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What Is Diabetic Myopathy?

Diabetic Myopathy Causes Muscular Degeneration

Diabetic Myopathy Causes Muscular Degeneration

Welcome to Health Clover for Good Fortune in Health Diabetic Myopathy Causes Muscular Degeneration Myopathy is a systemic muscular disease which causes muscle fibers not to work properly and causes general muscle weakness in the area that it is affecting. Myopathy may also cause muscle inflammation, spasms, and even paralysis. There are many different causes of myopathy, but when the condition is caused by persistent high glucose levels it is referred to as diabetic myopathy. It should not be confused with neuropathy which is used to describe damage and degeneration of nerve tissue, whereas myopathy refers to malfunction and degeneration of muscle tissue. As diabetes progresses, sufferers often notice that their muscle strength deteriorates, which is sometimes localized to one or more areas of the body, and sometimes across the body as a whole. The condition may manifest itself as muscle spasms or trembling in certain parts of the body such as the feet and hands. Myopathy associated with diabetes mellitus is fairly rare and there is scant research available on the topic at this time. Because the condition is systemic and often progresses, it is important to see your doctor to work out a proper treatment plan that is tailored to your specific symptoms and needs. Continue reading >>

Diabetic Myopathy | Diabetes Forum The Global Diabetes Community

Diabetic Myopathy | Diabetes Forum The Global Diabetes Community

Diabetes Forum The Global Diabetes Community This site uses cookies. By continuing to use this site, you are agreeing to our use of cookies. Learn More. Get the Diabetes Forum App for your phone - available on iOS and Android . Find support, ask questions and share your experiences. Join the community Have just returned from the rheumatologist and he thinks i may have Diabetic Myopathy. I have to go for further tests on the nerves although he did a basic test and said the nerves seem ok, however, my my right leg is that of an 80 year old as the muscle wastage is so severe. I also have osteoarthritis in both knees and hips. I am having trouble finding any information about this and if anyone has any experiance of it or if it can be reversed i would be really grateful, Thanks x Can I ask whether you are taking statins? The reason I ask is that muscle wasting is a known side effect (albeit relatively rare) of certain statins. HI,just a bit of information about joint or muscle pain.I was prescribed sitigliptin alongside metformin due to my bg being 8.1%.Have been type 2 for 5 years.Within days of taking the sitigliptin I experienced really bad pains in my shoulder-knees-wrists and worst of all my hips.Continued with the sitigliptin for another 3 weeks then went to GP who told me to stop taking sitigliptin and just continue with the metformin.Again within days the pains had vanished apart from what appeared to be a trapped nerve in my shoulder.But is it a trapped nerve.I take simvastatin 40mg and have done for 7 years so does anyone think,as I do,it could be myopathy caused by the simvastatin.Have mentioned this to GP but all he has done is refer me to physiotherapy. Continue reading >>

Proximal Diabetic Neuropathy

Proximal Diabetic Neuropathy

Proximal diabetic neuropathy, more commonly known as diabetic amyotrophy, is a nerve disorder that results as a complication of diabetes mellitus. It can affect the thighs, hips, buttocks or lower legs. Proximal diabetic neuropathy is a peripheral nerve disease (diabetic neuropathy) characterized by muscle wasting or weakness, pain, or changes in sensation/numbness of the leg.[1] Diabetic neuropathy is an uncommon complication of diabetes. It is a type of lumbosacral plexopathy, or adverse condition affecting the lumbosacral plexus. There are a number of ways that diabetes damages the nerves, all of which seem to be related to increased blood sugar levels over a long period of time. Proximal diabetic neuropathy is one of four types of diabetic neuropathy.[2] Proximal diabetic neuropathy can occur in type 2 and type 1 diabetes mellitus patients however, it is most commonly found in type 2 diabetics.[3] Proximal neuropathy is the second most common type of diabetic neuropathy and can be resolved with time and treatment.[4] Signs & symptoms[edit] Signs and symptoms of proximal diabetic neuropathy depend on the region of the plexus which is affected. The first symptom is usually pain in the buttocks, hips, thighs or legs. This pain most commonly affects one side of the body and can either start gradually or come on suddenly. This is often followed by variable weakness in the proximal muscles of the lower limbs. These symptoms, although often beginning on one side, can also spread to both sides.[1] Weakness in proximal diabetic neuropathy is caused by denervation of the specific muscles innervated by regions of the plexus affected and can thus these muscles may start exhibiting fasciculations. Note that diabetic amyotrophy is a condition caused by diabetes mellitus, but sepa Continue reading >>

