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Serological tests for which disease may give a false- positive result if the patient has Lyme disease? Hepatitis C Immunology/Evaluate laboratory data to determine possible inconsistent results/Lyme disease/Testing/3 55 erectile dysfunction how common purchase dapoxetine overnight. The virus is an opportunistic pathogen and has become a well-recognized cause of poor renal function in kidney transplant recipients erectile dysfunction at 25 order 90mg dapoxetine fast delivery. Although Legionella pneumophila can be diagnosed through a urinary antigen assay erectile dysfunction in young males discount dapoxetine 90mg amex, that organism is not a primary cause of renal insufficiency in transplant patients erectile dysfunction hypothyroidism best dapoxetine 90mg. When you call to find out what organism the physician wants to identify, you are told: A. The current antibody tests are either IgG-specific or an IgG/IgM combination assay. Aspergillus Immunology/Apply knowledge of special procedures/ Fungal testing/2 smear specimen to you for an assay designed to detect the presence of a virus associated with cervical cancer. A convalescent specimen is recommended in 4 weeks to determine if a fourfold rise in titer has occurred C. B the Cryptococcus antibody response is not a reliable indicator of a current infection; thus, an antigen assay is normally used to monitor the disease. The antigen assay may be used for serum or spinal fluid and will decline in response to treatment much faster than a traditional antibody test. A urinary antigen test is available for histoplasmosis, and a serum galactomannan assay is available for Aspergillus. No antigen test is available for Candida, thus antibody is the best serologic procedure for this organism. While a convalescent specimen may be useful in many cases, in an immunosuppressed patient the convalescent specimen may remain negative in the presence of an infection. A false-negative result could conceivably be caused by multiple whole blood or plasma transfusions, but retesting for antibody a month later would not be beneficial to the patient. What disease is indicated by a high titer of Immunology/Apply knowledge of fundamental biological characteristics/Autoimmunity/Definitions/1 2. B Autoimmunity is a loss of tolerance to self-antigens and the subsequent formation of autoantibodies. Complement testing would not be indicated with this low titer in a 55-year-old female. Which disease is least likely when a nucleolar pattern occurs in an immunofluorescence test for antinuclear antibodies? Which of the following is used in rapid slide tests for detection of rheumatoid factors? This pattern may be seen in most systemic autoimmune diseases and is especially common in patients with scleroderma. Laboratory tests cannot distinguish between these disorders Immunology/Evaluate laboratory data to recognize and report the need for additional testing/ Autoimmune/Testing/3 staining in interphase cells and dense chromatin staining in mitotic cells. Nucleolar Immunology/Evaluate laboratory data to recognize and report the need for additional testing/ Autoimmune/Testing/3 9. Ribosomal p antibody has nucleolar staining and a background homogeneous and cytoplasmic stain. A combination nucleolar/homogeneous specimen will also show homogeneous staining in the interphase cells. B Rheumatoid factors react with the Fc portion of the IgG molecule and are usually IgM. However, this pattern is seen in a wide range of systemic autoimmune diseases and in many normal persons at a titer below 10. B Antibodies to smooth muscle are found in the serum of up to 70% of patients with active chronic hepatitis and up to 50% of patients with primary biliary cirrhosis. If a positive result is found to thyroid peroxidase, thyroxine levels can be measured to distinguish between the two diseases. Which of the following diseases may show positive results with this type of assay? B While antibodies to tissue transglutaminase and gliadin are often found in celiac disease, their combined sensitivity is less than 100%. IgM level Immunology/Select routine laboratory procedures/ Autoimmune/Celiac disease/Testing/2 102 Chapter 3 Immunology 18. On which of the following substrates would this specimen display cytoplasmic speckling?

