Microfibre ankle high support socks from Propeds, giving you the soft and comfortable fit. Small criss-cross fishnet mesh fashion design. Tailored to stay in place and to retain shape. Great with loafers, sneakers and high-cut shoes. Quick dry. Microfibre provides a drapeable, soft and comfortable fit. Color chart. Colors Peach,Suntan. Freesize. Price: USD5.21

Informational article on Meryl® microfiber, a well known Nylstar speciality. The fineness of each filament (less than 10µ) is characterised by soft handle, breathability and resistance to wind and rain.

A new collection of microfibre full support pantyhose by GaLeries®. Full support with mild compression benefits for tired legs. Enhanced with Microfiber yarn to give a soft-feel and resilient support. Seamless sheer to waist. Sandal toe.

Gabriella deluxe opaque tights with microfiber in 80 denier. Braided with LYCRA® for greater elasticity and durability.

Sheer to waist. Flat seam. Semi sheer when stretched.

Size 2 to 5. See sizechart at:
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Music Legs® Opaque tights in microfibre.

Onesize (5'~5'10", 100~175lbs).

Mielofibrosis y su relación con la médula ósea.

Cuidados de la fibrosis pulmonar idiopática.

Colombia logra conectividad de fibra óptica con Brasil en el Amazonas

K Schoonjans
May 1, 1996; 37:907-925
Reviews

Systemic antibody light chains (AL) amyloidosis is characterized by deposition of amyloid fibrils derived from a particular antibody light chain. Cardiac involvement is a major risk factor for mortality. Using MAS solid-state NMR, we studied the fibril structure of a recombinant light chain fragment corresponding to the fibril protein from patient FOR005, together with fibrils formed by protein sequence variants that are derived from the closest germline (GL) sequence. Both analyzed fibril structures were seeded with ex-vivo amyloid fibrils purified from the explanted heart of this patient. We find that residues 11-42 and 69-102 adopt β-sheet conformation in patient protein fibrils. We identify arginine-49 as a key residue that forms a salt bridge to aspartate-25 in the patient protein fibril structure. In the germline sequence, this residue is replaced by a glycine. Fibrils from the GL protein and from the patient protein harboring the single point mutation R49G can be both heterologously seeded using patient ex-vivo fibrils. Seeded R49G fibrils show an increased heterogeneity in the C-terminal residues 80-102, which is reflected by the disappearance of all resonances of these residues. By contrast, residues 11-42 and 69-77, which are visible in the MAS solid-state NMR spectra, show 13Cα chemical shifts that are highly like patient fibrils. The mutation R49G thus induces a conformational heterogeneity at the C terminus in the fibril state, whereas the overall fibril topology is retained. These findings imply that patient mutations in FOR005 can stabilize the fibril structure.

Neurodegeneration in Parkinson's disease (PD) can be recapitulated in animals by administration of α-synuclein preformed fibrils (PFFs) into the brain. However, the mechanism by which these PFFs induce toxicity is unknown. Iron is implicated in PD pathophysiology, so we investigated whether α-synuclein PFFs induce ferroptosis, an iron-dependent cell death pathway. A range of ferroptosis inhibitors were added to a striatal neuron-derived cell line (STHdhQ7/7 cells), a dopaminergic neuron–derived cell line (SN4741 cells), and WT primary cortical neurons, all of which had been intoxicated with α-synuclein PFFs. Viability was not recovered by these inhibitors except for liproxstatin-1, a best-in-class ferroptosis inhibitor, when used at high doses. High-dose liproxstatin-1 visibly enlarged the area of a cell that contained acidic vesicles and elevated the expression of several proteins associated with the autophagy-lysosomal pathway similarly to the known lysosomal inhibitors, chloroquine and bafilomycin A1. Consistent with high-dose liproxstatin-1 protecting via a lysosomal mechanism, we further de-monstrated that loss of viability induced by α-synuclein PFFs was attenuated by chloroquine and bafilomycin A1 as well as the lysosomal cysteine protease inhibitors, leupeptin, E-64D, and Ca-074-Me, but not other autophagy or lysosomal enzyme inhibitors. We confirmed using immunofluorescence microscopy that heparin prevented uptake of α-synuclein PFFs into cells but that chloroquine did not stop α-synuclein uptake into lysosomes despite impairing lysosomal function and inhibiting α-synuclein toxicity. Together, these data suggested that α-synuclein PFFs are toxic in functional lysosomes in vitro. Therapeutic strategies that prevent α-synuclein fibril uptake into lysosomes may be of benefit in PD.

En France, environ 2 à 4 % de la population, souvent des femmes, est touchée par la fibromyalgie. Mais en réalité, qu’est-ce que la fibromyalgie ? Quelles sont les astuces naturelles permettant de soulager les patients qui présentent des symptômes de cette maladie ? Quels sont les symptômes de la fibromyalgie ? La fibromyalgie, ou syndrome fibromyalgique, […]

L’article Quelques remèdes de grand-mère pour soulager les symptômes de la fibromyalgie est apparu en premier sur Ortho Doc France.

