Damaged Muscle Cells Research Articles

Correlation Between Heart Disease Clinics Based on NYHA Classification and CTR on Thorax Photos at Ibnu Sina Hospital Makassar

Heart disease is caused by damaged heart muscle cells that pump blood throughout the body. The cause is due to a lack of oxygen carried by the blood to the blood vessels in the heart or because spasms in the heart muscle result in failure of the heart's function to pump blood. The heart cannot carry out its function properly, as many as 48% of Indonesians experience heart disease. To determine the level of heart disease, the New York Heart Association (NYHA) is used. Increasing NYHA in heart disease can result in an increase in heart size. To determine the correlation between clinical heart disease based on the NYHA classification and CTR results on chest x-rays. Total sampling through secondary data with certain criteria. NYHA 1 (P = 20.2), NYHA 2 (P = 33.3), NYHA 3 (P= 32.3), NYHA 4 (P= 14.1). The heart grade levels based on CTR examination results, no cardiomegaly (<50%) (p= 22.2), mild cardiomegaly (>50-55%) (p= 76.8), moderate cardiomegaly (56-60) (p=0 .0), severe cardiomegaly (>60%) (p=1.0) while symptoms of weakness (n = 57%), palpitations (n = 47%), no shortness of breath (n = 68%), no chest pain ( n = 50%). So there is a significant relationship between NYHA classification and CTR results on Thorax photos. In conclusion, there is a significant relationship between NYHA classification and CTR results on Thorax photos.

A Versatile Passivated Protein‐Adsorption Platform for Rapid Healing of Vascular Stents by Modulating the Microenvironment

AbstractBiodegradable stents have paved the way to treat coronary artery disease. However, rapid reendothelialization is required to solve the problems of mismatched degradation rates, localized inflammation, and insufficient biocompatibility. Herein, a novel passivated protein‐adsorption coating is synthesized by coordination chelation, oxidation, cross‐linking, polymerization, and deposition of dopamine, (‐)‐epigallocatechin gallate (EGCG), and copper ions (Cu2+) using two‐electron oxidation. This coating exhibits hierarchical functionality, that is, at the macroscale, its superhydrophilicity conveys antifouling ability; whereas at the microscale, the active groups (quinone‐, amino‐, hydroxyphenyl groups and aromatic ring) facilitate protein adsorption. Antifouling ability prevents acute thrombosis and inflammation and maintains initial microenvironment stability post‐implantation. The active groups facilitate gradual endothelial cells (ECs) adhesion. Meanwhile, the decomposition of nitric oxide (NO) donors to release NO is catalyzed by Cu2+, and EGCG alleviates or prevents oxidative stress damage, inflammatory responses, thrombosis formation, and excessive smooth muscle cells proliferation in the stent microenvironment. This provides favorable conditions for the rapid and healthy growth of ECs. This study proposes a novel strategy for rapid neointima formation comprising healthy ECs on the surfaces of biodegradable stents by depositing a passivated protein‐adsorption coating (polydopamine/EGCG/Cu), opening new possibilities for the efficient treatment of coronary artery disease.

Protective role of alpha-lipoic acid against rhabdomyolysis-induced acute kidney injury in rats.

Rhabdomyolysis, a potentially life-threatening condition, occurs when myoglobin is released from damaged muscle cells, leading to acute kidney injury (AKI). Alpha lipoic acid (ALA), an organosulfur compound known for its anti-oxidant and anti-inflammatory properties, was examined in this study for its potential impact on rhabdomyolysis-induced AKI in rats. Six groups of rats were included in the study, with each group consisting of six rats (n=6): Control, rhabdomyolysis, rhabdomyolysis treated with different doses of ALA (5, 10, and 20 mg/kg), and ALA alone (20 mg/kg) groups. Rhabdomyolysis was induced by intramuscular injection of glycerol on the first day of the experiment, while ALA was administered intraperitoneally for four consecutive days. Renal function parameters, oxidative stress markers, and histological changes in the kidneys were evaluated. Western blot analysis was performed to measure the levels of neutrophil gelatinase-associated lipocalin (NGAL) and tumor necrosis factor-alpha (TNF-α) proteins. A significant increase in serum urea, creatinine, renal malondialdehyde, NGAl, and TNF-α protein levels was observed in glycerol-injected rats. In addition, a significant decrease in glutathione was recorded. Compared to the rhabdomyolysis group, treatment with ALA recovered kidney histological and biochemical abnormalities. Results suggest that rhabdomyolysis-induced AKI is associated with increased oxidative stress and inflammation. Treatment with ALA improved kidney histological abnormalities and reduced oxidative stress markers in rats. Therefore, ALA may have a potential protective effect against rhabdomyolysis-induced AKI.

