A precolumn derivatization liquid chromatography (LC) method was developed for the analysis of various dietary supplement formulations and raw materials for glucosamine. A 1 mL sample or standard water solution (containing about 0.05 mg glucosamine) was mixed with 1 mL pH 8.3 buffer, 1 mL 5% phenylisothiocyanate methanolic solution, and derivatized at 80 degrees C in a water bath for 30 min. After derivatization, the solution was cooled in a cold water bath and centrifuged at 3000-5000 rpm. The clear upper layer was ready for injection. The LC system was equipped with a C18 reversed-phase column and an ultraviolet detector set at 240 nm. The column was developed with a linear gradient composed of 0.1% phosphoric acid in deionized water and 0.1% phosphoric acid in methanol. The method was subjected to Single Laboratory Validation. The method precision was 0.50% relative standard deviation, accuracy was less than +/-1.5%, method linearity in the range 0-2 mg glucosamine/mL was 1.00, the detection limit was 0.0705 microg/mL, and the quantitation limit was 0.235 microg/mL. Chondroitin sulfate, amino acids, and excipients did not interfere with glucosamine testing. After derivatization, both standard and sample preparations were stable for at least 48 h. Due to its high sensitivity, this method can be used to assay glucosamine in functional foods and pet foods. The validation data will be published separately.
OBJECTIVES A 67-year-old male patient was diagnosed with acute myeloid leukemia (AML) in April 2018. Chromosome analysis showed an abnormal male karyotype with an isodicentric chromosome 7q resulting in deletion 7q and two copies of 7p and a derivative chromosome 18 in 13 of the 20 metaphase cells examined. This karyotype was described as 46,XY,idic(7)(q11.2),der(18)t(1;18)(q23;q21.1)[13]/46,XY[7]. Additionally, subsequent sequencing analysis displayed FLT3-ITD and RUNX1 mutations (data not shown). The bone marrow showed an overwhelming number of blast cells, with co-expression of CD34, CD117, TdT, MPO, CD7, CD13, CD33, CD38, CD19, and HLA-DR. Molecular cytogenetic studies showed a deletion of one RELN/TES (7q22/7q31) signal in 80.5% of nuclei and a gain of a BCR/ABL1 (22q11.2/9q34) signal in 3.5% of interphase nuclei examined. These findings were described as nuc ish(RELN,TES)x1[161/200],(ABL1x2,BCRx3)[7/200], (EVI1,TAS2R1,EGR1,DEK,MYC,NUP214,KMT2A,DLEU1,DLEU2,Clone 163C9,PML,CBFB,RARA,PTPRT,MYBL2,RUNX1)x2[200]. The patient relapsed with AML in September 2019 and underwent treatment. However, all AML treatment options were exhausted by March 2020. An isodicentric chromosome 7 leading to two copies of the short arm of chromosome 7 (7p) and deletion 7q is a rare event in AML and is rarely described in the literature. The key element here is that this specific rearrangement leads to deletion 7q which is a well-known abnormality in AML that places the patient in the Poor/Adverse risk category.
Lymphoplasmacytic lymphoma (LPL, previously termed lymphoplasmacytoid lymphoma) is an uncommon mature B-cell lymphoma usually involving the bone marrow and less commonly the spleen and/or lymph nodes. The majority of patients with LPL have a circulating monoclonal immunoglobulin M (IgM) that can lead to a hyperviscosity syndrome known as Waldenström macroglobulinemia (WM). Although LPL appears to be a sporadic disease in the majority of cases, a familial predisposition is present in some cases. The main chromosomal abnormalities are trisomy 12, trisomy 3, isochromosome 6p, and 14q rearrangements involving IgH among complex karyotypes. Herein, we present an 89-year-old male patient who presents with LPL involving 80% of the marrow cellularity with circulating lymphoma cells. Chromosomal analysis detected two unrelated abnormal clonal populations: one clone has trisomy 12 as the sole abnormality in the stimulated culture, while the other clone has a 13q deletion as the sole abnormality in the cells from the non-stimulated culture. Trisomy 12 is one of the most common abnormalities in B-CLL and it is associated with an intermediate prognosis. Deletions 13q have been identified in B-cell malignancies, non-Hodgkin's lymphomas (NHL), as well as myelodysplastic syndromes and chronic myeloproliferative neoplasms (Heim and Mitelman, 2015). Trisomy 12/13q- FISH slide was reviewed looking at the segmented cells. Fifty segmented cells were scored and a 13q- pattern was detected in 36% (18/50) of the cells suggesting that this finding (the 13q- clone) may be myeloid in origin. Clinicopathologic correlation of these results was recommended.
