheters following dosimetric planning. There are several variations of the plastic tube technique, including: ­ Through-and-Through Technique this approach is mainly suited for tumor volumes when both sides are accessible for implantation, including the lip, buccal mucosa, skin and neck nodes. The first step is the identification of the intended implant target volume and the points of entry for the brachytherapy catheters, which are arranged in parallel, approximately 1 cm apart. Using a metal needle or trocar, the skin is pierced at the planned entry site, courses along in the tumor volume, and exits at the marked skin site at the other end of the target volume. Once in place, an afterloading catheter is threaded through the trocar, which is then removed along its original pathway while holding the implanted catheter in place. A metal button and a plastic button are threaded over the exposed ends of the catheter and crimped in place over the skin entry sites. The exposed end of the catheter is then cut off leaving at least several centimeters distal to the metal button. These steps are repeated with parallel catheters until adequate coverage is obtained. However, the catheters are looped, usually over a mucosal surface, and exit adjacent to the catheter entry site. Because this is commonly done for tongue implants, the technique is discussed for such an implant. From left to right: (1) A nylon afterloading flexible catheter, 60 cm long, with an inner wire to prevent kinking of catheter. Once the target volume has been assessed, the overall strategy for implantation should be planned out regarding the number of catheters, orientation, placement, and their entry and exit sites. A curved metal trocar is inserted through the submental region, traversing through the site of disease and exiting the dorsal mucosal surface of the tongue. An afterloading catheter is then threaded through the trocar, and held in place as the metal trocar is removed along its original entrance pathway. A similar insertion is then performed with the metal trocar adjacent to the prior entry point, and exiting out of the tongue approximately 1. While securing the catheter, the trocar is then carefully removed, and the exposed ends of the catheter are secured using metal buttons. These steps are repeated, resulting in a set of looped catheters in multiple planes covering the target volume. Although this technique is more commonly utilized outside the head and neck in situations when it is not pragmatic to have the catheters exit through both sides of an implant target volume, it can be used for the placement of interstitial catheters into the neck after neck dissection for recurrent disease. As before, the procedure begins with identification of skin entry points and target volume delineation, which often includes the tumor bed with margin. A metal trocar is percutaneously inserted, and an afterloading catheter is threaded through the trocar. After retraction of the trocar, absorbable sutures are used to tie the catheter in place at various intervals to stabilize its position. This step is then repeated, resulting in a parallel distribution of the catheters over the target volume. Typically, the catheters are approximately 1 cm apart in a singleplane implant, 1. Each of the catheters would then be secured using metal and halfmoon-shaped buttons crimped and sewn into place over the entry point. This technique with various modifications is used when both sides of the tumor are accessible for the implant. The spacing material is slipped into the ends, and lead caps are crimped into place. A modification of this technique includes threading the suture seeds into a mesh, which is then secured over the tumor bed. This requires meticulous planning and radiologic guidance for accurate placement of the seeds to achieve good geometry and dose distribution. The placement of the surgical incision, grafts, drains, tracheostomy, and wound closure techniques need to be meticulously planned and discussed before any surgical procedure to optimize the implant geometry and reduce the risk of wound complications. In patients with temporary implants, it should be ensured that surgical drains and wound dressings are appropriately placed to avoid hindrance to source loading and unloading. In addition, coordination of the wound closure procedure will minimize potential tension, damage, and distortion of the implanted catheters and geometry. In the postoperative period, a well-trained nursing staff is critical to ensure avoidance of wound complications, and for patient education with regard to self-care. Dummy seeds can be placed within the implanted catheters prior to imaging to provide the relative seed position. It is important to note that even the best optimization cannot overcome poor implant geometry. Additionally, a description of the sources, techniques, time pattern, and prescription dose should be documented. Specific dose recommendations by head and neck subsite are discussed