First Clinical Experience With Targeted REnal Nerve Demodulation (TREND-1) Using a Neurotropic Agent for the Treatment of Sympathetic Hypertension.

Aims: To evaluate the feasibility and safety of a novel targeted neuromodulatory treatment for sympathetic hypertension involving a one-time local injection of neurotropic agents near renal nerves.

Methods And Results: Seven patients suffering from uncontrolled hypertension per ESH-ESC guidelines were treated using a single dose of NW2013, a neurotropic Na+/K+ ATPase antagonist. A microneedle catheter was used to administer 1.

Safety and efficacy of local periadventitial delivery of sirolimus for improving hemodialysis graft patency: first human experience with a sirolimus-eluting collagen membrane (Coll-R).

Background: Neointimal hyperplasia causes a high rate of hemodialysis synthetic graft failure. Thus, therapies that inhibit neointimal hyperplasia are urgently needed. The Coll-R is a sirolimus-eluting collagen matrix designed for intra-operative perivascular implantation around the graft-venous anastomosis.

Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's disease.

Increased oxidative stress is implicated in the pathogenesis of Alzheimer's disease (AD). A large body of evidence suggests that mitochondrial dysfunction and increased reactive oxygen species occur prior to amyloid-β (Aβ) deposition. Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is well characterized as a neuroprotective antioxidant in animal models and human trials of Huntington's disease and Parkinson's disease, and reduces plaque burden in AβPP/PS1 mice.

Endovascular treatment of stenosis of autogenous arteriovenous access for hemodialysis.

Retrospectively review of long-term outcome of balloon angioplasty (TBA) in the treatment of native dialysis A-V fistulae stenosis was conducted. From February 2008 to January 2009, seven hemodialysis patients (5 women and 2 men; mean age 46.4 years) were treated for stenosis of the A-V fistula at the venous outflow tract.

[Multispiral computed tomography-assisted angiography in diagnosis of diseases of the aorta and lower limb arteries].

Purpose Of The Study: Our work was aimed at determining the diagnostic value of multislice computed tomography-assisted angiography in atherosclerotic lesions of the aorta and arteries of the lower limbs, taking into consideration the condition of the peripheral bed, as well as at making an angiographic assessment of the quality of the reconstructive operations performed.

Material And Methods: Over the period from October 2005 to July 2006, multispiral computed tomography-assisted angiography (hereinafter referred to as MSCTA) followed by an operative intervention was carried out in a total of 59 patients who were diagnosed with diseases of the aorta and arteries of the lower extremities. The average age of the patients was 59.

Matrix metalloproteinase-9 regulates TNF-alpha and FasL expression in neuronal, glial cells and its absence extends life in a transgenic mouse model of amyotrophic lateral sclerosis.

Whether increased levels of matrix metalloproteinases (MMPs) correspond to a role in the pathogenesis of amyotrophic lateral sclerosis (ALS) needs to be determined and it is actively being pursued. Here we present evidence suggesting that MMP-9 contributes to the motor neuron cell death in ALS. We examined the role of MMP-9 in a mouse model of familial ALS and found that lack of MMP-9 increased survival (31%) in G93A SOD1 mice.

Celastrol blocks neuronal cell death and extends life in transgenic mouse model of amyotrophic lateral sclerosis.

There is substantial evidence that both inflammation and oxidative damage contribute to the pathogenesis of motor neuron degeneration in the G93A SOD1 transgenic mouse model of amyotrophic lateral sclerosis (ALS). Celastrol is a natural product from Southern China, which exerts potent anti-inflammatory and antioxidative effects. It also acts potently to increase expression of heat shock proteins including HSP70.

[Effect of patients' preoperative condition on the outcome of the surgical repair of the infrarenal abdominal aortic aneurism].

During the past decades there is an evidence of the increase in the number of patients with the aneurism of the infrarenal abdominal aorta (IRAAA). As a rule, there is an increased operative risk among these patients due to presence of concomitant diseases. The aim of this study was to investigate effect of patients' preoperative condition on the outcome after the surgical repair of the IRAAA.

Thalidomide and lenalidomide extend survival in a transgenic mouse model of amyotrophic lateral sclerosis.

Accumulating evidence suggests that inflammation plays a major role in the pathogenesis of motor neuron death in amyotrophic lateral sclerosis (ALS). Important mediators of inflammation such as the cytokine tumor necrosis factor-alpha (TNF-alpha) and its superfamily member fibroblast-associated cell-surface ligand (FasL) have been implicated in apoptosis. We found increased TNF-alpha and FasL immunoreactivity in lumbar spinal cord sections of ALS patients and G93A transgenic mice.