Wenczek, Carl. Chemical Galaxy II. Digital image. Born Digital Ltd, n.d. Web. 3 Oct. 2013. . Over 200 years since the creation of the periodic system, it would not be surprising to see more variations or completely different versions of the periodic table. Some examples of these innovative ways people thought of to organize the elements are featured and evaluated on this poster. Of course, these are only a small sum of a vast number of alternative periodic tables out here today. • It can be utilized to find out how many protons, electrons, and neutrons are in an atom of an element
Glioblastoma Multiforme (GBM) is the most malignant and frequently occurring primary brain tumor out of the different types of primary astrocytomas. It presents with an extremely poor prognosis, with a median survival of 14 to 15 months from the diagnosis. Herein, we present an 83-year-old female patient with a right frontal brain mass. A craniotomy for the frontal brain mass was performed, which revealed a tumor with high-grade glioma, necrosis, atypia, and vascular proliferation. The patient was subsequently diagnosed with Glioblastoma Multiforme Grade IV (GBM). Molecular cytogenetic studies showed an amplification of the EGFR gene in 100% nuclei scored. Amplification of EGFR appears in around 40-50% of individuals with Glioblastoma Multiforme Grade IV, leading to high levels of EGFR protein levels that contribute to tumorigenesis. Chromosomal deletions involving 1p36 and 19q13 are characteristic molecular features of solid tumors such as oligodendrocytes and mixed oligoastrocytomas, but in this case there was no evidence of a co-deletion of 1p36/19q13 in this case of glioblastoma.
Transient myeloproliferative disorder (TMD), now more commonly known as transient abnormal myelopoiesis (TAM), is a condition closely associated with Down syndrome. Ninety-five percent of Down syndrome cases occur as a result of chromosomal nondisjunction and are rarely due to mosaicism or translocation. TMD is found exclusively in neonates and is most commonly characterized by trisomy 21, somatic GATA1 mutation, and the increased presence of megakaryoblasts. TMD often does not manifest clinically, but patients may show hepatomegaly, splenomegaly and other symptoms. While TMD is almost always present with trisomy 21, there are not many other cytogenetic abnormalities associated with TMD, with a few rare cases such as monosomy 7 and trisomy 8. Recent studies have suggested liver hematopoietic progenitor cells as the candidate for TMD origin. Furthermore, GATA1 mutations associated with TMD are found to encode for a stop codon in the N-terminal activation region of gene sequences. It has been shown that those mutations can cause overproliferation of megakaryocytes, which can cooperate with Down syndrome cells, which have trisomy 21, in the progression of TMD into acute megakaryoblastic leukemia (AMKL). Since GATA1 mutations are present in all cases of myeloid leukemia of Down Syndrome, monitoring GATA1 in patients with trisomy 21 may assist with earlier diagnosis of TMD. Another likely cause of TMD is the amplification of the RUNX1 transcription factor gene located on chromosome 21. It has been shown that RUNX1 is associated with leukemias of myeloid lineage. While most cases of TMD will spontaneously resolve, some will evolve into acute myeloid leukemia (AML). In this review, we will discuss the cytogenetic, molecular genetics and clinical aspects of TMD.
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