in the following text; here we discuss considerations with regard to dose rate. In addition, because of the decreased radiation delivery time, there is less likelihood of organ movement, and a higher likelihood of treating the patient as an outpatient. The data are reviewed under each subsite, but generally speaking, doses between 3 and 4 Gy per fraction are recommended (10,12). Twice-daily fractions are often delivered, with an inter-fraction interval of at least 6 hours. The optimal dose per pulse and the time interval between pulses remain under debate. Other authors have suggested a slightly higher dose per pulse, delivered once every 3 hours, with or without a night break; however, there are no prospective long-term data as of yet to support this approach (12,15). Prophylactic antibiotics are often prescribed to prevent skin or soft tissue infection. Following completion of brachytherapy, removal of the catheters should be done with the coordination of the head and neck surgical team. A possible complication that may occur during the removal of the implanted catheters is arterial hemorrhage, which can be effectively controlled with bi-digital compression. A review of the procedure, including a discussion of possible bleeding, should be clearly discussed with the patient to ensure proper cooperation and safety. Prior to discharge, expected radiation side effects, including potential mucositis, pain, and decreased nutritional and fluid intake, should be carefully reviewed with the patient. Patients can expect to develop mucositis approximately 1 week after completion of brachytherapy, with symptoms peaking by week 3, and subsiding around week 6. Education about this expected reaction is an important part of patient care, as is ensuring availability of analgesics, mouthwashes, and alimentation. Follow-up should be arranged approximately 2 to 3 weeks following discharge from the hospital. The nasopharynx is surrounded by multiple critical structures such as the brainstem, pituitary, optic chiasm, temporal lobes, cochlea, and salivary glands. Treatment of nasopharyngeal tumors can be particularly challenging, especially for those that are locally advanced or recurrent. Local control is paramount because it is one of the most important prognostic factors, and is an independent prognostic indicator of distant metastases, besides T and N stage (17). Tumor recurrences are particularly challenging because the surrounding critical structures have received the upper safe limits of radiation exposure. However, carefully delivered brachytherapy can provide the most conformal treatment approach because of its steep dose falloff and dose optimization potential. Evidence Basis of the Practice There is considerable experience using intracavitary brachytherapy as a boost for the primary treatment of early stage nasopharyngeal carcinoma, or for persistent localized disease. There are also data supporting the use of intracavitary or interstitial brachytherapy in the setting of recurrent disease. Their initial report demonstrated high rates of local control relative to nonbrachytherapy patients, with little significant late grade 3 toxicity other than synechiae of the nasal mucosa in three (7%) patients. With these high radiation doses (range: 73-95 Gy), they found a 15% increase in local control with every additional 10 Gy over 60 Gy. They found that for early T-stage patients, local control was significantly improved with the brachytherapy boost: 100% versus 86% without brachytherapy (P =. The benefit of intracavitary brachytherapy among early T-stage patients was corroborated by a large study of 509 patients by Teo et al (22). Complications were low with only 10 (6%) patients developing nasopharyngeal ulceration. Although the addition of brachytherapy had a significant local control and survival benefit, 9% experienced palate or sphenoid sinus floor perforation or nasopharynx necrosis, leading the authors to recommend decreasing the fraction size. Intracavitary or Interstitial Brachytherapy for Recurrent Disease Several institutional series have reported sustained local control rates of approximately 50% for locally recurrent disease, depending upon the extent of disease and dose administered. Fu et al treated patients with a combination of limited external radiation and brachytherapy, obtaining a 5-year survival rate of 41% (25). This study demonstrated the importance of delivering adequate radiation dose (60 Gy) in the recurrent setting, and reported relatively low morbidity with the integration of brachytherapy. Palatal fistula and mucosal necrosis occurred in 19% and 16% of patients, respectively. Syed et al reported on the use of a brachytherapy implant alone (50­58 Gy) for 34 patients with recurrent or persistent nasopharyngeal carcinoma, with a 5-year local control rate of 59% (28). Late complications were reported in 45% of patients, most often soft tissue necrosis (14%), dysphagia (11%), soft palate atrophy (11%), and nasal crusting (11%).

