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Guttate hypomelanosis and progressive hypomelanosis of the trunk (progressive macular hypomelanosis)
Published in Electra Nicolaidou, Clio Dessinioti, Andreas D. Katsambas, Hypopigmentation, 2019
Alexander Katoulis, Efthymia Soura
It is uncertain whether genetic factors play a role in the pathogenesis of IGH, although a correlation with specific HLAs (human leukocytic antigens) has been established.10,11 One the other hand, continuous microtrauma may play an important role in the appearance of IGH.4 Defective local melaninogenesis has also been included in the possible causes of IGH.12–15
Fluorescence In Situ Hybridization and Polymerase Chain Reaction
Published in Wojciech Gorczyca, Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
The immunoglobulin molecule is made up of two heavy chains and two light chains, joined by disulfide bonds. Both heavy and light chains have variable and constant regions corresponding to the V and Cμ genes. The genes encoding heavy chains are located on chromosome 14, and the genes encoding light chains are located on chromosomes 2 (kappa) and 22 (lambda). During the maturation of lymphocytes, B cells rearrange their genes producing fusion gene composed of variable (V), diversity (D), joining (J), and constant (C) segments, which encode an antigen receptor that is expressed on the surface of B cells and become secreted when B cells differentiate into plasma cells. All maturing B cells rearrange their genes differently by splicing out and deleting a portion of the IGH gene, in which 1 of 30 D regions is juxtaposed first with 1 of 6 J regions, followed by joining of 1 of ~200 V regions. Antibody type (IgA, IgM, IgD, IgE, and IgG) depends on which C region (Cα, Cμ, Cδ, Cε, or Cγ) joins the rearranged VDJ genes. The heavy-chain protein (IGH) joins either kappa (κ) or lambda (λ) light-chain proteins (which are encoded by genes rearranged in a similar manner) to produce antibody. The unique coding sequence for both heavy- and light-chain genes ensures the diversity of antibody production by the plasma cells. Normal B-cell population, therefore, consists of polyclonal IG gene rearrangements.
MALT lymphoma pathology, initial diagnosis, and post-treatment evaluation
Published in Franco Cavalli, Harald Stein, Emanuele Zucca, Extranodal Lymphomas, 2008
Christiane Copie-Bergman, Andrew Wotherspoon
Several studies have tried to clarify this issue by using PCR for the immunoglobulin heavy chain (IGH) gene.19 Molecular evidence of monoclonality detected by PCR may help to assess the remission status; however, its usefulness is jeopardized by the possibility of false-negative results and conflicting reports on detectable monoclonality in histologically reactive lesions.17,19–21 Furthermore, persistent monoclonal disease may be observed in up to 44% of the patients after eradication therapy despite apparent histological remission.22–26 Whether these monoclonal bands represent active neoplastic cells or resting memory B cells in the gastric mucosa remains to be established. The significance of a persistent malignant clone is still unclear and PCR results should be interpreted only in the context of histology.
Prognostic value of t(4;14) translocation in newly diagnosed multiple myeloma patients in novel agent era
Published in Hematology, 2023
Chuanying Geng, Guangzhong Yang, Huixing Zhou, Huijuan Wang, Yanchen Li, Yun Leng, Zhiyao Zhang, Yuan Jian, Wenming Chen
Multiple myeloma (MM) is a malignant hematological disease originating from monoclonal plasma cells, mainly manifested as hypercalcemia, renal insufficiency, anemia and bone lesions [1,2]. MM is a highly heterogeneous disease with significant discrepancies in survival, ranging from a few months to more than ten years. So it is very important to clarify the prognostic factors of MM patients and design personalized treatment to improve the outcome of patients. Cytogenetic abnormalities represent the biological characteristics of myeloma cells and play an important role in the prognosis of multiple myeloma patients. Fluorescence in situ hybridization (FISH) is a common method to detect cytogenetic abnormalities in MM patients. IGH gene locates at 14q32 and several cytogenetic abnormalities based on 14q32 translocations are identified which have special prognostic significance for MM patients. These translocations mainly include t(4;14)(p16;q32), t(14;16)(q32;q23), t(11;14)(q13;q32), and t(14;20)(q32;q12). In prior reports, t(4;14) translocation could be detected by FISH in 10–30% patients with newly diagnosed MM [3–6]. Several studies found that the t(4;14) was a poor prognostic factor for the outcome of MM patients [7–16]. However, some studies suggested that t(4;14) was not associated with the prognosis of MM patients [3,5,17–19]. At present, the prognostic value of t(4; 14) in newly diagnosed MM patients is still controversial.
International global health education for doctor of physical therapy students: a scoping review
Published in Physical Therapy Reviews, 2022
Cara E. Felter, Leslie B. Glickman, Kelly Westlake, Andrea G. Shipper, Victoria Marchese
Results were organized by study design including outcome measures used (Table 1), global program locations (Table 2), academic program year for participating PT students, required or non-required course, number and type of participating students (Table 3), and the nature of the global activities (Table 4A–C) sorted by pre-immersion, immersion, and post-immersion categories (Figure 2). Some articles offered specific details about the pre- and post-immersion activities, while others merely mentioned or implied that they took place. Table 4A–C indicates articles that described at least basic details about the pre-immersion, immersion, and post immersion activities. The primary purposes of IGH as defined by the academic programs included one or more of the following: service learning, clinical education, cultural immersion, and research (Table 4B).
Immunological Role of IgG Subclasses
Published in Immunological Investigations, 2021
Cecilia Napodano, MariaPaola Marino, Annunziata Stefanile, Krizia Pocino, Roberto Scatena, Francesca Gulli, Gian Lodovico Rapaccini, Stefano Delli Noci, Giovanna Capozio, Donato Rigante, Umberto Basile
IgG act by binding Fcγ receptors (FcγR) on target cells and/or activating the complement system (Kapur et al. 2014). In humans, IgG are the predominant antibody class (7–15 g/L), and the four IgG subclasses, named IgG1, IgG2, IgG3, and IgG4, functionally distinct because of different heavy chain genes, differ in their ability to fix complement (IgG3> IgG1> IgG2> IgG4) and bind Fc receptors (Engelhart et al. 2017) Figure 1(a,b). The biological activities of each subclass of IgG are not completely understood. IgG receptors are surprisingly abundant in humans, and they comprise high- and low-affinity ones (Sigal 2012; Vidarsson et al. 2014). The genes of IgG subclass constant regions are positioned in the order of IgG3, IgG1, IgG2, and IgG4 in the human IgH region (Lowe et al. 2013; Tan et al. 2015).