What Is Diabetic Myopathy? | Diabetes Healthy Solutions

What Is Diabetic Myopathy? | Diabetes Healthy Solutions

Therefore, myopathy is a systemic disease caused by neuropathy (nerve damage) that impairs proper functioning of muscle fibers causing general muscle weakness in affected areas. Myopathy also causes muscle spasms, inflammation and paralysis. Diabetes sufferers may notice deterioration in the strength of their muscles as the disease progresses which may be localized in one area or across various parts of the body. Signs and symptoms of vary among individuals and they may be very mild such as temporary trembling and clamps or very serious including paralysis and wasting. Weakness occurs mainly in the proximal muscles such as the upper arms, shoulders, pelvis and thighs. In the advanced stages, the distal muscles of the feet and hands may also be involved. This is a motor speech disorder which is primarily characterized by difficulty expressing and forming words. It is mainly a result of pathology or injury of the nervous system due to diabetes myopathy. The muscles of the respiratory system, face and mouth move very slowly or do not move at all. However, severity depends on the areas of the muscular and nervous systems that have been affected. Symptoms include; slow or rapid rate of speech with a mumbling quality, limited lip, jaw and tongue movement, changes in vocal quality, abnormal intonation, drooling and chewing or swallowing difficulty. As diabetes progresses, sufferers may also experience failure of voluntary muscle coordination. It implies dysfunction of some parts of the nervous system that usually coordinate movement. Fatigue is an abnormal feeling of weariness, tiredness, weakness, exhaustion or low energy. It may impact the persons ability to function properly in their everyday life. Although fatigue may be mild at the onset of diabetic myopathy, it becomes Continue reading >>

Diabetes Mellitus, Myopathy

Diabetes Mellitus, Myopathy

Diabetic myopathy ; Insulin-dependent diabetic myopathy ; Juvenile-onset diabetic myopathy Diabetic myopathy refers to the broad spectrum of pathophysiological alterations to skeletal muscle in response to the diabetic biochemical, hormonal, and cellular environment. This chapter will describe those alterations specific to type 1 diabetes mellitus (T1DM). T1DM causes a host of changes in muscle that can be detected with molecular or biochemical techniques, with microscopy of histochemically prepared tissue samples, or with functional testing (e.g., exercise testing). Typically T1DM is associated with a loss of muscle mass and strength, the former presumably causing the latter [ 1 ]. Many studies have examined exercise capacity in T1DM, the most common findings being small, but significant losses in maximal aerobic capacity or peak work capacity. The studies that detected significant decreases in aerobic fitness usually... This is a preview of subscription content, log in to check access. Krause MP, Riddell MC, Hawke TJ (2011) Effects of type 1 diabetes mellitus on skeletal muscle: clinical observations and physiological mechanisms. Pediatr Diabetes 12(4 Pt 1):345364 Google Scholar Jakobsen J, Reske-Nielsen E (1986) Diffuse muscle fiber atrophy in newly diagnosed diabetes. Clin Neuropathol 5:7377 PubMed Google Scholar Iscoe KE, Campbell JE, Jamnik V, Perkins BA, Riddell MC (2006) Efficacy of continuous real-time blood glucose monitoring during and after prolonged high-intensity cycling exercise: spinning with a continuous glucose monitoring system. Diabetes Technol Ther 8:627635 CrossRef PubMed Google Scholar Andersen H (1998) Muscular endurance in long-term IDDM patients. Diabetes Care 21:604609 CrossRef PubMed Google Scholar Gulati AK, Swamy MS (1991) Regeneration of Continue reading >>

(pdf) Diabetic Myopathy: Impact Of Diabetes Mellitus On Skeletal Muscle Progenitor Cells

(pdf) Diabetic Myopathy: Impact Of Diabetes Mellitus On Skeletal Muscle Progenitor Cells