Ivanyi B: A primer on recurrent and de novo glomerulonephritis in renal allografts treatment endometriosis cyclophosphamide 50 mg discount. Vlaminck H xerostomia medications side effects 50 mg cyclophosphamide with visa, Maes B symptoms shingles purchase generic cyclophosphamide online, Evers G 5 medications related to the lymphatic system cyclophosphamide 50 mg order visa, et al: Prospective study on late consequences of subclinical non-compliance with immunosuppressive therapy in renal transplant patients treatment lyme disease cyclophosphamide 50 mg order fast delivery. Pascual J, Quereda C, Zamora J, et al: Steroid withdrawal in renal transplant patients on triple therapy with a calcineurin inhibitor and mycophenolate mofetil: a meta-analysis of randomized, controlled trials. Denhaerynck K, Dobbels F, Cleemput I, et al: Prevalence, consequences, and determinants of nonadherence in adult renal transplant patients: a literature review. Webster A, Pankhurst T, Rinaldi F, et al: Polyclonal and monoclonal antibodies for treating acute rejection episodes in kidney transplant recipients. Briggs D, Dudley C, Pattison J, et al: Effects of immediate switch from cyclosporine microemulsion to tacrolimus at first acute rejection in renal allograft recipients. Zarkhin V, Li L, Kambham N, et al: A randomized, prospective trial of rituximab for acute rejection in pediatric renal transplantation. Jorgensen K, Povlsen J, Madsen S, et al: C2 (2-h) levels are not superior to trough levels as estimates of the area under the curve in tacrolimus-treated renal-transplant patients. Audard V, Matignon M, Hemery F, et al: Risk factors and longterm outcome of transplant renal artery stenosis in adult recipients after treatment by percutaneous transluminal angioplasty. Ghazanfar A, Tavakoli A, Augustine T, et al: Management of transplant renal artery stenosis and its impact on long-term allograft survival: a single-centre experience. Fabrizi F, Lunghi G, Dixit V, et al: Meta-analysis: anti-viral therapy of hepatitis C virus-related liver disease in renal transplant patients. Agrawal V, Swami A, Kosuri R, et al: Contrast-induced acute kidney injury in renal transplant recipients after cardiac catheterization. Ohmacht C, Kliem V, Burg M, et al: Recurrent immunoglobulin A nephropathy after renal transplantation: a significant contributor to graft loss. Oka K, Imai E, Moriyama T, et al: A clinicopathological study of IgA nephropathy in renal transplant recipients: beneficial effect of angiotensin-converting enzyme inhibitor. Contreras G, Mattiazzi A, Guerra G, et al: Recurrence of lupus nephritis after kidney transplantation. Debout A, Foucher Y, Trébern-Launay K, et al: Each additional hour of cold ischemia time significantly increases the risk of graft failure and mortality following renal transplantation. Kootstra G, van Heurn E: Non-heartbeating donation of kidneys for transplantation. Press R, Carrasquillo O, Nickolas T, et al: Race/ethnicity, poverty status, and renal transplant outcomes. Pallet N, Thervet E, Alberti C, et al: Kidney transplant in black recipients: are African Europeans different from African Americans Opelz G, Dohler B: Effect of human leukocyte antigen compatibility on kidney graft survival: comparative analysis of two decades. Gratwohl A, Dohler B, Stern M, et al: H-Y as a minor histocompatibility antigen in kidney transplantation: a retrospective cohort study. Fabrizi F, Martin P, Dixit V, et al: Hepatitis C virus antibody status and survival after renal transplantation: meta-analysis of observational studies. Opelz G, Dohler B: Improved long-term outcomes after renal transplantation associated with blood pressure control. Messa P, Sindici C, Cannella G, et al: Persistent secondary hyperparathyroidism after renal transplantation. Evenepoel P, Cooper K, Holdaas H, et al: A randomized study evaluating cinacalcet to treat hypercalcemia in renal transplant recipients with persistent hyperparathyroidism. Sofue T, Inui M, Hara T, et al: Efficacy and safety of febuxostat in the treatment of hyperuricemia in stable kidney transplant recipients. Aroldi A, Tarantino A, Montagnino G, et al: Effects of three immunosuppressive regimens on vertebral bone density in renal transplant recipients: a prospective study. Conley E, Muth B, Samaniego M, et al: Bisphosphonates and bone fractures in long-term kidney transplant recipients. Torres A, García S, Gómez A, et al: Treatment with intermittent calcitriol and calcium reduces bone loss after renal transplantation. Rostaing L, Cantarovich D, Mourad G, et al: Corticosteroid-free immunosuppression with tacrolimus, mycophenolate mofetil, and daclizumab induction in renal transplantation. Hojo M, Morimoto T, Maluccio M, et al: Cyclosporine