Panum Institute

About: Panum Institute is a based out in . It is known for research contribution in the topics: Peptide nucleic acid & Nucleic acid. The organization has 857 authors who have published 998 publications receiving 69046 citations.

Sequence-selective recognition of DNA by strand displacement with a thymine-substituted polyamide

Abstract: A polyamide nucleic acid (PNA) was designed by detaching the deoxyribose phosphate backbone of DNA in a computer model and replacing it with an achiral polyamide backbone. On the basis of this model, oligomers consisting of thymine-linked aminoethylglycyl units were prepared. These oligomers recognize their complementary target in double-stranded DNA by strand displacement. The displacement is made possible by the extraordinarily high stability of the PNA-DNA hybrids. The results show that the backbone of DNA can be replaced by a polyamide, with the resulting oligomer retaining base-specific hybridization.

PNA hybridizes to complementary oligonucleotides obeying the Watson–Crick hydrogen-bonding rules

Abstract: DNA analogues are currently being intensely investigated owing to their potential as gene-targeted drugs. Furthermore, their properties and interaction with DNA and RNA could provide a better understanding of the structural features of natural DNA that determine its unique chemical, biological and genetic properties. We recently designed a DNA analogue, PNA, in which the backbone is structurally homomorphous with the deoxyribose backbone and consists of N-(2-aminoethyl)glycine units to which the nucleobases are attached. We showed that PNA oligomers containing solely thymine and cytosine can hybridize to complementary oligonucleotides, presumably by forming Watson-Crick-Hoogsteen (PNA)2-DNA triplexes, which are much more stable than the corresponding DNA-DNA duplexes, and bind to double-stranded DNA by strand displacement. We report here that PNA containing all four natural nucleobases hybridizes to complementary oligonucleotides obeying the Watson-Crick base-pairing rules, and thus is a true DNA mimic in terms of base-pair recognition.

Increased rate of force development and neural drive of human skeletal muscle following resistance training

Abstract: The maximal rate of rise in muscle force [rate of force development (RFD)] has important functional consequences as it determines the force that can be generated in the early phase of muscle contraction (0-200 ms). The present study examined the effect of resistance training on contractile RFD and efferent motor outflow ("neural drive") during maximal muscle contraction. Contractile RFD (slope of force-time curve), impulse (time-integrated force), electromyography (EMG) signal amplitude (mean average voltage), and rate of EMG rise (slope of EMG-time curve) were determined (1-kHz sampling rate) during maximal isometric muscle contraction (quadriceps femoris) in 15 male subjects before and after 14 wk of heavy-resistance strength training (38 sessions). Maximal isometric muscle strength [maximal voluntary contraction (MVC)] increased from 291.1 +/- 9.8 to 339.0 +/- 10.2 N. m after training. Contractile RFD determined within time intervals of 30, 50, 100, and 200 ms relative to onset of contraction increased from 1,601 +/- 117 to 2,020 +/- 119 (P < 0.05), 1,802 +/- 121 to 2,201 +/- 106 (P < 0.01), 1,543 +/- 83 to 1,806 +/- 69 (P < 0.01), and 1,141 +/- 45 to 1,363 +/- 44 N. m. s(-1) (P < 0.01), respectively. Corresponding increases were observed in contractile impulse (P < 0.01-0.05). When normalized relative to MVC, contractile RFD increased 15% after training (at zero to one-sixth MVC; P < 0.05). Furthermore, muscle EMG increased (P < 0.01-0.05) 22-143% (mean average voltage) and 41-106% (rate of EMG rise) in the early contraction phase (0-200 ms). In conclusion, increases in explosive muscle strength (contractile RFD and impulse) were observed after heavy-resistance strength training. These findings could be explained by an enhanced neural drive, as evidenced by marked increases in EMG signal amplitude and rate of EMG rise in the early phase of muscle contraction.

Aminoacyl-tRNA synthesis.

Abstract: Aminoacyl-tRNAs are substrates for translation and are pivotal in determining how the genetic code is interpreted as amino acids. The function of aminoacyl-tRNA synthesis is to precisely match amino acids with tRNAs containing the corresponding anticodon. This is primarily achieved by the direct attachment of an amino acid to the corresponding tRNA by an aminoacyl-tRNA synthetase, although intrinsic proofreading and extrinsic editing are also essential in several cases. Recent studies of aminoacyl-tRNA synthesis, mainly prompted by the advent of whole genome sequencing and the availability of a vast body of structural data, have led to an expanded and more detailed picture of how aminoacyl-tRNAs are synthesized. This article reviews current knowledge of the biochemical, structural, and evolutionary facets of aminoacyl-tRNA synthesis.

Normalization of fasting hyperglycaemia by exogenous glucagon-like peptide 1 (7-36 amide) in type 2 (non-insulin-dependent) diabetic patients.

Abstract: Glucagon-like peptide 1 (GLP-1) (7-36 amide) is a physiological incretin hormone that is released after nutrient intake from the lower gut and stimulates insulin secretion at elevated plasma glucose concentrations. Previous work has shown that even in Type 2 (non-insulin-dependent) diabetic patients GLP-1 (7-36 amide) retains much of its insulinotropic action. However, it is not known whether the magnitude of this response is sufficient to normalize plasma glucose in Type 2 diabetic patients with poor metabolic control. Therefore, in 10 Type 2 diabetic patients with unsatisfactory metabolic control (HbA1c 11.6 +/- 1.7%) on diet and sulphonylurea therapy (in some patients supplemented by metformin or acarbose), 1.2 pmol x kg-1 x min-1 GLP-1 (7-36 amide) or placebo was infused intravenously in the fasting state (plasma glucose 13.1 +/- 0.6 mmol/l). In all patients, insulin (by 17.4 +/- 4.7 nmol x 1-1 x min; p = 0.0157) and C-peptide (by 228.0 +/- 39.1 nmol x 1-1 x min; p = 0.0019) increased significantly over basal levels, glucagon was reduced (by -1418 +/- 308 pmol x 1-1 x min) and plasma glucose reached normal fasting concentrations (4.9 +/- 0.3 mmol/l) within 4 h of GLP-1 (7-36 amide) administration, but not with placebo. When normal fasting plasma glucose concentrations were reached insulin returned towards basal levels and plasma glucose concentrations remained stable despite the ongoing infusion of GLP-1 (7-36 amide). Therefore, exogenous GLP-1 (7-36 amide) is an effective means of normalizing fasting plasma glucose concentrations in poorly-controlled Type 2 diabetic patients.(ABSTRACT TRUNCATED AT 250 WORDS)