لطفا نظرات خود را برای ما ارسال کنید : 👇🏻 @Takmililab این کانال به همت چندین فلوشیپ و فارغ التحصیل دکتری تخصصی راه اندازه شده است . در این کانال سعی بر آن است تا از 0 تا 100 با شما باشیم دکتر شکوه امیری : فلوشیپ دکتر محمد نژاد : فلوشیپ
🌟 به دنیای پرانرژی و جذاب کانالهای ارشد وزارت بهداشت و پزشکی خوش آمدید! 🌟
🩸هماتولوژی،ایمنولوژی 👩⚕داروخانه،پرستاری
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🥇بهترین کانال های اساتید ارشد دکترا وزارت بهداشت وپزشکی پرستاری که حتما باید در تمامی آنها عضو شوید⬇️
Читать полностью…پاسخ سوال 104)
گزینه د صحیح است
پاسخ سوال 102) در کلید گزینه الف بیان شده است.
Читать полностью…پاسخ سوال 99)
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Antinuclear Autoantibodies
The target antigens of ANA are heterogeneous and not well defined. ANA have been shown to be reactive with single-and double-stranded DNA, centromeres, histones, chromatin, and cyclin A. Human epithelial type 2 (HEp2) cells have prominent nuclei, hence nuclear patterns are easier to analyze and additional diagnostic information pointing to variant syndromes may be obtained, therefore IFL is now performed on this cell line in many laboratories (Sebode et al., 2017). A homogeneous staining pattern is the most common pattern in type 1 AIH, and coarse or speckled patterns are less frequently observed. In adults, a clinically significant titer is 1:40 and in children it is 1:20. Titers greater than 1:80, in conjunction with other criteria, are considered diagnostic of autoimmune hepatitis by the International Autoimmune Hepatitis Group ........
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💥قبولی در آزمون لیسانس پزشکی آسان شد.......
❌حذف شرط سن
❌حذف شرط معدل
✅کلیه رشته های کارشناسی مجاز به شرکت
✅کل طول تحصیل پزشکی فقط ۴ سال
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اطلاعیه شماره 3: ثبت نام آزمون ورودی دوره تکمیلی تخصصی علوم آزمایشگاهی (1404/04/11) (جدید)
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88) Recent advances in immunotherapy appear to be able to identify predictive biomarkers of responsiveness to immunotherapy. NGS has made the determination of tumor burden possible. Tumor burden is defined as the rate of peptide-changing single-nucleotide variants per million pairs. Hypermutated tumors have an increased tumor burden and a higher rate of somatic mutations. This is associated with the development of neoantigens as well as responsiveness to immune checkpoint inhibitors. Along with exogenous and endogenous mutagens, microsatellite instability (MSI) is a leading mechanism resulting in hypermutation. Detection of MSI is vital in the assessment of hypermutation, particularly in colorectal and gastric cancers (Nagahashi, 2019).
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85)
X AND Y CHROMOSOME MARKERS
Sex determination is commonly performed using the amelogenin locus (see Fig. 74.1). The primer for this locus amplifies an X-specific
band (Xp22.1 to 22.3) and a Y-specific band (Yp11.2). This locus is coamplified and coanalyzed with most multiplexed STR systems designed for human identity testing. Sex determination marks a departure from all other routine identity markers, in that it provides specific phenotypic information about the source individual (i.e., male or female). It may also be important in the investigation of potential suspects as well as in the categorization of specimens as originating from a victim or suspect. Although polymorphic Y chromosome markers (Fig. 74.3) are not used for sex determination, they are extremely useful in the typing of casework when there is a mixture of a male and female and a mixture of males. For example, an excellent use of Y-STRs is sexual assault evidence that displays a mixture of both the female epithelial cell DNA and male sperm DNA. When the quantity of male DNA is much less than the female DNA, Y-STRs are excellent in obtaining a profile of the male subject with no interference from the female subject since Y-STR results are only obtained from males. They also are used to characterize the paternal lineage in human remains identifications (Box 74.3). A haplotype is generated from Y-STRs versus a phenotype in autosomal STRs; haplotypes do not afford the same level of discrimination as autosomal STR profiles.