induces cancer progression by a cell-autonomous mechanism. Svensson M, Jardine A, Fellström B, et al: Prevention of cardiovascular disease after renal transplantation. Asberg A, Hartmann A, Fjeldså E, et al: Bilateral pharmacokinetic interaction between cyclosporine A and atorvastatin in renal transplant recipients. Viewed through the lens of embryology, normal tissue architecture indicates that patterning of renal tissue elements is normal. Dysplastic kidneys also vary in the presence of epithelial cysts, the number of cysts, and cyst size. Renal tubular dysgenesis represents a particular form of renal dysplasia and is characterized by the absence or poor development of proximal tubules and is accompanied by thickening of the renal arterial vasculature from the arcuate to the afferent arteries. Simple non-crossed (nonfused) ectopy refers to a kidney that lies on the correct side of the body but lies in an abnormal position. Crossed renal ectopy can occur with and without fusion to the contralateral kidney. Ectopic kidneys that do not ascend above the pelvic brim are commonly called pelvic kidneys. This differs from crossed fused renal ectopy, which usually involves abnormal movement of only one kidney across the midline with fusion of the contralateral noncrossing kidney. Renal ectopia is bilateral in 10% of cases; when unilateral, there is a slight predilection for the left side. The incidence of fusion anomalies is estimated to be approximately 1 per 600 infants. The reported incidence of horseshoe kidney based upon data from birth defect registries varies from 0. In the majority of affected patients, congenital renal malformations occur as sporadic events. In approximately 30% of affected individuals, these malformations occur as part of a multiorgan genetic syndrome. Renal­urinary tract malformations and extrarenal malformations can go unrecognized unless a careful phenotypic examination is performed. Over 200 distinct genetic syndromes feature some type of kidney and urinary tract malformation. Incomplete penetrance with variable expressivity is frequent in affected families. That is, within any particular family in which affected members carry the same mutation, the renal phenotype can vary from agenesis to dysplasia to isolated abnormalities of the collecting system. In probands with bilateral renal agenesis or bilateral renal dysgenesis and without evidence of a genetic syndrome or a family history, 9% of first-degree relatives were shown by ultrasonography to have some type of malformation in the kidney and/or lower urinary tract. The incidence of renal and urinary tract malformations identified in fetal ultrasonography is 0. These anomalies include vesicoureteral reflux (25%), ureteropelvic junction obstruction (11%), and ureterovesical junction obstruction (11%). Complete or partial duplication of the renal collecting system is the most common congenital anomaly of the urinary tract. Unilateral renal agenesis has been reported with a prevalence of 1 per1000 autopsies. Briefly summarized, formation of the human kidney is initiated at 5 weeks of gestation in the human when the ureteric duct is induced to undergo lateral outgrowth from the wolffian duct and to invade the adjacent metanephric mesenchyme. The ureteric bud then undergoes repetitive branching events, so termed because each event consists of expansion of the advancing ureteric bud branch at its leading tip, division of the ampulla resulting in formation of new branches, and elongation of the newly formed branches. Beginning with the tenth- to eleventh-branch generation, the pattern of branching becomes terminally bifid. During branching morphogenesis 65,000 collecting ducts are formed, both as cortical and medullary collecting ducts, a process that is essential to the function of the mature kidney. During the latter stages of kidney development, tubular segments formed from the first five generations of ureteric bud branching undergo remodeling to form the kidney pelvis and calyces. The position at which the ureteric bud arises from the wolffian duct relative to the metanephric mesenchyme is critical to the nature of the interactions between the ureteric bud and the metanephric mesenchyme. Ectopic positioning of the ureteric bud is associated with renal tissue malformation (dysplasia) due to abnormal ureteric bud­metanephric mesenchyme interactions and is also thought to contribute to the integrity of the ureterovesical junction. Mackie and Stephens postulated that an abnormal position of the ureteral orifice in the bladder is associated with vesicoureteral reflux in humans. Interestingly, the domain of Gdnf expression is expanded anteriorly in these mice, which suggests that loss of