Diabetes mellitus is dened as a group of metabolic diseases that are associated with the presence of a hyperglycemic state due to impairments in insulin release and/or function. While the development of each form of diabetes (Type 1 or Type 2) drastically differs, resultant pathologies often overlap. In each diabetic condition, a failure to maintain healthy muscle is often observed, and is termed diabetic myopathy. This signicant, but often overlooked, complication is believed to contribute to the progression of additional diabetic complications due to the vital importance of skeletal muscle for our physical and metabolic well-being. While studies have investigated the link between changes to skeletal muscle metabolic health following diabetes mellitus onset (particularly Type 2 diabetes mellitus), few have examined the negative impact of diabetes mellitus on the growth and reparative capacities of skeletal muscle that often coincides with disease development. Importantly, evidence is accumulating that the muscle progenitor cell population (particularly the muscle satellite cell population) is also negatively affected by the diabetic environment, and as such, likely contributes to the declining skeletal muscle health observed in diabetes mellitus. In this review, we summarize the current knowledge surrounding the inuence of diabetes mellitus on skeletal muscle growth and repair, with a particular emphasis on the impact of diabetes mellitus on skeletal muscle progenitor cell populations. Keywords: diabetes mellitus, muscle satellite cells, PICs, skeletal muscle, muscle regeneration, Type 1 diabetes SKELETAL MUSCLE AND MUSCLE PROGENITOR CELLS Skeletal muscle is capable of adapting to numerous stimuli, with these responses manifested through changes in muscle size, ber- t Continue reading >>

Reversing Diabetic Muscle Myopathy By Exercise And Exosomes Tyagi, Suresh C. University Of Louisville, Louisville, Ky, United States

Reversing Diabetic Muscle Myopathy By Exercise And Exosomes Tyagi, Suresh C. University Of Louisville, Louisville, Ky, United States

Reversing diabetic muscle myopathy by exercise and exosomes Although exercise mitigates diabetic complications and myopathy, the mechanism is unclear. The long-term goal of this project is to understand the mechanism of diabetic myopathy. Studies from previous funding period revealed causative role of endothelial-myocyte (E-M) uncoupling in cardiomyopathy. The connexin -37 and -43 are associated with endothelial and myocyte coupling; and mitochondria contains connexin-43. Matrix metalloproteinase-9 (MMP-9) disrupts connexins and is activated in diabetes, unequivocally. Interestingly, the exercise decreases MMP-9 activity. Exosomes, 50-100 nm, nanovesicles, contain mir-RNAs and are released from myocytes. In this renewal application we will determine the role of exercise-mediated release in exosome containing mir-RNAs that mitigates the endothelium-myocyte, myocyte-myocyte and mitochondrial-myocyte uncoupling by down regulating the MMP-9. The central hypothesis of this proposal is that MMP-9 degrades connexins and causes endothelial-myocyte, myocyte-myocyte and mitochondria-myocyte uncoupling in diabetes. Exercise releases exosomes containing mir-RNAs that decreases MMP-9 and mitigates uncoupling. We will test the central hypothesis by following three specific aims. Specific aim #1 : To determine whether the exercise releases exosomes that contain mir-29b, mir-323, mir-455 and mir-466 which negatively regulate MMP-9 and mitigate fibrosis and uncoupling. Specific aim #2 : To determine whether endothelial-myocyte uncoupling is caused by perivascular/pericapillary fibrosis and myocyte-myocyte uncoupling is caused by interstitial fibrosis in diabetes and exercise mitigates these conditions. Specific aim #3 : To determine whether the dys-synchronization of mitochondrial fusi Continue reading >>