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Schrock E et al (1996) Recurrent gain of chromosome arm 7q in low-grade astrocytic tumors studied by comparative genomic hybridization erectile dysfunction drugs from india order dapoxetine master card. Walker C et al (2001) Characterisation of molecular alterations in microdissected archival gliomas erectile dysfunction pills canada purchase dapoxetine line. Liu C et al (2011) Mosaic analysis with double markers reveals tumor cell of origin in glioma erectile dysfunction natural order dapoxetine with a visa. Bouvier C et al (2003) Shared oligodendrocyte lineage gene expression in gliomas and oligodendrocyte progenitor cells erectile dysfunction causes cancer purchase discount dapoxetine. Colin C et al (2006) In vitro identification and functional characterization of glial precursor cells in human gliomas. Colin C et al (2007) Relevance of combinatorial profiles of intermediate filaments and transcription factors for glioma histogenesis. Potter N et al (2008) Genomic deletions correlate with underexpression of novel candidate genes at six loci in pediatric pilocytic astrocytoma. Shoshan Y et al (1999) Expression of oligodendrocyte progenitor cell antigens by gliomas: implications for the histogenesis of brain tumors. Genes Dev 21(21):2683­2710 Ichimura K et al (2004) Molecular pathogenesis of astrocytic tumours. Prevalence, fitness, mutation rate, and effect of parental transmission on severity. J Med Genet 26(11):704­711 Takano T et al (1992) Genetics of neurofibromatosis 1 in Japan: mutation rate and paternal age effect. In: Garner A, Klintworth G (eds) Pathobiology of ocular disease: a dynamic approach, 2nd edn, vol. Jacob K et al (2009) Duplication of 7q34 is specific to juvenile pilocytic astrocytomas and a hallmark of cerebellar and optic pathway tumours. Cheng Y et al (2000) Pilocytic astrocytomas do not show most of the genetic changes commonly seen in diffuse astrocytomas. Courtois-Cox S et al (2006) A negative feedback signaling network underlies oncogene-induced senescence. Ding H et al (2001) Astrocyte-specific expression of activated p21-ras results in malignant astrocytoma formation in a transgenic mouse model of human gliomas. Marumoto T et al (2009) Development of a novel mouse glioma model using lentiviral vectors. Uhrbom L et al (2005) Cell type-specific tumor suppression by Ink4a and Arf in Kras-induced mouse gliomagenesis. Jacks T et al (1994) Tumour predisposition in mice heterozygous for a targeted mutation in Nf1. Lyustikman Y et al (2008) Constitutive activation of Raf-1 induces glioma formation in mice. Perilongo G (2005) Considerations on the role of chemotherapy and modern radiotherapy in the treatment of childhood low grade glioma. Olson a,b,c Purpose of review Most children diagnosed with cancer today are expected to be cured. Medulloblastoma, the most common pediatric malignant brain tumor, is an example of a disease that has benefitted from advances in diagnostic imaging, surgical techniques, radiation therapy and combination chemotherapy over the past decades. It was an incurable disease 50 years ago, but approximately 70% of children with medulloblastoma are now cured of their disease. However, the pace of increasing the cure rate has slowed over the past 2 decades, and we have likely reached the maximal benefit that can be achieved with cytotoxic therapy and clinical risk stratification. Recent findings Using genome-based high-throughput analytic techniques, several groups have independently reported methods of molecular classification of medulloblastoma within the past year. Summary Novel classification and risk stratification based on biologic subtypes of disease will form the basis of further study in medulloblastoma and identify specific subtypes that warrant greater research focus. Risk stratification in medulloblastoma is currently based on age, metastatic status, extent of surgical resection and histological presence or absence of diffuse anaplasia. Standard risk patients are over the age of 3 years with localized disease and without anaplastic subtype. Incorporation of molecular factors will greatly improve risk stratification for pediatric patients with medulloblastoma. Several studies are ongoing to incorporate children who are 4 or 5 years old into this strategy [20]. Increased gene or protein expression occurs more frequently even without amplification in 20­40% of medulloblastoma cases [32,33].