Cytogenetic Findings
Several large CNVs were reported, most notably deletions on both
15q13.3 and 1q21.1. Subsequently, large-scale “mega-analysis” in the PGC confirmed this and showed a more or less specific increase in burden in genes with synaptic function as well as those implicated in animal models of illness. Furthermore, a number of specific loci showed significant enrichment in CNVs, including 1q21.1, 2p16.3 (neurexin1), 3q29, 7q11.2, 15q13.3, 16p11.2, and 22q11.2 (Marshall et al., 2017).
81)
ARRAY TECHNOLOGY IN CLINICAL DISEASE
Microarray technology has provided the ability to screen genes that are differentially regulated in experimental and clinical disease and allow further correlation of select genes with their function. For example, Ji and colleagues (2003) used microarray technology to screen for genes that are upregulated in the early stage of acute pancreatitis using two different experimental models of the disease. Many genes were upregulated in both experimental systems, suggesting their importance in the human condition. However, one gene in particular, EGR1, further analyzed through classical approaches (gene knockout), was shown to be a key regulator that may be important in the development of early acute pancreatitis. Others (Iacobuzio-Donahue et al., 2003) have performed a comprehensive evaluation and comparison of gene expression profiles of 39 samples of pancreatic cancer and identified between 6 and 40 genes that were highly expressed when examined by multiple methods (oligonucleotide arrays, cDNA arrays, or SAGE). These may eventually be translated into clinically useful targets for therapy or diagnosis.
سوال79 ) در صفحه 1430 داریم
Miller-Dieker syndrome clearly illustrates the overlap between microdeletion and contiguous gene syndromes. The disorder has been associated with a microdeletion of the distal short arm of chromosome 17 (17p13.3), and the cardinal clinical features are lissencephaly (smooth brain) and craniofacial anomalies. Isolated lissencephaly has also been recognized as an independent entity, so Miller-Dieker syndrome is a more complex presentation that couples the brain defect with characteristic facial features. Molecular analysis has shown there are at least two genes involved in Miller-Dieker syndrome, so it is a true contiguous gene syndrome resulting from a microdeletion. A smaller deletion of the LIS1 gene only would result in isolated lissencephaly (Ledbetter et al., 1992).
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بااحترام به
دوستانی که گزینه بله رو انتخاب کردن لینک کانال ها رو در زیر قرار میدم👇🌹🌹
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📚📚📚📚📚📚📚📚📚📚📚📚📚📚📚
💥قبولی در آزمون لیسانس پزشکی آسان شد.......
❌حذف شرط سن
❌حذف شرط معدل
✅کلیه رشته های کارشناسی مجاز به شرکت
✅کل طول تحصیل پزشکی فقط ۴ سال
پاسخ سوال 105)
گزینه ب صحیح است
103) ANCA Is a Marker for Primary Sclerosing Cholangitis Primary sclerosing cholangitis (PSC) is an autoimmune disease associated with destruction of extrahepatic and intrahepatic bile ducts. More than 80% (26%–94%) of patients with this disease have circulating perinuclear antineutrophil cytoplasmic antibodies (p-ANCAs) (Chapman, 2005; Hov et al., 2008; Hov et al., 2017) with specificities against antigens such as bactericidal/ permeability-increasing protein, cathepsin G, elastase, and/or lactoferrin (Mulder et al., 1993; Roozendaal et al., 1998; Hov et al., 2008; Kyriakidi et al., 2016). Up to 75% also have other autoantibodies, such as antinuclear antibodies (ANAs) or anti–smooth muscle antibodies (ASMAs) (Chapman et al., 1986; Björnsson et al., 2002; Hov et al., 2008). There is some question as to whether pANCA, which is a reliable indicator of large cholangiole disease, can likewise serve as a reliable biomarker for PSC involving small cholangioles
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101)
گزینه های الف و ج صحیح است.