Diabetic Amyotrophy

Diabetic Amyotrophy

Diabetic amyotrophy is a nerve disorder complication of diabetes mellitus. It affects the thighs, hips, buttocks and legs, causing pain and muscle wasting. What is diabetic amyotrophy? Diabetic amyotrophy is a nerve disorder which is a complication of diabetes mellitus. It affects the thighs, hips, buttocks and legs, causing pain and muscle wasting. It is also called by several other names, including proximal diabetic neuropathy, lumbosacral radiculoplexus neurophagy and femoral neurophagy. What is diabetic amyotrophy like? The main features of diabetic amyotrophy are: Weakness of the lower legs, buttocks or hip. Muscle wasting, usually in the front of the thigh, which follows within weeks. Pain, sometimes severe, usually in the front of the thigh but sometimes in the hip, buttock or back. Other features which occur in some (but not all) patients are: Altered sensation and tingling in the thigh, hip or buttock, which tends to be mild in comparison to the pain and weakness. About half of patients also have distal neuropathy, meaning that sensation in the nerves of the lower legs and feet may be separately affected by this condition (which is the most common form of diabetic neuropathy). Learn more about diabetic neuropathy. About half of people affected lose weight. Symptoms generally begin on one side and then spread to the other in a stepwise progression. The condition may come on quickly or more slowly and usually remains asymmetrical (ie the two sides of the body are unequally affected) throughout its course. About half of patients also have distal symmetrical polyneuropathy, which means the sensation in their feet and toes on both sides is also affected. The condition tends to go on for several months but can last up to three years. By the end of this time it usuall Continue reading >>

Myopathy And Diabetes Mellitus

Myopathy And Diabetes Mellitus

Prevention - Myopathy and diabetes mellitus Diagnosis - Myopathy and diabetes mellitus * High Cholesterol Testing: - Cholesterol Tests - Triglycerides Tests - Blood Pressure Tests * High Blood Pressure Testing - Blood Pressure Monitors - Heart Tests * Heart Health Testing: - Heart Rate Monitors - Irregular Heartbeat Detection - Heart Electrocardiogram (ECG) * Thyroid: Home Testing: - Thyroid Function Tests - TSH Tests - Adrenal Function Tests * Diet & Weight Loss Testing: - Weight Testing - Body Fat Testing (BMI) - Body Fat Monitoring - Fitness Testing * Diabetes Testing: - Diabetes Tests - Blood Glucose Tests - Urine Glucose Tests - Urine Ketone Tests - Diabetes HbA1c Tests - Microalbumin Tests (Kidney) - Urine Protein Tests (Kidney) - Kidney Tests - Eye Tests Prognosis - Myopathy and diabetes mellitus Treatment - Myopathy and diabetes mellitus Resources - Myopathy and diabetes mellitus Continue reading >>

Diabetic Neuropathy

Diabetic Neuropathy

Print Overview Diabetic neuropathy is a type of nerve damage that can occur if you have diabetes. High blood sugar (glucose) can injure nerve fibers throughout your body, but diabetic neuropathy most often damages nerves in your legs and feet. Depending on the affected nerves, symptoms of diabetic neuropathy can range from pain and numbness in your extremities to problems with your digestive system, urinary tract, blood vessels and heart. For some people, these symptoms are mild; for others, diabetic neuropathy can be painful, disabling and even fatal. Diabetic neuropathy is a common serious complication of diabetes. Yet you can often prevent diabetic neuropathy or slow its progress with tight blood sugar control and a healthy lifestyle. Symptoms There are four main types of diabetic neuropathy. You may have just one type or symptoms of several types. Most develop gradually, and you may not notice problems until considerable damage has occurred. The signs and symptoms of diabetic neuropathy vary, depending on the type of neuropathy and which nerves are affected. Peripheral neuropathy Peripheral neuropathy is the most common form of diabetic neuropathy. Your feet and legs are often affected first, followed by your hands and arms. Signs and symptoms of peripheral neuropathy are often worse at night, and may include: Numbness or reduced ability to feel pain or temperature changes A tingling or burning sensation Sharp pains or cramps Increased sensitivity to touch — for some people, even the weight of a bed sheet can be agonizing Muscle weakness Loss of reflexes, especially in the ankle Loss of balance and coordination Serious foot problems, such as ulcers, infections, deformities, and bone and joint pain Autonomic neuropathy The autonomic nervous system controls your hea Continue reading >>

Diabetic Myopathy: Impact Of Diabetes Mellitus On Skeletal Muscle Progenitor Cells

Diabetic Myopathy: Impact Of Diabetes Mellitus On Skeletal Muscle Progenitor Cells