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B Biuret is a compound with two carbonyl groups and three amino groups and forms coordinate bonds with Cu+2 in the same manner as does protein impotence with gabapentin cheap 60 mg dapoxetine visa. The reaction of phosphomolybdic acid with protein Chemistry/Apply principles of basic laboratory procedures/Proteins and enzymes/1 3 erectile dysfunction drugs lloyds 30mg dapoxetine mastercard. Slight hemolysis does not cause falsely high results erectile dysfunction treatment washington dc discount 30 mg dapoxetine with visa, if the absorbance of the Cu+2-protein complexes is measured bichromatically erectile dysfunction young men dapoxetine 30mg without a prescription. However, frankly hemolyzed samples contain sufficient globin to cause positive interference. The reagent reacts with peptides containing at least two peptide bonds, but due to the high concentration of proteins in plasma relative to peptides present this reactivity causes insignificant bias. Hemolysis will not interfere Chemistry/Apply knowledge to identify sources of error/Proteins and enzymes/2 highest analytical sensitivity? Direct ultraviolet absorption Chemistry/Apply knowledge of special procedures/ Proteins and enzymes/2 4. These, in turn, reduce the Cu+2 in the biuret reagent, increasing sensitivity about 100-fold. Albumin normally accounts for about one-third of the cerebrospinal fluid total protein D. Transudative serous fluid protein is about two-thirds of the serum total protein Chemistry/Evaluate laboratory data to recognize health and disease states/Proteins and enzymes/2 Answers to Questions 5­9 5. A Water pools in the vascular bed in nonambulatory patients, lowering the total protein, albumin, hematocrit, and calcium. A A high serum albumin level is caused only by dehydration or administration of albumin. Liver disease, burns, gastroenteropathy, nephrosis, starvation, and malignancy cause hypoalbuminemia. A In multiple myeloma, synthesis of large quantities of monoclonal immunoglobulin by plasma cells often results in decreased synthesis of albumin. In glomerulonephritis and nephrotic syndrome, both total protein and albumin are low owing to loss of proteins through the glomeruli. In hepatic cirrhosis, decreased hepatic production of protein results in low total protein and albumin. Nephrotic syndrome Chemistry/Correlate clinical and laboratory data/ Proteins and enzymes/2 commonly associated with an elevated level of total protein? Malignancy Chemistry/Correlate clinical and laboratory data/ Proteins and enzymes/2 for measurement of albumin? Tetrabromphenol blue Chemistry/Apply principles of basic laboratory procedures/Proteins and enzymes/1 8. D Malignant disease is usually associated with increased immunoglobulin and acute-phase protein production. However, nutrients required for protein synthesis are consumed, causing reduced hepatic albumin production. Glomerular damage causes albumin and other low molecular weight proteins to be lost through the kidneys. B Tetrabromphenol blue and tetrabromosulfophthalein are dyes that change pKa in the presence of protein. Although they have greater affinity for albumin than globulins, they are not sufficiently specific to apply to measurement of serum albumin. Reaction of both dyes with globulins requires a longer incubation time than with albumin, and reaction times are kept at 30 seconds or less to increase specificity. Which of the following dyes is the most specific 248 Chapter 5 Clinical Chemistry 10. Lipemia Chemistry/Apply knowledge to recognize sources of error/Proteins and enzymes/2 migrate toward the. Negatively, cathode Chemistry/Apply knowledge of fundamental biological characteristics/Electrophoresis/1 anode will decrease by increasing the: A. Voltage Chemistry/Apply principles of basic laboratory procedures/Electrophoresis/2 is caused by: A.