inhibition of Gdnf expression by Robo2 dependent signaling expands the domain of Gdnf expression and results in ectopic ureteric budding. Bmp4 is expressed in stromal cells immediately adjacent to the wolffian duct and the ureteric bud. The number of ureteric bud branches elaborated is considered to be a major determinant of final nephron number because each ureteric bud branch tip induces a discrete subset of metanephric mesenchyme cells to undergo nephrogenesis (see Chapter 1). Regulation of ureteric branch number has been informed by complementary studies in humans and mice. The most common finding is an optic disc pit associated with vascular abnormalities and cilioretinal arteries, with mild visual impairment limited to blind spot enlargement. It encodes a transcription factor that belongs to the paired box family of homeotic genes. In 1995, Sanyanusin and colleagues reported heterozygous mutations in two families with renal-coloboma syndrome. Studies in the 1Neu mouse strain, which is characterized by a Pax2 mutation, demonstrated decreased ureteric branching in association with decreased nephron number. Decreased ureteric branch number and nephron number are rescued by inhibition of apoptosis in the ureteric lineage. In the metanephric mesenchyme, Sall1, Eya1, and Six1 positively control Gdnf expression. Sall1, a member of the Spalt family of transcriptional factors,47 is expressed in the metanephric mesenchyme before and during ureteric bud invasion. Mutational inactivation of Sall1 in mice causes renal agenesis or severe dysgenesis and a marked decrease in Gdnf expression. However, variability of the phenotype even with the same mutation does not permit accurate prediction of the disease severity. Within the same family a given mutation may be associated with renal malformation in some individuals, but not in others. Pallister-Hall syndrome is an autosomal dominant multiorgan disorder characterized by multiple renal abnormalities, including agenesis or dysplasia, hypoplasia, and hydronephrosis. Remarkably, renal dysgenesis in the absence of Shh is completely rescued by homozygous inactivation of Gli3. During kidney development in mice, Tcf2 is expressed in the wolffian duct, ureteric bud, comma- and S-shaped bodies, and proximal and distal tubules. Mutations in angiotensinogen and in the angiotensinogen type 1 receptor genes occur much less frequently. Low birth weight or intrauterine growth restriction is generally considered to be due to a suboptimal in utero environment. Here, the fetal kidney is particularly susceptible, which leads to reduced nephron number. In humans intrauterine growth restriction is most often due to uteroplacental insufficiency and maternal undernutrition. Modeling of these disorders in animals causes a significant reduction in nephron endowment. In animal models, offspring of hyperglycemic or diabetic mothers demonstrate a significant nephron deficit. The expression of Gdnf and Wnt11, both of which are required during ureteric branching was reduced, consistent with a decrease in nephrogenesis. Infants with simple renal hypoplasia or a moderate to severe degree of hypodysplasia exhibit renal insufficiency. A more subtle deficiency in nephron number has been associated with adult-onset hypertension. Growth of renal tubules and expansion of glomerular cross-sectional area in utero and after birth is critical to renal functional capacity. The developmental maturation of renal structures is discussed in this chapter in the context of their functions. Illustrative examples are provided for how abnormal differentiation, growth, and maturation in the malformed kidney can limit these functions. Existing knowledge has been generated, for the most part, from the study of maturing preterm and term animals. In contrast, very few data have been derived from the study of animals, such as mutant mice, with renal malformation. Thus interpretation of physiologic abnormalities in humans and experimental animals with renal malformation is largely an extrapolation from developmental studies in experimental animals with normal kidney development. The responsiveness of collecting duct cells to vasopressin is limited in newborns. This is thought to be due to high intrarenal levels of prostaglandins, which antagonize vasopressin. Normal newborn infants are limited in their capacity to respond to sodium restriction by reducing urinary sodium excretion. Interruption of tubule generation, differentiation, and growth, which are hallmark features of renal dysplasia, contributes to an exaggerated limitation in the capacity to absorb sodium in affected infants and children. The proximal tubule exhibits dramatic growth and maturation during renal development.