98) RHEUMATOID ARTHRITIS
RA is a systemic autoimmune disorder characterized by chronic, symmetric, and erosive arthritis of the peripheral joints (Scott et al., 2010). A large percentage of patients have elevated titers of serum rheumatoid factors. There may be associated nonarticular manifestations such as subcutaneous nodules, vasculitis, interstitial fibrosis, and normochromic, normocytic anemia. Sjögren and Felty syndromes may occur in RA. The primary cause of the disease is unknown. RA is associated with several autoantibodies, which can serve as diagnostic and prognostic markers (Aho et al., 1994; Firestein, 2003; Pincus et al., 2014) (Fig. 53.4). These include: 1. Rheumatoid factor (RF): IgA, IgG, IgM 2. Antifillagrin antibodies (also known as anticitrullinated proteins antibodies, ACPA) (Table 53.4):
a. Antikeratin antibodies (AKA)
b. Antiperinuclear factor (APF), not commercially available
c. Antibodies to citrullinated peptides (many times referred to as anti-CCP, anticyclic citrullinated peptide)
d. Anti-Sa antibodies, targeting citrullinated vimentin (Rodriguez-Mahou et al., 2006)
3. Anticarbamylated proteins antibodies (Shi et al., 2019)
4. Anti-PAD 2/3/4 They all may possibly precede the onset of clinical RA (Klareskog et al., 2004; Bos et al., 2014; Gan et al., 2015; Verheul et al., 2018).
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فرصت را از دست ندهید! لیستی از بهترین کانال های ارشد وزارت بهداشت ،آزمایشگاهی ،استخدامی ،پرستاری،پزشکی💥 تا دقایقی دیگر لیست حذف میشود.
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سریعتر عضو شوید و از مزایا بهرهمند شوید!👆👆🌺🌺
اطلاعیه شماره 3: ثبت نام آزمون ورودی دوره تکمیلی تخصصی علوم آزمایشگاهی (1404/04/11) (جدید)
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93)
Given valence conditions that allow the formation of large aggregates, the size of the antigen–antibody complexes that form depends critically on the relative molar concentrations of the two reactants. If an excess of antigen or antibody is present, large complexes are unlikely to form (Fig. 47.2). This property is crucial to understanding seemingly paradoxical reactions in some immunoassays that depend on antigen–antibody complex formation. For example, a vast excess of antigen can completely saturate all antibody-binding sites, leading to a negative signal (i.e., no agglutination). This phenomenon is sometimes referred to as the prozone effect. The prozone effect remains a potential problem for modern assay systems, including syphilis testing, in which extremely high-titer antibodies can be missed unless the specimen is tested at dilutions (Smith & Holman, 2004) and even in immunofixation electrophoresis (see later discussion, Fig. 47.6E). The prozone effect, or hook effect, occurs in many different immunoassays, particularly those based on sandwich formation involving a capture antibody (usually solid phase) that binds antigen plus a second reporter antibody (typically labeled with an enzyme, fluorescent or chemiluminescent dye, or radioactivity) also directed against the antigen. When antigen is present in excess, it can saturate both capture and reporter antibodies, thereby preventing sandwich formation. This situation is analogous in part to the right side of Figure 47.2, where signal strength diminishes at high antigen concentration.
اما
Specimen Matrix Effects
Common biochemical analytes—such as electrolytes, small molecules, enzymes, and so on—are generally distributed in the water phase of plasma or serum. Consequently, specimens with reduced water phase due to hyperproteinemia (e.g., from very high concentrations of a myeloma protein) or hyperlipidemia (e.g., high chylomicron content) can have reduced content of those solvent analytes even though other properties, such as ionic activities in those specimens, may be within normal physiologic range. This phenomenon is termed the solvent exclusion effect, referring to the exclusion of water and small molecules in the aqueous phase when more volume within a specimen is occupied by protein or lipid that excludes water. The content of small molecules per volume is the osmolarity (which is the measurement that can be erroneous), whereas the physiologically important aspect, such as ionic activities, is the osmolality. If excess lipids are the cause, they may be removed by ultracentrifugation. If interference is due to excess protein, an alternative mode of analysis, such as ion-selective electrode in undiluted specimen, can be employed to yield correct electrolyte activity (i.e., equivalent of osmolality). Matrix effects from very high or very low concentrations of proteins and other constituents may be problematic when dealing with other body fluids, especially when the specimens are highly viscous or otherwise atypical. In those situations, it may be necessary to qualify results in the report to indicate the site of the body fluid and possible limitations in accuracy of measurement.
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91) Fluorescent immunoassays (FIAs) use fluorophores as labels. Fluorophores require optimal wavelength light energy for their excitation to produce detectable emission light. FIA sensitivity is likely to decrease because of the nonspecific background fluorescence present in biological specimens. Fluorophores that have a delayed fluorescence emission time of 100 ns (nanoseconds) are suitable for application on time-resolved FIA.
