Publications by authors named "Freidin A"

The feasibility of a novel composite rubber sealing material to improve sealing under transient cooling (in a so-called blowdown scenario) is investigated here. A composite of hydrogenated nitrile butadiene rubber (HNBR) filled with Micro Encapsulated Phase Change Materials (MEPCM) is described. The fillers contain phase change materials that release heat during the phase transformation from liquid to solid while cooling.

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Glucocorticoids are widely used as therapeutic agents to treat immune-mediated diseases in humans because of their anti-inflammatory and immunosuppressive effects. However, glucocorticoids have various adverse effects, in particular rapid and pronounced bone loss associated with fractures in glucocorticoid-induced osteoporosis, a common form of secondary osteoporosis. In zebrafish, which are increasingly used to study processes of bone regeneration and disease, glucocorticoids show detrimental effects on bone tissue; however, the underlying cellular mechanisms are incompletely understood.

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Introduction: Understanding the factors affecting success of extracorporeal shockwave lithotripsy (SWL) would improve informed decision-making on the most appropriate treatment modality for an individual patient. Although stone size and skin-to-stone distance do correlate with fragmentation efficacy, it has been shown that stone composition and architecture, as reflected by structural heterogeneity on CT, are also important factors. This study aims to determine if CT texture analysis (CTTA), a novel, nondestructive, and objective tool that generates statistical metrics reflecting stone heterogeneity, could have utility in predicting likelihood of SWL success.

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Heterozygous germline gain-of-function mutations of G-protein subunit α (Gα), a signaling partner for the calcium-sensing receptor (CaSR), result in autosomal dominant hypocalcemia type 2 (ADH2). ADH2 may cause symptomatic hypocalcemia with low circulating parathyroid hormone (PTH) concentrations. Effective therapies for ADH2 are currently not available, and a mouse model for ADH2 would help in assessment of potential therapies.

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Objective: To investigate whether molecules found to be up-regulated within hours of surgical joint destabilization in the mouse are also elevated in the analogous human setting of acute knee injury, how this molecular response varies between individuals, and whether it is related to patient-reported outcomes in the 3 months after injury.

Methods: Seven candidate molecules were analyzed in blood and synovial fluid (SF) from 150 participants with recent structural knee injury at baseline (<8 weeks from injury) and in blood at 14 days and 3 months following baseline. Knee Injury and Osteoarthritis Outcome Score 4 (KOOS4 ) was obtained at baseline and 3 months.

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The treatment of autoimmune disorders has been revolutionised by the introduction of biologics such as anti-tumour necrosis factor (anti-TNF). Although in rheumatoid arthritis patients a bone sparing effect of anti-TNF has been shown, the mechanism is not fully understood. Anti-TNF molecules block tumour necrosis factor (TNF) and prevent signalling via both TNF receptor 1 (TNFR1; p55) and TNF receptor 2 (TNFR2; p75).

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Article Synopsis
  • * Research shows that GSL synthesis is crucial for osteoclast activation in MM, and myeloma cells produce GSLs that enhance this activation, particularly GM3.
  • * Inhibiting GSL synthesis with drugs like NB-DNJ can prevent OC development, reduce bone damage in MM cases, and shows promise for treating osteolytic bone diseases.
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The mechanism by which trauma initiates healing remains unclear. Precise understanding of these events may define interventions for accelerating healing that could be translated to the clinical arena. We previously reported that addition of low-dose recombinant human TNF (rhTNF) at the fracture site augmented fracture repair in a murine tibial fracture model.

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Objective: DIP joint OA is common but has few cost-effective, evidence-based interventions. Pain and deformity [radial or ulnar deviation of the joint or loss of full extension (extension lag)] frequently lead to functional and cosmetic issues. We investigated whether splinting the DIP joint would improve pain, function and deformity.

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Objectives: To test the sensitivity to change of ultrasonographic endpoints in early phase clinical trials in subjects with active rheumatoid arthritis (RA).

Methods: A double-blind, placebo and comparator controlled, randomised, two-centre study investigated the effect on synovial thickness and vascularity of 28 days repeat daily oral dosing of 60 mg of the inducible nitric oxide synthase inhibitor GW274150 or 7.5 mg prednisolone in RA.

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Objective: Bone formation and destruction are usually tightly linked; however, in disorders such as rheumatoid arthritis, periodontal disease, and osteoporosis, elevated osteoclast activity leads to bone destruction. Osteoclast formation and activation are controlled by many signaling pathways, including p38 MAPK. Dual-specificity phosphatase 1 (DUSP-1) is a factor involved in the negative regulation of p38 MAPK.

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With an aging population, skeletal fractures are increasing in incidence, including the typical closed and the less common open fractures in normal bone, as well as fragility fractures in patients with osteoporosis. For the older age group, there is an urgent unmet need to induce predictable bone formation as well as improve implant fixation in situations such as hip joint replacement. Using a murine model of slow-healing fractures, we have previously shown that coverage of the fracture with muscle accelerated fracture healing and increased union strength.

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Purpose: Objective outcomes data after excision of the distal ulna in rheumatoid arthritis are lacking. The aim of this study was to evaluate the functional results of this surgery in the long term.

Methods: We prospectively collected data on range of motion (22 wrists), visual analog pain scores (14 wrists), and grip strength measured using a Jamar dynamometer (20 hands) in a group of 23 patients (26 wrists) preoperatively and at 3 months, 12 months, and a minimum of 5 years postoperatively (range, 5.

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It has been shown by affinity chromatography on calmodulin-sepharose that transducin, a G protein of bovine retinal rod outer segments interacts with Ca(2+)-calmodulin. This result assumes that the main part of calmodulin in dark retinal rod outer segments is associated with transducin. It has been suggested that photoactivation of retinal rods induces changes in intracellular calmodulin concentration, which may be one of the steps involved in the light adaptation of photoreceptor.

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At least two kinetically different kinds of calcium current are shown to exist in the frog atrial cells. The current with faster activation kinetics is usually depressed by insulin. Insulin also increases the amplitude of the slower calcium current.

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The inhibitory effect of insulin on Ca2+-current was supposed to be due to activation of phosphoproteinphosphotases stimulated by a specific intracellular insulin messenger. The results obtained support the above suggestion. Pretreatment of myocardial preparation with cycloheximide in low concentrations completely blocks the inhibitory insulin effect on Ca2+-current due, probably, to a decrease in peptide formation.

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The experiments on frog atra tuberculae revealed that insulin could induce biphasic changes of calcium currents of different directions. The current is inhibited with hormone due to a decrease both in the conductivity of channel system and reversal potential. In some cases prior to inhibition of calcium current, a short rise of this current occurred (3-6 min) induced by increased reversal potential.

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Low voltage myocardial automaticity (LVA) was investigated by pharmacological modulations of the presynaptic and postsynaptic processes. The sensitivity of LVA both to inhibitor and stimulator of neurotransmitter release suggests its involvement in LVA genesis. Moreover, LVA is blocked by the inhibition of the cyclic AMP system, supporting the participation of the c-AMP-dependent membrane phosphorylation in calcium-mediated cardiac electrogenesis.

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