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1.  Revision to reverse shoulder arthroplasty with retention of the humeral component 
Acta Orthopaedica  2013;84(5):473-478.
Background
Revision in failed shoulder arthroplasty often requires removal of the humeral component with a significant risk of fracture and bone loss. Newer modular systems allow conversion from anatomic to reverse shoulder arthroplasty with retention of a well-fixed humeral stem. We report on a prospectively evaluated series of conversions from hemiarthroplasty to reverse shoulder arthroplasty.
Methods
In 14 cases of failed hemiarthroplasty due to rotator cuff deficiency and painful pseudoparalysis (in 13 women), revision to reverse shoulder arthroplasty was performed between October 2006 and 2010, with retention of the humeral component using modular systems. Mean age at the time of operation was 70 (56–80) years. Pre- and postoperative evaluation followed a standardized protocol including Constant score, range of motion, and radiographic analysis. Mean follow-up time was 2.5 (2–5.5) years.
Results
Mean Constant score improved from 9 (2–16) to 41 (17–74) points. Mean lengthening of the arm was 2.6 (0.9–4.7) cm without any neurological complications. One patient required revision due to infection.
Interpretation
Modular systems allow retainment of a well-fixed humeral stem with good outcome. There is a risk of excessive humeral lengthening.
doi:10.3109/17453674.2013.842433
PMCID: PMC3822132  PMID: 24032523
2.  Side chain modified peptide nucleic acids (PNA) for knock-down of six3 in medaka embryos 
BMC Biotechnology  2012;12:50.
Background
Synthetic antisense molecules have an enormous potential for therapeutic applications in humans. The major aim of such strategies is to specifically interfere with gene function, thus modulating cellular pathways according to the therapeutic demands. Among the molecules which can block mRNA function in a sequence specific manner are peptide nucleic acids (PNA). They are highly stable and efficiently and selectively interact with RNA. However, some properties of non-modified aminoethyl glycine PNAs (aegPNA) hamper their in vivo applications.
Results
We generated new backbone modifications of PNAs, which exhibit more hydrophilic properties. When we examined the activity and specificity of these novel phosphonic ester PNAs (pePNA) molecules in medaka (Oryzias latipes) embryos, high solubility and selective binding to mRNA was observed. In particular, mixing of the novel components with aegPNA components resulted in mixed PNAs with superior properties. Injection of mixed PNAs directed against the medaka six3 gene, which is important for eye and brain development, resulted in specific six3 phenotypes.
Conclusions
PNAs are well established as powerful antisense molecules. Modification of the backbone with phosphonic ester side chains further improves their properties and allows the efficient knock down of a single gene in fish embryos.
doi:10.1186/1472-6750-12-50
PMCID: PMC3469332  PMID: 22901024
PNA; Knock down; Medaka; Six3
3.  Inhibition of Human Immunodeficiency Virus Replication by Cell Membrane–Crossing Oligomers 
Molecular Medicine  2011;18(1):111-122.
Although rapidly becoming a valuable tool for gene silencing, regulation or editing in vitro, the direct transfer of small interfering ribonucleic acids (siRNAs) into cells is still an unsolved problem for in vivo applications. For the first time, we show that specific modifications of antisense oligomers allow autonomous passage into cell lines and primary cells without further adjuvant or coupling to a cell-penetrating peptide. For this reason, we termed the specifically modified oligonucleotides “cell membrane–crossing oligomers” (CMCOs). CMCOs targeted to various conserved regions of human immunodeficiency virus (HIV)-1 were tested and compared with nontargeting CMCOs. Analyses of uninfected and infected cells incubated with labeled CMCOs revealed that the compounds were enriched in infected cells and some of the tested CMCOs exhibited a potent antiviral effect. Finally, the CMCOs did not exert any cytotoxicity and did not inhibit proliferation of the cells. In vitro, our CMCOs are promising candidates as biologically active anti-HIV reagents for future in vivo applications.
doi:10.2119/molmed.2011.00128
PMCID: PMC3276398  PMID: 22105607
4.  Does Methylphenidate Cause a Cytogenetic Effect in Children with Attention Deficit Hyperactivity Disorder? 
Environmental Health Perspectives  2007;115(6):936-940.
Background and objective
Attention deficit hyperactivity disorder (ADHD) is the most common psychiatric disorder in children and adolescents (6–12% affected). Treatment with methylphenidate (MPH) in the United States has increased to a current prescription rate of > 5 million per year. However, a 2005 study by El-Zein and co-workers [Cancer Lett 230:284–291] reporting a 3-fold increase in genomic damage in all 12 analyzed children after 3 months of therapy with MPH resulted in much concern about potential carcinogenic effects. Here we provide new information concerning the cytogenetic effect of MPH in children.
Design, participants, and methods
In a prospective study, we analyzed the genomic damage in children with ADHD (initial sample size 38 children) before and 1 (30 children), 3 (21 children), and 6 (8 children) months after initiation of MPH therapy. In addition, we investigated a group of 9 children receiving chronic MPH therapy. Patients were recruited within a study of our Clinical Research Group on ADHD in the Department of Child and Adolescent Psychiatry and Psychotherapy of the University of Würzburg. Assessment and treatment of patients were performed during inpatient or outpatient health care. The measure for genomic damage was the frequency of micronuclei, a subset of chromosomal aberrations, in peripheral lymphocytes.
Results
MPH treatment resulted in no significant alteration in the micronucleus frequency.
Conclusions
Because the findings published in 2005 by El-Zein and co-workers could not be replicated, the concern regarding a potential increase in the risk of developing cancer later in life after long-term MPH treatment is not supported.
doi:10.1289/ehp.9866
PMCID: PMC1892117  PMID: 17589603
ADHD; cytogenetic effects; methylphenidate; micronuclei; psychostimulants

Results 1-4 (4)