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Histopathologically similar tumours had previously been described as pseudopapillary ganglioglioneurocytoma [29] and pseudopapillary neurocytoma with glial diVerentiation [23] erectile dysfunction drug overdose buy cheap dapoxetine on line. This tumour is part of the growing list of relatively benign glioneuronal tumours erectile dysfunction bipolar medication buy dapoxetine with visa. Layers of tumour cells surround vessels erectile dysfunction medications side effects buy generic dapoxetine 90mg line, forming pseudopapillary structures with b pseudopapillae covered by inner cells with hyperchromatic and outer cells with vesicular nuclei erectile dysfunction doctor pune purchase dapoxetine 30mg free shipping. Pseudorosette with ring-like arrangement of neurocytic tumour cell nuclei around an eosinophilic neuropil core which d shows strong immunoreactivity to synaptophysin. Hainfellner Acta Neuropathol (2007) 114:97­109 [32], was established as distinct disease entity in a report of 11 cases by Komori et al. It often occupies the fourth ventricle and/or aqueduct, and may show parenchymal extension. The neuronal component consists of neurocytes that form neurocytic rosettes with eosinophilic, synaptophysin-positive cores and/or perivascular pseudorosettes. The glial component dominates and typically exhibits features of pilocytic astrocytoma. Although macroscopically indistinguishable from pineocytoma, the histology is incompatible with a pineal parenchymal tumour. In the past, the term pituicytoma was also applied to other tumours in the sellar and suprasellar region, particularly granular cell tumours and pilocytic astrocytomas. Presently, it is reserved for low-grade glial neoplasms that originate in the neurohypophysis or infundibulum and are distinct from pilocytic astrocytoma. To date, less than 30 bona Wde examples have been described, often as case reports. Clinical signs and symptoms include visual disturbance, headache and features of hypopituitarism. Pituicytomas are well-circumscribed, solid masses that can measure up to several centimetres. Histologically, they show a compact architecture consisting of elongate, bipolar spindle cells arranged in interlacing fascicles or assuming a storiform pattern [2, 48]. Local recurrences and cerebrospinal spread are more likely to occur in pilomyxoid than in pilocytic astrocytomas. It occurs in infants and diVers from the desmoplastic nodular variant by exhibiting a markedly expanded lobular architecture, due to the fact that the reticulin-free zones become unusually large and rich in neuropil-like tissue. Such zones contain a population of small cells resembling those of a central neurocytoma and exhibit a streaming pattern. The internodular reticulin-rich component, which dominates in the desmoplastic/nodular variant, is markedly reduced. Following radiotherapy and/or chemotherapy, medulloblastomas with extensive nodularity may occasionally undergo further maturation to tumours dominated by ganglion cells. A more favourable outcome than for patients with classic medulloblastomas is recognized for both, the desmoplastic/nodular medulloblastoma variant and medulloblastoma with extensive nodularity. Although all medulloblastomas show some degree of atypia, these changes are particularly pronounced and widespread in the anaplastic variant. Histological progression from classic to anaplastic medulloblastomas may be observed, even within the same biopsy. The highly malignant large cell medulloblastomas and anaplastic medulloblastomas have considerable cytological overlap. The large cell variant features often spherical cells with round nuclei, open chromatin and prominent central nucleoli. Surgical pathologists need to know such divergent patterns of diVerentiation but not every pattern warrants designation as a variant, since some patterns do not have distinct clinical or genetic features. The majority of pathologists thought that more clinico-pathological data should be available before this tumour is considered a new disease entity. In particular, it should be established whether or not these tumours carry a better prognosis than standard glioblastomas [13, 16, 31]. Glioneuronal tumour with neuropil-like islands Small cell glioblastoma Although small cells are common in glioblastoma, they are predominant or exclusive in a subset known as small cell glioblastoma [38]. This glioblastoma subtype displays a monomorphic cell population characterized by small, round to slightly elongated, densely packed cells with mildly hyperchromatic nuclei, high nuclear:cytoplasmic ratios and only minor atypia. This glioblastoma type appears to have a poor prognosis [38] although in one population-based study there was no signiWcant overall survival diVerence when compared to nonsmall cell glioblastoma [16]. Rare inWltrating gliomas contain focal, sharply delineated, round to oval islands composed of a delicate, neuropil-like matrix with granular immunolabeling for synaptophysin.

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