Diseases

• Bone tumor (generic term)
• Leprechaunism
• Cutaneous anthrax
• Plague, pneumonic
• Pulmonary surfactant protein B, deficiency of
• Costocoracoid ligament congenitally short

This increase in proteasome activity acts as a feed-forward mechanism to degrade large amounts of protein in muscles medications to avoid during pregnancy cyclophosphamide 50 mg buy line. Satellite cells are present under the sarcolemmal membrane of myofibers and medications gout cheap cyclophosphamide 50 mg otc, in response to muscle injury medicine wheel images cyclophosphamide 50 mg purchase online, they proliferate and fuse with myofibers to repair the injury treatment tinea versicolor order cheap cyclophosphamide online. We have shown that caspase-3 is at least one protease that performs this initial cleavage of the complex structure of proteins in muscle medications during pregnancy discount cyclophosphamide 50 mg buy line. Caspase-3 in muscle has been found to be activated in several catabolic conditions. Interestingly, the initial cleavage of muscle proteins in catabolic conditions can be monitored by examination of muscle biopsies. The kinases phosphorylate Smad2 and Smad3 and recruit Smad4 to form a Smad complex that translocates into the nucleus and stimulates transcription of genes, which results in muscle wasting. The possibility that abnormalities in the metabolism of fatty acids can stimulate protein breakdown in muscle was evaluated by Li and Wassner. There was no change in protein synthesis, and the pathway responsible for the degradation of muscle protein was not identified. In skeletal muscle, the parent molecule is prepromyostatin, which is cleaved to produce promyostatin and an inactive, latent protein complex that contains myostatin. Myostatin is released from the promyostatin complex by proteolysis or in response to free radicals. For example, in mice, deletion of the myostatin gene results in a dramatic increase in the size and number of skeletal muscle fibers. In dog races, whippets bearing a single copy of the mutated myostatin gene are among the fastest dogs, but those with two mutated copies have such massive muscles that they are barely mobile. Similarly, administration of myostatin or activin A experimentally leads to about a 30% decrease in muscle mass, documenting its importance as a catabolic factor in muscle. The myostatin peptibody also increased p-Akt and led to improvements in satellite cell function. Hyperparathyroidism can also inhibit insulin release, and low levels of insulin cause muscle protein degradation in vivo. Consequently, the optimal diet is one in which protein synthesis equals protein degradation. The daily rates of protein synthesis and degradation are very high, so even a small increase in protein degradation or decrease in protein synthesis persisting for several weeks can cause a marked loss of lean body mass. Notably, results of measured nitrogen balance do not identify whether protein synthesis or degradation is abnormal nor does it give insights into mechanisms that can cause loss of protein stores. Consequently, plasma proteins and indirect indices have been used to assess protein stores. Hypoalbuminemia is among the most frequently cited indicator of decreased protein stores, but the serum albumin concentration can be confounded by many factors. Thus, the serum albumin level is reduced by inflammation, acidosis, and urinary or other losses of albumin, but the presence of a low serum albumin level does not elucidate which fraction of the protein stores has been lost. The half-life of urea disappearance in a normal adult is about 7 hours, so even a large load of urea. For this reason, changes in the urea pool of normal adults can be ignored when their nitrogen balance is being calculated. When the serum creatinine level rises from 10 to 15 mg/dL, the retained nitrogen increases by only 0. The urea appearance equals the sum of urinary urea nitrogen excretion plus its accumulation (positive or negative). Although a surfeit or deficiency of dietary protein or calories may influence serum albumin levels, this is not sufficient to diagnose malnutrition. Malnutrition is defined as a complex of abnormalities due to an inadequate or unbalanced diet. This syndrome includes symptoms such as fatigue plus a loss of lean body mass and a decrease in serum albumin and other plasma protein levels. Second, in the absence of these metabolic abnormalities, a poor diet (or even starvation in the short term) does not cause a meaningful change in serum albumin. Third, correcting a low serum albumin level by increasing dietary protein and calories has been difficult to establish. The serum albumin level responds relatively slowly to changes in protein stores because it has a half-life of about 20 days; thus, its use in identifying malnourished patients is compromised during trials of protein refeeding. In fact, chronic inflammation is a major cause of morbidity and mortality in dialysis patients. Kaysen and coworkers207 have shown that albumin synthesis falls sharply in patients on hemodialysis with inflammatory illnesses. Changes in dietary protein estimated by urea kinetics have indicated that changes in the diet protein have minimal impact on changes in serum albumin levels. The authors concluded