Carpal tunnel release can be a risk factor for trigger finger: National Health Insurance data analysis.

PURPOSE: We aimed to compare trigger finger (TF) development between patients with carpal tunnel syndrome (CTS) treated with carpal tunnel release (CTR) and those treated conservatively, using the National Health Insurance Services data of Korea. We also aimed to investigate risk factors for post-CTR TF development. METHODS: We selected CTS patients with or without CTR (3543 patients in each group) between 2002 and 2015. Sex, age, follow-up duration after CTS diagnosis, and comorbidities associated with TF-development were matched using propensity score. We compared the rates of TF diagnosis and subsequent TF operations between groups. Thereafter, we selected patients with CTS undergoing CTR, for whom minimum follow-up exceeded five years. We compared sex, age, height, weight, and comorbidities associated with TF risk factors between the TF-occurrence and non-TF-occurrence groups. RESULTS: On comparing CTR-treated patients with those treated conservatively for CTS, CTR-treated patients presented with significantly higher rates of TF diagnosis (12.2%) and TF operations (4.7%) than patients without CTR (6.2% and 1.2%, respectively). Among 433 TF-diagnosed patients and 166 TF-operated patients after CTR, most were identified < 5 years after CTR, with 379 diagnosed (87.5%) and 147 operated (88.5%) patients. A total of 240 patients presented with newly developed TF over a five year period. Patients with subsequent TF exhibited a higher female sex rate and shorter height. None of the variables was significant risk factors for TF development in logistic regression analysis. CONCLUSION: We confirmed high incidences of post-CTR TF diagnosis and operations. TF develops most frequently in the first postoperative year.

Low serum vitamin B12 levels are associated with degenerative rotator cuff tear.

BACKGROUND: Vitamin B12 (Vit B12) deficiency results in elevated homocysteine levels and interference with collagen cross-linking, which may affect tendon integrity. The purpose of this study was to investigate whether serum Vit B12 levels were correlated with degenerative rotator cuff (RC) tear. METHODS: Eighty-seven consecutive patients with or without degenerative RC tear were enrolled as study participants. Possible risk factors (age, sex, medical history, bone mineral density, and serum chemistries including glucose, magnesium, calcium, phosphorus, zinc, homocysteine, Vitamin D, Vit B12, homocysteine, and folate) were assessed. Significant variables were selected based on the results of univariate analyses, and a logistic regression model (backward elimination) was constructed to predict the presence of degenerative RC tear. RESULTS: In the univariate analysis, the group of patients with degenerative RC tear had a mean concentration of 528.4 pg/mL Vit B12, which was significantly lower than the healthy control group (627.1 pg/mL). Logistic regression analysis using Vit B12 as an independent variable revealed that Vit B12 concentrations were significantly correlated with degenerative RC tear (p = 0.044). However, Vit B12 levels were not associated with tear size. CONCLUSION: Low serum levels of Vit B12 were independently related to degenerative RC tear. Further investigations are warranted to determine if Vit B12 supplementation can decrease the risk of this condition.

Enhanced splicing correction effect by an oligo-aspartic acid-PNA conjugate and cationic carrier complexes.

Peptide nucleic acids (PNAs) are synthetic structural analogues of DNA and RNA. They recognize specific cellular nucleic acid sequences and form stable complexes with complementary DNA or RNA. Here, we designed an oligo-aspartic acid-PNA conjugate and showed its enhanced delivery into cells with high gene correction efficiency using conventional cationic carriers, such as polyethylenimine (PEI) and Lipofectamine 2000. The negatively charged oligo-aspartic acid-PNA (Asp(n)-PNA) formed complexes with PEI and Lipofectamine, and the resulting Asp(n)-PNA/PEI and Asp(n)-PNA/Lipofectamine complexes were introduced into cells. We observed significantly enhanced cellular uptake of Asp(n)-PNA by cationic carriers and detected an active splicing correction effect even at nanomolar concentrations. We found that the splicing correction efficiency of the complex depended on the kind of the cationic carriers and on the number of repeating aspartic acid units. By enhancing the cellular uptake efficiency of PNAs, these results may provide a novel platform technology of PNAs as bioactive substances for their biological and therapeutic applications.

Cloning, expression and characterization of the catalase-peroxidase (KatG) gene from a fast-growing Mycobacterium sp. strain JC1 DSM 3803.

The gene encoding a catalase-peroxidase (KatG) was cloned from chromosomal DNA of a fast-growing Mycobacterium sp. strain JC1 DSM 3803. The nucleotide sequence of a 5.7 kb EcoRI fragment containing the katG and its flanking regions was determined. The fragment (5,706 bps) contained two complete open reading frames (ORFs) encoding putative ferric uptake regulator A (FurA) and KatG proteins. The cloned gene, katG, had an ORF of 2241 nt, encoding a protein with calculated molecular mass of 81,748 Da. The furA was located in the upstream of the katG with the same transcriptional direction and there was a 38 bp gap space between them. The deduced KatG and FurA protein sequences showed significant homologies to KatG2 and Fur2 of Mycobacterium smegmatis and clustered with other mycobacterial KatG and Fur-like proteins in phylogenetic trees, respectively. The recombinant KatG overproduced in Escherichia coli was nearly indistinguishable from the native JC1 catalase-peroxidase in enzymatic properties and also possessed the resistance to organic solvents, indicating that the cloned katG truly encodes the Mycobacterium sp. JC1 catalase-peroxidase. Difference spectroscopy revealed Mn(II) binding near the haem of the KatG. Transcript analysis of the furA-katG using RT-PCR suggests that the katG is independently transcribed from the furA.