Oct. 25, 2024 — Aggregation of proteins underlies many human disorders, including Alzheimer’s. Teams from the New Jersey Institute of Technology and Princeton University joined forces to study how the amyloid […]

The post PSC: Anton Simulations Reveal How Alzheimer’s Fibril Growth May Accelerate appeared first on HPCwire.

Bharat Sanchar Nigam Limited (BSNL) has announced the launch of the first fibre-based intranet TV service in select regions in India. This service, dubbed IFTV, was first introduced last month alongside the unveiling of the state-owned telecommunications provider’s new logo and six other new facilities.

Calculations show that nerve fibres in the brain could emit pairs of entangled particles, and this quantum phenomenon might explain how different parts of the brain work together

The networks of fibre optic cables that criss-cross the planet could be used to better understand what’s happening inside it

Fibres in wet wipes and clothes often make their way into soil - and natural versions could be more damaging than synthetic ones

Title: Study: Acupuncture Helps Fibromyalgia
Category: Health News
Created: 8/25/2005 12:00:00 AM
Last Editorial Review: 8/25/2005 12:00:00 AM

Title: Gene Mutation Found in Uterine Fibroids
Category: Health News
Created: 8/26/2011 11:01:00 AM
Last Editorial Review: 8/26/2011 12:00:00 AM

Title: Health Tip: Living With Fibromyalgia
Category: Health News
Created: 8/30/2012 8:05:00 AM
Last Editorial Review: 8/30/2012 12:00:00 AM

Title: New Defibrillator Works Without Wires Touching Heart
Category: Health News
Created: 8/26/2013 4:36:00 PM
Last Editorial Review: 8/27/2013 12:00:00 AM

Title: Gene Study Helps Advance Diagnosis of Cystic Fibrosis
Category: Health News
Created: 8/26/2013 2:36:00 PM
Last Editorial Review: 8/27/2013 12:00:00 AM

Title: Use of Cancer-Linked Fibroid Device Declines After FDA Warning
Category: Health News
Created: 8/23/2016 12:00:00 AM
Last Editorial Review: 8/24/2016 12:00:00 AM

Title: Many U.S. Women Unaware of Fibroid Treatments: Poll
Category: Health News
Created: 8/29/2017 12:00:00 AM
Last Editorial Review: 8/30/2017 12:00:00 AM

Title: fenofibrate
Category: Medications
Created: 3/30/2022 12:00:00 AM
Last Editorial Review: 3/30/2022 12:00:00 AM

The prognosis of people with cystic fibrosis (pwCF) has improved dramatically with the introduction of cystic fibrosis transmembrane conductance regulator (CFTR) modulators (CFTRm). The ageing of the cystic fibrosis (CF) population is changing the disease landscape with the emergence of different needs and increasing comorbidities related to both age and long-term exposure to multiple treatments including CFTRm. Although the number of pwCF eligible for this treatment is expected to increase, major disparities in care and outcomes still exist in this population. Moreover, the long-term impact of the use of CFTRm is still partly unknown due to the current short follow-up and experience with their use, thus generating some uncertainties. The future spread and initiation of these drugs at an earlier stage of the disease is expected to reduce the systemic burden of systemic inflammation and its consequences on health. However, the prolonged life expectancy is accompanied by an increasing burden of age-related comorbidities, especially in the context of chronic disease. The clinical manifestations of the comorbidities directly or indirectly associated with CFTR dysfunction are changing, along with the disease dynamics and outcomes. Current protocols used to monitor slow disease progression will need continuous updates, including the composition of the multidisciplinary team for CF care, with a greater focus on the needs of the adult population.

Extract

In cystic fibrosis (CF), Pseudomonas aeruginosa acquisition represents a turning point in disease progression. The presence of chronic P. aeruginosa infection is associated with worsening lung function and increased risk of earlier death, whereas treatment substantially improves lung function and survival [1, 2]. Efforts to diagnose and eradicate early P. aeruginosa provide lasting benefits for children with CF [3, 4]. However, the timing of infection varies considerably between individuals with CF, treatment centres [5, 6], and different birth cohorts of people with the disease [7, 8].

Background

Pseudomonas aeruginosa is a common pathogen that contributes to progressive lung disease in cystic fibrosis (CF). Genetic factors other than CF-causing CFTR (CF transmembrane conductance regulator) variations contribute ~85% of the variation in chronic P. aeruginosa infection age in CF according to twin studies, but the susceptibility loci remain unknown. Our objective is to advance understanding of the genetic basis of host susceptibility to P. aeruginosa infection.

