Some evidence exists and provides tentative evidence of impulsivity as a vulnerability marker for BD (e.g. Kwapil et al. 2000; Fulford et al. 2008; Giovanelli et al. 2013).
Expression of NCAM is highly indicative of neuroendocrine differentiation and is a potential tumour marker for SCLC (e.g. Ledermann et al, 1994).
Comparison of representative laboratory markers for inflammation (e.g. leukocytes, CRP, ferritin) or malnutrition (e.g. total serum protein), recorded at the date when the swab cultures were obtained, revealed no significant differences between MRSA carriers and noncarriers (Table 1).
The protein sequences and SSR markers of the two species were first prepared, and the protein sequences compared against themselves by BLAST analysis, and SSR markers selected for e-PCR against their own genomes.
No molecular markers for pathogenicity (e.g. PB2 E627K) were detected.
Co-localisation with markers for mitochondria (e.g., HSP60) demonstrated that these fragments were targeted to the mitochondrial network.
We explored its possible co-localisation with cell markers for Golgi, e.r. and mitochondria, and found no convincing co-localisation (not shown).
While several studies investigated the potential use of biologic markers for FM (e.g. cytokines, antipolymer antibodies), correlation of these markers with symptoms was equivocal at best [ 9- 12], rendering them ineffective as indicators of severity.
Other prognostic markers for glioblastoma (e.g., gender, age, steroid use, type of first surgery, time from original diagnosis, and maximum tumor diameter) were also not predictive of survival, findings that were consistent with those in previous studies [ 22, 34].
In particular, murine VSELs not only possess the primitive morphology of early developmental cells but also express typical markers for PSCs (e.g., Oct-4, Nanog, and Rex-1) [ 31, 33, 34, 37, 71].