Diabetic myopathy: impact of diabetes mellitus on skeletal muscle progenitor cells Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada Edited by: Lucas Guimares-Ferreira, Federal University of Espirito Santo, Brazil Reviewed by: Espen Spangenburg, University of Maryland, USA; Carlos Hermano J. Pinheiro, University of So Paulo, Brazil; Rebecca Berdeaux, University of Texas Health Science Center at Houston, USA *Correspondence: Thomas J. Hawke, Department of Pathology and Molecular Medicine, McMaster University, 1280 Main Street West, Hamilton, ON L8S 4L8, Canada e-mail: [email protected] This article was submitted to Striated Muscle Physiology, a section of the journal Frontiers in Physiology. Received 2013 Oct 31; Accepted 2013 Dec 4. Copyright 2013 D'Souza, Al-Sajee and Hawke. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. This article has been cited by other articles in PMC. Diabetes mellitus is defined as a group of metabolic diseases that are associated with the presence of a hyperglycemic state due to impairments in insulin release and/or function. While the development of each form of diabetes (Type 1 or Type 2) drastically differs, resultant pathologies often overlap. In each diabetic condition, a failure to maintain healthy muscle is often observed, and is termed diabetic myopathy. This significant, but often overlooked, complication is believe Continue reading >>

The Underlying Mechanisms Of Diabetic Myopathy

The Underlying Mechanisms Of Diabetic Myopathy

The Underlying Mechanisms of Diabetic Myopathy The clinical history of both type-1 (T1D) and type-2 (T2D) diabetes differs drastically; however, the resultant conditions and complications often overlap. A common feature of both TD1 and TD2 is the failure to preserve muscle mass and function, here designated as diabetic myopathy. This complication, which is often overlooked, is believed to contribute to the progression of diabetic complications because the key role skeletal muscle plays in glucose homeostasis and locomotion. Despite the wealth of information on muscle weakness and muscle wasting, the specific triggering events of diabetic myopathy in people with diabetes remain unknown. Unfortunately, this condition currently also receives little attention in the clinical setting. Several studies have investigated the link between diabetic myopathy and diverse cellular processes; however, further knowledge of the pathophysiological and molecular mechanisms involved in the onset and progression of diabetic myopathy is needed for the development of new pharmacological tools to ameliorate diabetic myopathy. New studies in the field of muscle biomedical research will propel novel insights to further our understanding of diabetic myopathy. In this special issue of the Journal of Diabetes Research entitle The Underlying Mechanisms of Diabetic Myopathy, we call for original and review articles from leading and emerging scientists who study diabetic myopathy in different muscle tissues (cardiac, smooth, or skeletal) and with diverse expertise and interests, aiming to stimulate the continuing effort to understand the impact of diabetes on muscle function. In vitro and in vivo studies using diabetes animal models as well as interventional and/or translational studies are welcome. Continue reading >>

Diabetic Myopathy And Mechanisms Of Disease

Diabetic Myopathy And Mechanisms Of Disease

Diabetic Myopathy and Mechanisms of Disease Erick O. Hernndez-Ochoa * and Camilo Vanegas Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene St., Baltimore, MD, 21201, USA *Corresponding author: Erick O. Hernndez-Ochoa, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene St., Baltimore, MD, 21201, USA, Tel: 1+(410) 706-5787; [email protected] This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The publisher's final edited version of this article is available at Biochem Pharmacol (Los Angel) See other articles in PMC that cite the published article. Humans build muscle mass over the first two decades of life; begin to lose muscle mass and strength between the third and fourth decades, and the decline accelerates during the sixth decade [ 1 , 2 ]. Sarcopenia and dynapenia are age-related loss of skeletal muscle mass and muscle strength, respectively [ 1 3 ]. Loss of muscle mass and strength are associated with a reduction in vitality, manifested as poor mobility and physical function [ 3 ], and are accentuated by many common chronic diseases including long-term diabetes. Diabetes mellitus (DM) is characterized by chronic hyperglycemia due to insulin deficiency, resistance, or both. Late complications affect patients quality of life and longevity, and changes in morbidity and mortality result in major health costs. The pathogenesis and the clinical history of both type-1 (T1D) and type-2 (T2D) diabetes drastically differ; however, the resultant syndromes and complica Continue reading >>

The Effects Of Alpha-lipoic Acid On Diabetic Myopathy.