Neural mitochondrial Ca2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn-superoxide dismutase mutant mice.

Mitochondrial respiratory chain dysfunction, impaired intracellular Ca2+ homeostasis and activation of the mitochondrial apoptotic pathway are pathological hallmarks in animal and cellular models of familial amyotrophic lateral sclerosis associated with Cu/Zn-superoxide dismutase mutations. Although intracellular Ca2+ homeostasis is thought to be intimately associated with mitochondrial functions, the temporal and causal correlation between mitochondrial Ca2+ uptake dysfunction and motor neuron death in familial amyotrophic lateral sclerosis remains to be established. We investigated mitochondrial Ca2+ handling in isolated brain, spinal cord and liver of mutant Cu/Zn-superoxide dismutase transgenic mice at different disease stages.

Additive neuroprotective effects of a histone deacetylase inhibitor and a catalytic antioxidant in a transgenic mouse model of amyotrophic lateral sclerosis.

ALS is a devastating neurodegenerative disorder for which no effective treatment exists. Multiple molecular mechanisms are involved in the pathogenesis. We tested the catalytic antioxidant AEOL 10150, the histone deacetylase inhibitor phenylbutyrate (PBA), and the combination of PBA and AEOL 10150 in the G93A transgenic mouse model, administered from disease onset.

Protection from Alzheimer's-like disease in the mouse by genetic ablation of inducible nitric oxide synthase.

Brains from subjects who have Alzheimer's disease (AD) express inducible nitric oxide synthase (iNOS). We tested the hypothesis that iNOS contributes to AD pathogenesis. Immunoreactive iNOS was detected in brains of mice with AD-like disease resulting from transgenic expression of mutant human beta-amyloid precursor protein (hAPP) and presenilin-1 (hPS1).

Integrative role of cPLA with COX-2 and the effect of non-steriodal anti-inflammatory drugs in a transgenic mouse model of amyotrophic lateral sclerosis.

Cyclooxygenase-2 (COX-2) is a key molecule in the inflammatory pathway in amyotrophic lateral sclerosis (ALS). Cytosolic phospholipase A (cPLA2) is an important enzyme providing substrate for cyclooxygenases. We therefore examined cPLA2 expression in human ALS and mutant Cu/Zn superoxide dismutase (SOD1) transgenic mice and its relation to COX-2.

Peroxisome proliferator-activated receptor-gamma agonist extends survival in transgenic mouse model of amyotrophic lateral sclerosis.

Accumulating evidence suggests that inflammation plays a major role in the pathogenesis of motoneuron death in amyotrophic lateral sclerosis (ALS) both in humans and transgenic mouse models. Peroxisome proliferator-activated receptors (PPARs) are involved in the inflammatory process. Agonists of PPAR-alpha, -gamma, and -delta show anti-inflammatory effects both in vitro and in vivo.

Therapeutic angiogenesis for patients with limb ischemia by utilization of fibrin meshwork. Pilot randomized controlled study.

Aim: The aim of this paper is to assess the feasibility and efficacy of fibrin in inducing neovascularization as an angiogenic substance and/or carrier for vascular endothelial growth factor (VEGF) in patients with limb ischemia.

Methods: Twenty-three patients with limb ischemia and referred for below the knee amputations were randomized for treatment: group 1, 7 patients received only a saline injection; group 2, 9 received intramuscular injection of fibrin and group 3, 7 received the fibrin composition with deferoxamine and added VEGF(165). The fibrin meshwork was introduced into the popliteal area of the diseased limbs using a dual syringe system (1 contained thrombin solution [1 mg, 5000 U] and 1 contained fibrinogen [1 mg, Baxter Hyland Immuno] solution).

[Diagnosis and surgical treatment of renovascular hypertension in patients with a single kidney].

The study is based on an analysis of the results in operative treatment of 55 patients with vasorenal hypertension, when a functional single kidney is existing. The examinations showed that in the majority of patients function of the kidneys and renin activity in the peripheral blood were normal. The operation performed most frequently in this group of patients were the transaortal endarterectomy by means of the turning-up technique and the resection of the renal arteries with following reimplantation into the aorta or the end-to-end anastomosis.

[Our experience with the surgical treatment of renovascular hypertension].

The experience with 785 operations performed for the period from 1962 to 1983 on 697 patients is presented. The advantage of direct reconstructive operations over restorative interventions with the employment of explantation materials is proved. In the remote period after operation positive results were noted in 85% of patients with fibrose-muscular dysplasia of renal arteries and in 70% of patients with non-specific aorto-arteritis.