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Related Concept Videos

Alkyl Halides02:45

Alkyl Halides

21.0K
Structural Properties
Alkyl halides are halogen-substituted alkanes wherein one or more hydrogen atoms of an alkane is replaced by a halogen atom such as fluorine, chlorine, bromine, or iodine. The carbon atom in an alkyl halide is bonded to the halogen atom, which is sp3-hybridized and exhibits a tetrahedral shape.
Unlike alkyl halides, compounds in which a halogen atom is bonded to an sp2 -hybridized carbon atom of a carbon-carbon double bond (C=C) are called vinyl halides. Whereas aryl...
21.0K
Amides to Amines: LiAlH4 Reduction01:20

Amides to Amines: LiAlH4 Reduction

6.5K
Amide reduction with strong reducing agents like lithium aluminum hydride proceeds through a nucleophilic acyl substitution to form amines. Primary, secondary, and tertiary amides yield primary, secondary, and tertiary amines, respectively.
Amide reduction requires two equivalents of the reducing agent, acting as a source of hydride ions. As shown in the figure, the reaction is initiated with a nucleophilic attack by the hydride ion at the carbonyl carbon to form a tetrahedral intermediate.
6.5K
Mass Spectrometry: Alkyl Halide Fragmentation01:22

Mass Spectrometry: Alkyl Halide Fragmentation

1.6K
Chlorine isotopes exist as 35Cl and 37Cl in a 3:1 ratio, while bromine isotopes exist as 79Br and 81Br in a 1:1 ratio. The mass spectrum of alkyl halides typically produces two distinct molecular ion peaks, the molecular ion peak, [M], and the molecular ion plus two, [M + 2] peak. The relative heights of these two peaks are proportional to the isotopic abundance ratios of the halide. For example, 2‐chloropropane and 1‐bromopropane display two peaks with relative peak heights in a 3:1 and...
1.6K
Amyloid Fibrils03:03

Amyloid Fibrils

6.9K
6.9K
Amyloid Fibrils03:03

Amyloid Fibrils

12.5K
Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
12.5K
Acid-Catalyzed α-Halogenation of Aldehydes and Ketones01:21

Acid-Catalyzed α-Halogenation of Aldehydes and Ketones

5.1K
By replacing an α-hydrogen with a halogen, acid-catalyzed α-halogenation of aldehydes or ketones yields a monohalogenated product
In the first step of the mechanism, the acid protonates the carbonyl oxygen resulting in a resonance-stabilized cation, which subsequently loses an α-hydrogen to form an enol tautomer. The C=C bond in an enol is highly nucleophilic because of the electron-donating nature of the –OH group. Consequently, the double bond attacks an electrophilic halogen to form a...
5.1K

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Related Experiment Video

Updated: Mar 11, 2026

Use of Alu Element Containing Minigenes to Analyze Circular RNAs
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AML in 2016: Where we are now?

Jacob M Rowe1

  • 1Technion Israel Institute of Technology, Haifa, Israel; Department of Hematology, Rambam Health Care Campus, Haifa, Israel; Northwestern University Feinberg School of Medicine, Chicago, IL, USA; Department of Hematology, Shaare Zedek Medical Center, Jerusalem, Israel.

Best Practice & Research. Clinical Haematology
|November 29, 2016
PubMed
Summary

High relapse rates in acute myeloid leukemia (AML) persist, but advances in genomic analysis, minimal residual disease monitoring, and targeted therapies like IDH and FLT3 inhibitors offer improved survival outcomes for adult patients.

Keywords:
ALLAMLAcute leukemia forumAcute lymphoblastic leukemiaAcute myeloid leukemiaBlinatumomabGenomicsIDHMRDMinimal residual disease

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Area of Science:

  • Hematology
  • Oncology
  • Genetics

Background:

  • Acute myeloid leukemia (AML) presents a significant challenge to long-term patient survival due to high relapse rates.
  • Despite challenges, substantial advancements in understanding AML biology and therapeutic strategies are emerging.

Purpose of the Study:

  • To review recent progress in AML biology and therapy.
  • To highlight key areas driving improved patient survival outcomes.

Main Methods:

  • Review of integrated genomic analysis for prognostic insights.
  • Assessment of minimal residual disease (MRD) monitoring in clinical settings.
  • Evaluation of novel therapeutic agents, including targeted inhibitors.

Main Results:

  • Integrated genomic analysis is enhancing prognostic accuracy.
  • Minimal residual disease (MRD) monitoring is increasingly utilized in clinical practice.
  • Targeted therapies, such as IDH and FLT3 inhibitors, are effectively used as a bridge to transplant.

Conclusions:

  • Continued research in AML biology and therapy is crucial.
  • Advancements in genomics, MRD monitoring, and targeted therapies are essential for improving survival in adult AML patients.