The Effects Of Alpha-lipoic Acid On Diabetic Myopathy.

The effects of alpha-lipoic acid on diabetic myopathy. July 28, 2017 Consumer Blog By GeroNova Research Increased oxidative stress and impaired antioxidant defense are important mechanisms in the pathogenesis of diabetic myopathy. Since diabetes mellitus type 1 decreases muscle regeneration capacity the present study was designed to determine the influence of alpha-lipoic acid (ALA), a potent biological antioxidant, on the process of regeneration of diabetic rat skeletal muscles. 40 Wistar rats were divided into three groups: control (n=8), untreated diabetic group (n=16) and ALA treated diabetic group (n=16). The regeneration process was provoked in streptozotocin-induced diabetic rats in both slow (m.soleus, SOL) and fast (m.extensor digitorum longus, EDL) skeletal muscles by intramuscular injection of myotoxin bupivacaine. At intervals of 10 days and 4 weeks, muscle histochemical and morphometrical analysis (fiber cross areas and fiber type distribution) was performed. Changes induced by diabetes are evident in redistribution of muscle fibers and in significant level of atrophy. After 4 weeks of diabetes, glycolytic muscle fibers are dominant in both slow and fast muscles. Muscle atrophy is present in all fiber types except in type I of slow skeletal muscle. Treatment with ALA reduce changes in the morphological properties caused by diabetes mellitus type 1 in slow and fast rat skeletal muscles during the process of regeneration. Treatment with lipoic acid during 4 weeks has shown effects on the redistribution of muscle fibers, and can prevent atrophy in slow and fast diabetic muscle. J Endocrinol Invest. 2017 Jun 28. doi: 10.1007/s40618-017-0720-0. [Epub ahead of print] Jurisic-Erzen D1, Starcevic-Klasan G2, Ivanac D3, Peharec S4, Girotto D5, Jerkovic R6. Continue reading >>

Acute Myopathy In A Patient With Type 2 Diabetes (t2dm) Receiving Metformin, Fenofibrate And Rosiglitazone

Acute Myopathy In A Patient With Type 2 Diabetes (t2dm) Receiving Metformin, Fenofibrate And Rosiglitazone

Acute Myopathy in a Patient with Type 2 Diabetes (T2DM) Receiving Metformin, Fenofibrate and Rosiglitazone A 75-year old Caucasian male w A 75-year old Caucasian male was admitted to the clinical ward because of acute onset of pain and cramps in both calf muscles. Serum enzymes indicating myopathy were markedly elevated (creatine kinase , CK 6897 U/l, myoglobine 902 ng/ml) and kidney function was impaired (serum creatinine 1.94 mg/dl). He had a 11-years history of type 2 diabetes mellitus with related complications including hypertension, hyperlipidemia, hepatic steatosis and mild neuropathy. Nine years ago he underwent cardiac bypass surgery and received a mechanic aortic valve. His drug treatment consisted of phenprocoumon, an angiotensine-receptor-blocker and inhalative sympathomimetics. Few months before admission, the lipid-lowering medication with simvastatin was switched to fenofibrate. Three weeks before hospital admission, rosiglitazone was added to the pre-existing metformin therapy (1000 mg twice daily) because of worsening metabolic control (HbA1c [gt]7.0%). Electromyography indicated myopathy in the right rectus femoris muscle and electroneurography showed loss of sensoric potentials from the peronaeus nerves consistent with polyneuropathy. An open biopsy taken from the left vastus lateralis muscle revealed multiple damages of the myofibrilliar architecture, but biochemical analysis disclosed neither deletions/insertions in mitochondrial DNA nor common tRNA mutations which are associated with mitochondrial myopathies. Screening for polymorphisms in the cytochrome P450 system detected no functional limitations in the subunits CYP2C9, CYP2C19 and CYP2D6. Upon admission, metformin, fenofibrate and rosiglitazone were withdrawn. During 13-days iv therapy with m Continue reading >>

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