that responses to inflammatory cytokines but not changes in dietary protein were the major factors producing hypoalbuminemia in patients undergoing hemodialysis. Instead, inflammatory cytokines and acute phase reactant proteins can actually initiate loss of muscle protein. With this diet, 30% of total calories from fat is recommended; saturated fat should not exceed 20% of total calories, and cholesterol intake should be below 300 mg/day. If high levels of triglycerides are present, the exclusion of purified sugars should be reduced in the diet and the patient should be evaluated for type 2 diabetes and/or insulin resistance. This should include withdrawal of alcohol and intake of complex carbohydrates instead of purified sugars. Weight reduction is obligatory for obese patients; many patients with insulin resistance who are not obese but exhibit mild-to-moderate weight excess may also benefit from caloric restriction and other dietary modifications. Medications that can reduce hypertriglyceridemia include a supplement of -3 fatty acids, fibric acid derivatives, and nicotinic acid. On the other hand, statin administration to patients on dialysis may not be useful because large randomized trials have not revealed a beneficial influence on survival in hemodialysis patients, including patients with and without type 2 diabetes mellitus. Notably, prescription of a low-protein diet normally includes a reduction of protein from animals. In the general population, a high plasma homocysteine level is associated with the development of atherosclerosis and mortality. However, serum transferrin levels change in response to nondietary factors; the serum transferrin level rises when iron stores are depleted and, with chronic inflammatory disorders, transferrin can decrease by as much as 50%, producing artificially low values in patients with inflammation. Interestingly, erythropoietin therapy causes no significant change in serum transferrin concentrations, at least in patients on dialysis, nor does it change nutritional status in terms of serum albumin levels, anthropometry, or muscle protein content. Most importantly, when the influence of early dialysis on mortality was analyzed, it was concluded that early dialysis does not prolong life. Plasma valine is usually low, and leucine and isoleucine levels are lower, but to a more modest extent. Statistical significance cannot be evaluated in view of the variety of sources of the data. There is growing evidence that the concentrations of sulfur-containing amino acids. One abnormality is that binding of homocysteine to albumin seems be abnormal, while abnormal intracellular levels of free sulfur-containing amino acids can aggravate the high plasma levels of these amino acids. Generally, their concentrations decrease when protein intake is reduced and urea appearance falls (see Chapter 54). Because the degree of acidosis is related to creatinine clearance and intake of protein, it is not surprising to find the serum bicarbonate level so low unless it is properly addressed by restricting the amount of protein in the diet or by supplementation with oral sodium bicarbonate. The energy required during daily activities is measured by indirect calorimetry over relatively brief periods and then extrapolating the result to 24 hours. This leads to the development of calorie malnutrition and possibly negative nitrogen balance, with loss of protein stores. The authors concluded that on average, the energy expenditure of patients on dialysis is no different from that of normal subjects. One possibility is to increase the pasta content of meals as these are complex carbohydrates and will not aggravate diabetes as much as increasing simple sugars. There also needs to be careful monitoring because providing extra calories may only create more body fat rather than increase protein stores. The open circle represent the patient who had the lowest resting energy expenditure. If blood pressure rises when the salt intake increases, a patient is labelled salt-sensitive, and he or she will achieve neutral salt balance more slowly. In contrast, persons who are salt-resistant rapidly excrete additional salt and do not have an increase in blood pressure. This is relevant because salt sensitivity has several negative features, such as the following: (1) it precedes established hypertension; (2) constitutes a cardiovascular risk factor; (3) complicates antihypertensive therapy; and (4) contributes to progressive loss of kidney function by exacerbating proteinuria and diminishing antiproteinuric responses. It should also be emphasized that treatment with diuretics alone will fail if salt intake is unrestricted because the excess salt will overcome the effectiveness of the diuretic. The frequency of salt-sensitive hypertension is rather high, especially in African Americans, and the frequency increases with age, especially when kidney function declines. For example, with furosemide treatment, normal adults experience a sharp increase in sodium excretion, producing an initial negative sodium balance. However, over the remaining 18 to 20 hours, dietary salt and fluid are retained, counteracting the effectiveness of the diuretic. We recommend that diuretic therapy must be accompanied by restricting salt intake to 2 g