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90) Hairy Cell Leukemia
HCL is often readily diagnosed based on its cytologic features, pattern of bone marrow infiltration, and characteristic immunophenotype (Swerdlow et al., 2017). Occasionally however, HCL can be difficult to distinguish from other small B-cell neoplasms, particularly splenic MZL. In these difficult cases, molecular analysis for BRAF Val600Glu mutation
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87) This mirrors the clinically defined subsets of patients who were most likely to respond to EGFR TK inhibitors. NSCLC patients whose tumors present with EGFR TK–activating mutations show better overall response, longer progression-free survival, and overall survival after chronic gefitinib or erlotinib treatment, as compared to those without these activating mutations (Gazdar, 2009). Acquired resistance
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TP53. TP53 is located at chromosome 17p13 and encodes a transcription factor that acts as a tumor suppressor through induction of apoptosis or growth arrest (see also Chapter 77). TP53 is upregulated in response to a variety of cellular proliferative stress and DNA damage signals (Junttila & Evan, 2009; Kato et al., 2003; Willis, et al., 2004). P53 protein activity or its loss from mutation or other mechanisms has complex effects on normal hematopoiesis (Pant et al., 2012). Somatic TP53 mutations are seen in approximately 5% to 10% of patients with MDS, with 25% showing high-grade diseases, 10% of de novo AML, and half of therapy-related myeloid neoplasms. TP53 mutations often coexist with complex karyotypes with a high frequency of del(5q) and 17p loss of heterozygosity (LOH). These mutations confer chemoresistance and poor prognosis in myeloid neoplasms regardless of clinical or pathological diagnoses
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82)
MICROARRAY FABRICATION
3′-End functionalization (i.e., chemical modification) of nucleic acids—oligonucleotides, PCR products, cDNAs, or peptide nucleic acid oligomers— is required for covalent immobilization on either glass or polypropylene surfaces (Matson et al., 1995; Beier & Hoheisel, 1999). For example, treatment of glass slides with silane allows amino-covered glass to bind amino-linked probes, using bifunctional molecules such as a dialdehyde or a diisothiocyanate (Case-Green & Southern, 1994; Guo et al., 1994). Alternatively, glass coating with a polycation (e.g., polylysine) allows direct charge-coupled binding of polyanionic DNA probes (Maskos & Southern, 1993a); an ultraviolet photo-cross- linking step adds covalent bonds to the ionic interaction. Covalent binding is essential to permit stringent washes and therefore accurate discrimination of hybridized species. Several protocols have been published to address surface activation (Maskos & Southern, 1992; Beattie et al., 1995; Matson et al., 1995; Beier & Hoheisel, 1999). An interesting alternative consists of deposition of small patches of activated polyacrylamide to which presynthesized oligonucleotides are attached by microinjection (Khrapko et al., 1991; Yershov et al., 1996; Guschin et al., 1997). The packing density
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A phenotypic male with an XX sex chromosome complement may also result from a cryptic translocation between the X and Y chromosomes. The distal ends of the short arms of the X and Y chromosomes are homologous and comprise what is termed the pseudoautosomal regions (see Fig. 71.23). This is the primary site of X and Y chromosome pairing during meiosis, and recombination may occur between X and Y alleles. Rarely, a recombination event outside the boundaries of the pseudoautosomal region takes place, resulting in the transfer of unique Y loci, including SRY, to the tip of the X chromosome. The amount of chromosome material involved in such an exchange is extremely small and cannot be cytogenetically detected. In a male with such a balanced translocation, there would be no clinical abnormalities, because the genes are all present, although in alternate locations. However, if this male transmits his rearranged X chromosome to an offspring who has received an X from the mother, the resultant child will have an apparent XX chromosome complement but a phenotype that is male or Klinefelter male due to the presence of the TDF protein that triggers the male developmental pathway.
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one or more globin chains with hundreds of sequence variants known, and their diagnosis at the molecular level is correspondingly more complex than that of sickle cell anemia. α-Thalassemia is the more straightforward because it is usually caused by deletion of either or both of the two contiguous α (HBA) genes on one or the other or both chromosomes 16. This can be detected by Southern blot, MLPA, or quantitative PCR, allowing differentiation of the silent carrier state (one α gene missing) from the very severe hydrops fetalis (all four genes missing) and the two intermediate states (Zhou et al., 2013). For the minority of cases caused by point mutations, Sanger sequencing or allele-specific probe hybridization can be used
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