Late markers

Pauluhn, J., Carsom, A., Costa, D.L., Gordon, T., Kodavanti, U., Last, J.A., Matthay, M.A., Pinkerton, K.E., Sciuto, A.M. (2007). Workshop summary phosgene-induced pulmonary toxicity revisited appraisal of early and late markers of pulmonary injury from animal models with emphasis on human significance. Inhal. Toxicol. 19 789-810. 

Consequently, in addition to hydroperoxides, a lot of secondary oxidized lipidic compounds, mainly short-chain aldehydes, may appear and represent late markers of lipid peroxidation. As an example, malondialdehyde (MDA, Fig. 6) is known to be the most abundant lipid peroxidation aldehyde whose determination by 2-thiobarbituric acid (TBA) is one ofthe most common assays in lipid peroxidation studies [20]. However, it can be noticed that the TBA assay method [21] is not specific of MDA titration since it also can detect a variety of peroxides and secondary degradation products of lipid peroxidation called... 

LDH 135,000 8-12 48-72 10-15 days Late marker not cardiac specific LD1/LD2 determination increases cardiac specificity. 

Lipid accumulation and expression of late transcription factors, e.g., PPARy and C/EBPa and late markers of differentiation, e.g., PEPCK, AFABP/aP2, FATP... 

Late markers are not shared by undifferentiated neuroepithelial cells in their resident or itinerant status, and often not even after neuroblasts settle in their stable niche, but only after they become functional and mature neurons, with regard to the biosynthesis of neurotransmitters, resting membrane potential, membrane receptors, and synaptic contacts. The start of those markers expression should be kept in mind not only with reference to brain sections from the fetal to the neonatal stage but also, with particular attention, when the same tissues are used as starting material for growing cell cultures. For this purpose. Table 1 summarizes the most useful and predictive immunocytochemical markers found in the course of neuronal differentiation. 

Figure 4 shows cultured mouse embryonic stem immunola-beled for DCX (early marker) and NeuN (late marker). Cultures were counterstained with Hoechst 33342 [15]. 

Fig. 6.—One of the Molecular-ion Clusters Obtained from a Sample of Deuteropermethy-lated. Cyclic /3(l- 2)-Glucans (see Section VI,S). [All high-mass samples give unresolved clusters of this type if the mass spectrometer is operated at low resolution. The peak is 6 mass units wide at half height. The mass is assigned by using the mass marker, which gives marks every 4 mass units, as shown. The center of the peak corresponds to the chemical molecular weight of an [M + NKJ species.]...

Saito Y, Sharer LR, Epstein LG, Michaels J, Mintz M, Louder M, Golding K, Cvetkovich TA, Blumberg BM (1994) Overexpression of nef as a marker for restricted HIV-1 infection of astrocytes in postmortem pediatric central nervous tissues. Neurology 44 474-481 Sargeant TJ, Day DJ, Mrkusich EM, Eoo DE, Miller JH (2007) Mu opioid receptors are expressed on radial glia but not migrating neuroblasts in the late embryonic mouse brain. Brain Res 1175 28-38... 

The genetic basis for the more common late-onset AD appears more complex. Genetic susceptibility is more sporadic and it may be more dependent on environmental factors.9 The apolipoprotein E (apo E) gene on chromosome 19 has been identified as a strong risk factor for late-onset AD. There are three variants of apo E however, carriers of two or more of the apo E4 allele have an earlier onset of AD (approximately 6 years earlier) compared with non-carriers.9 Only 50% of AD patients have the apo E4 allele, thus indicating it is only a susceptibility marker. 

In 1993/1994 a series of publications caused a stir in the AD research community, since for the first time they linked a specific neuropathological process in late-onset AD to a genetic marker. Researchers looking at the composition of plaques found that the protein apolipoprotein E (ApoE) was associated with p-amyloid in the cerebrospinal fluid (CSF) of AD patients (Strittmatter et al., 1993). The gene for ApoE is on the same human chromosome (number 19) which was a risk factor in some AD pedigrees. The gene for ApoE comes in three versions (alleles) Apo s2, Apo s3 and, most importantly, Apo s4 these result in three slightly different variants of the protein. Humans carry two versions of the allele and so can have none, one or two of any of the versions of the Apo... 

Deciphering the cause(s) of the Late Wisconsin dust interval will be the subject of many future studies, but the interval serves as a useful time marker at present. Koerner and Fisher [34] have used elevated microparticle concentrations in the Devon Island ice core as an indicator of Wisconsin-aged ice. Similarly high continental dust concentrations are expected in the recently recovered cores from the East Antarctic plateau. 

Only recently has the mouse placenta been demonstrated to be a major hematopoietic organ. In the late 1970s, using major histocompatability haplotypes as markers, Melchers69 demonstrated that the placenta of day 9 to day 12 mouse embryos harbored... 

PCNA is a 36 kDa molecular weight protein also known as cyclin. PCNA is expressed in the nuclei of cells during the DNA-synthesis phase of the cell cycle. In early S phase, PCNA has a very granular distribution and is absent from the nucleoli. At late S phase, PCNA is prominent in the nucleoli. PCNA is a useful marker of cells with proliferative potential and for identifying the proliferation status of tumor tissue, which is relevant to prognosis. 

This procedure, which complements other methods for distinguishing apoptotic and necrotic cell death, employs annexin V-PE as a marker for early apoptotic cells, and 7-AAD for late apoptotic or necrotic cells. Although other versions of this assay have used annexin V-fluorescein together with PI, that combination precludes the use of a third fluorescence color to measure an additional parameter, such as a phenotypic marker, because PI, unlike 7-AAD, has a broad emission spectrum that includes both orange and red fluorescence. 

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