sodium/day. Since 95% of sodium ingested is excreted by the kidneys, a 24-hour sodium excretion is the best indicator of sodium intake. Other estimates are less accurate because sodium excretion fluctuates widely during the day. Consequently, a spot urine to measure the sodium/ creatinine ratio is not useful for assessing salt intake. It is important to note that patients accustomed to a high salt intake can experience salt craving when they begin reducing salt intake; this lasts about 2 weeks, so patients should be reassured that the craving will disappear with time. Optimally, home blood pressure recording or ambulatory 24-hour blood pressure recordings should be obtained to assess the effectiveness of therapy. Treatment must include plans for altering dietary salt intake, and the effectiveness of the plan should be assessed by a 24-hour urine collection for sodium excretion. The same collection can be used to determine creatinine clearance and estimate protein intake and the excretion of microalbumin and other minerals. Once the goals of dietary salt and blood pressure have been met, blood pressure values and periodic measurements of 24-hour sodium excretion are necessary to assess long-term compliance. If sodium excretion is excessive and blood pressure increases, visits to the nutritionist and repeating measurements of 24-hour urine sodium excretion will make dietary planning easier. Counteracting these problems are adaptations that increase the excretion of potassium via the kidney and gut. There is substantial evidence that diets rich in potassium, particularly when the intake of fruits and vegetables is high, have a reduced likelihood of developing chronic diseases such as coronary heart disease and diabetes. Clinically important reductions in blood pressure have also been documented in subjects with normal blood pressures or mild hypertension, as long as they consume a potassium-rich diet. In this study, 459 subjects with a systolic blood pressure lower than 160 mm Hg and diastolic blood pressure of 80 to 95 mm Hg were randomly assigned to different diets. Subsequently, subjects were randomly assigned to one of three diets for 8 weeks: (1) the control diet, rich in fruits and vegetables; (2) a combined diet, rich in fruits and vegetables, with limited dairy products; and (3) a diet with reduced content of saturated and total fats. For all three groups, sodium intake and body weight were maintained at constant levels. Compared to the control diet, the mean reductions in systolic and diastolic blood pressures associated with the combination diet were 5. For the 133 subjects who were hypertensive, the results were more pronounced; systolic and diastolic pressures were lowered by 11. This is recommended because a diet restricted in potassium and sodium is difficult to achieve. First, this amount of dietary protein is not needed by all subjects as some will require less than this amount and others require more. In adults, eating more than this amount does not improve body protein stores because the catabolic pathways described earlier stimulate losses of protein stores. Patients with Nephrotic Syndrome Patients with hypercholesterolemia, edema, and more than 3 g urinary protein/day. Similarly, these adaptive metabolic responses occur when the diet is restricted to only 0. There is a significant correlation between the amount of dietary protein and leucine oxidation during fasting and feeding, showing the adaptive response to dietary protein changes. Notably, the defect cannot be corrected by giving nephrotic patients a protein-rich diet. Unfortunately, some of the published studies are of low methodologic quality because they were retrospective studies with only a small number of patients or serious design flaws. Instead, outcomes in reported trials were based on estimating differences in changes in serum creatinine levels or the degree of proteinuria. There are different types of phosphate anions, and the proportions of these anions depend critically on the blood pH and other factors, making the interpretation of the plasma phosphates complex. Because of the marked influence of pH on the different types of phosphates, clinical laboratories do not report phosphate concentrations but report the serum concentration of phosphorus, which represents the concentration of all types of phosphates. Therefore, patients and physicians concentrate on regulating the amount of phosphorus in the diet, even though all physiologically important reactions are based on phosphate metabolism. The intake of phosphates is linked to dietary protein by a predictable relationship-approximately 1 g of protein contains 13 mg of phosphate-and, consequently, variations in the amount of protein eaten will predictably change phosphorus intake. The serum phosphorus level, therefore, is influenced by the amount of protein in the diet as well as processes that regulate phosphate metabolism, including the intestinal absorption of dietary phosphates, excretion of phosphates by renal tubules, and changes in bone metabolism. This finding suggests that phosphate retention is not a prominent reason for the development of secondary hyperparathyroidism (see Chapters 55), but there are flaws in this suggestion.

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