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Heavy Metal Index

Erik van der Wal,* SeyedYahya Anvar,* gressive neurodegenerative disorders, such as Hunting-

Source

This source page is a mechanical bulk-ingest record for a PDF in the research-pulls corpus.

Page snapshot
Cited by3 pages
Metals measured1
Evidence tierB
Year2011

Overview

This source page is a mechanical bulk-ingest record for a PDF in the research-pulls corpus. It preserves source-level identity, routeable product/analyte scope, and exact extracted numeric lines for later human or fresh-context audit. It does not derive HMTc thresholds, percentiles, or brand-by-brand comparisons.

Key numbers

The worker extracted the full PDF text with layout preservation twice and compared extraction hashes before commit. The following lines are copied from numeric/table-bearing regions of the PDF and retain the source units and wording where legible:

  • expPABPN1 were identified. These differences are asso- medium (Invitrogen), supplemented with 20% fetal bo-
  • the reduced amount of the soluble form is likely to be in a humidified 10% CO2 air atmosphere. Terminal differ-
  • becco’s modified Eagle’s medium containing 5% horse
  • Total RNA was extracted from myotube cultures after (pH 6.8), 10 mmol/L dithiothreitol (freshly added), 2%
  • cated in Table 1. The specificity of RT-PCR products was de-ubiquitinating enzyme (DUB) inhibition, 10 mmol/L
  • Table 1. Primers Used for RT-qPCR Analysis
  • turated and resolved by SDS-PAGE on 10% polyacryl- Myotube Cultures at Low Expression Levels
  • Immunofluorescence and Fluorescence in Situ the use of the 3= half of the HBB gene.43– 46 Stable clones
  • fusion, intense fluorescent foci were detected (INIs, Fig- represented ⬎10% of the genes in a given pathway (see
  • ure 1F and Figure 2A) and were visualized by either Supplemental Table S1 at http://ajp.amjpathol.org). In a
  • PABPN1. In addition, PABPN1 foci colocalized with ubiq- OPMD-deregulated pathways (see Supplemental Table
  • of differences in PABPN1 transgene expression levels (see ubiquitin proteasome system (Table 2). More important,
  • Supplemental Table S2 at http://ajp.amjpathol.org). These these pathways are commonly deregulated in patients
  • WTA-deregulated genes were mapped to 41 KEGG path- with D7E and OPMD (see Supplemental Table S1 at
  • model of OPMD (see Supplemental Table S2 at http://ajp. are involved in OPMD disease etiology.
  • ulated because of PABPN1 expression levels (Table 2). pathway in a cross-species study29 for OPMD. In the D7E
  • paring the effect of expression level (Figure 3). In the expPABPN1 expression (see Supplemental Table S1 at
  • A17.1 mouse, apoptosis was listed among the top 20 de- http://ajp.amjpathol.org). Approximately 20% of the pro-
  • has been subjected to extensive studies.22,47,48 In our D7E among which 80% were down-regulated. Validation of
  • plemental Table S1 at http://ajp.amjpathol.org). The acti- is regulated by the proteasome. In this experiment,
  • reported in affected muscles of patients with OPMD, we imate 20% increase in nuclei containing INIs in D7E

Methods (brief)

  • Kirsten R. Straasheijm,* Rinse Klooster,* ton’s disease,1 polyalanine tract expansions have also

Implications

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Update history

The five most recent substantive edits to this page, classified major (evidence or structure moved), correction (a published value or statement was wrong and has been fixed), or minor (narrative rewritten without changing the underlying evidence). Each description is derived from what the edit did to this page; the linked commit is the authoritative record, routine regeneration passes are excluded, and the full version history lives in git. When DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.

CommitDateChangeDescription
b01ec52c2026-08-04major2 sections added
d49e450f2026-08-03major5 sections added; narrative text revised