Oxidative stress, fibrosis, and inflammasome activation from advanced glycation end product (AGE)–receptor of advanced glycation end product (RAGE) interaction contribute to diabetic cardiomyopathy (DCM) formation and progression. Our study revealed the impact of β-caryophyllene (BCP) on activating cannabinoid type 2 receptors (CB2Rs) against diabetic complication, mainly cardiomyopathy and investigated the underlying cell signaling pathways in mice. The murine model of DCM was developed by feeding a high-fat diet with streptozotocin injections. After the development of diabetes, the animals received a 12-week oral BCP treatment at a dose of 50 mg/kg/body weight. BCP treatment showed significant improvement in glucose tolerance and insulin resistance and enhanced serum insulin levels in diabetic animals. BCP treatment effectively reversed the heart remodeling and restored the phosphorylated troponin I and sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a expression. Ultrastructural examination showed reduced myocardial cell injury in DCM mice treated with BCP. The preserved myocytes were found to be associated with reduced expression of AGE/RAGE in DCM mice hearts. BCP treatment mitigated oxidative stress by inhibiting expression of NADPH oxidase 4 and activating phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/nuclear factor erythroid 2–related factor 2 (Nrf2) signaling. Also, BCP suppressed cardiac fibrosis and endothelial-to-mesenchymal transition in DCM mice by inhibiting transforming growth factor β (TGF-β)/suppressor of mothers against decapentaplegic (Smad) signaling. Further, BCP treatment suppressed nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome activation in DCM mice and alleviated cellular injury to the pancreatic tissues evidenced by significant elevation of the number of insulin-positive cells. To demonstrate a CB2R-dependent mechanism of BCP, another group of DCM mice were pretreated with AM630, a CB2R antagonist. AM630 was observed to abrogate the beneficial effects of BCP in DCM mice. Taken together, BCP demonstrated the potential to protect the myocardium and pancreas of DCM mice mediating CB2R-dependent mechanisms.

Chronic hypertension leads to injury and fibrosis in major organs. Fibroblast activation protein (FAP) is one of key molecules in tissue fibrosis, and ⁶⁸Ga-labeled FAP inhibitor-46 (FAPI46) PET is a recently developed method for evaluating FAP. The aim of this study was to evaluate FAP expression and fibrosis in a hypertension model and to test the feasibility of ⁶⁸Ga-FAPI46 PET in hypertension. Methods: Hypertension was induced in mice by angiotensin II infusion for 4 wk. ⁶⁸Ga-FAPI46 biodistribution studies and PET scanning were conducted at 1, 2, and 4 wk after hypertension modeling, and uptake in the major organs was measured. The FAP expression and fibrosis formation of the heart and kidney tissues were analyzed and compared with ⁶⁸Ga-FAPI46 uptake. Subgroups of the hypertension model underwent angiotensin receptor blocker administration and high-dose FAPI46 blocking, for comparison. As a preliminary human study, ⁶⁸Ga-FAPI46 PET images of lung cancer patients were analyzed and compared between hypertension and control groups. Results: Uptake of ⁶⁸Ga-FAPI46 in the heart and kidneys was significantly higher in the hypertension group than in the sham group as early as week 1 and decreased after week 2. The uptake was specifically blocked in the high-dose blocking study. Immunohistochemistry also revealed FAP expression in both heart and kidney tissues. However, overt fibrosis was observed in the heart, whereas it was absent from the kidneys. The angiotensin receptor blocker–treated group showed lower uptake in the heart and kidneys than did the hypertension group. In the pilot human study, renal uptake of ⁶⁸Ga-FAPI46 significantly differed between the hypertension and control groups. Conclusion: In hypertension, FAP expression is increased in the heart and kidneys from the early phases and decreases over time. FAP expression appears to represent fibrosis activity preceding or underlying fibrotic tissue formation. ⁶⁸Ga-FAPI46 PET has potential as an effective imaging method for evaluating FAP expression in progressive fibrosis by hypertension.

Two runners saved by the same public defibrillator appeal for all the life-saving devices to be publicly available. Tens of thousands of defibs are unregistered so ‘invisible’ in an emergency.

Fibres in wet wipes and clothes often make their way into soil - and natural versions could be more damaging than synthetic ones

Wearable devices like smart watches and health trackers can adversely affect health and increase medlinkanxiety/medlink among patients with irregular heart rhythm.

Doctors at King George's Medical University (KGMU) have successfully removed a massive four-kg fibroid (!--ref1--) tumor from the uterus of a 30-year-old woman.

Defibrillators can now save lives while consuming 1,000 times less power, according to a new study. The findings of the study are published in a paper i Chaos/i, by AIP Publishing (!--ref1--).

Anti-Fibrotic Data from Amira Pharmaceuticals' LPA1 Receptor Antagonist Program Published in the British Journal of Phar