PINK1/Parkin pathway-mediated mitophagy by AS-IV to explore the molecular mechanism of muscle cell damage

BackgroundFunctional disorders of mitochondria are closely related to muscle diseases. Many studies have also shown that oxidative stress can stimulate the production of a large number of reactive oxygen species (ROS), which have various adverse effects on mitochondria and can damage muscle cells. PurposeIn this study, based on our previous research, we focused on the PINK1/Parkin pathway to explore the mechanism by which AS-IV alleviates muscle injury by inhibiting excessive mitophagy. MethodsL6 myoblasts were treated with AS-IV after stimulation with hydrogen peroxide (H2O2) and carbonyl cyanide m-chlorophenylhydrazone (CCCP). Then, we detected the related indices of oxidative stress and mitophagy by different methods. A PINK1 knockdown cell line was established by lentiviral infection to obtain further evidence that AS-IV reduces mitochondrial damage through PINK1/Parkin. ResultsAfter mitochondrial damage, the expression of malondialdehyde (MDA) and intracellular ROS in L6 myoblasts significantly increased, while the expression of superoxide dismutase (SOD) and ATP decreased. The mRNA and protein expression levels of Tom20 and Tim23 were decreased, while those of VDAC1 were increased. PINK1, Parkin, and LC3 II mRNA and protein expression increased, and P62 mRNA and protein expression decreased·H2O2 combined with CCCP strongly activated the mitophagy pathway and impaired mitochondrial function. However, abnormal expression of these factors could be reversed after treatment with AS-IV, and excessive mitochondrial autophagy could also be reversed, thus restoring the regulatory function of mitochondria. However, AS-IV-adjusted function was resisted after PINK1 knockdown. ConclusionAS-IV is a potential drug for myasthenia gravis (MG), and its treatment mechanism is related to mediating mitophagy and restoring mitochondrial function through the PINK1/Parkin pathway.

Being an Expert Does Not Mean You Know Everything

Being an Expert Does Not Mean You Know Everything

Effects of Red-Fleshed Pitaya (Selenicereus polyrhizus) Ingestion after Strenuous Exercise on Creatine Kinase and Mitochondrial Function in Rat Muscle Cells

BACKGROUND: Free radicals formed during strenuous exercise through an increase in reactive oxygen species induce damage to tissues (e.g., muscle and liver) and cause oxidative damage to cells, resulting in mitochondrial dysfunction. AIM: As an effective method to repair mitochondrial muscle cell function, this study investigated the effects of red-fleshed pitaya (RFP) ingestion on creatine kinase (CK), which is a biomarker for muscle tissue damage, and malondialdehyde (MDA) levels during strenuous exercise. METHODS: This study involved 25 3-month-old male rats with an average weight of 200 g. The RFP extract was obtained through ethanol extraction and concentrated using an air-drying method. Rats were randomly allocated into five groups as follows: Two control groups (K1 [no-exercise, no RFP] and K2 [exercise, no RFP]) and three test groups (P1, P2, and P3; subjected to exercise and treated with 75, 150, and 300 mg kg−1 body weight of RFP, respectively). The exercise was in the form of swimming for 20 min 3 times/week for 31 days. CK and MDA were measured through an enzyme-linked immunosorbent assay, and histopathological examinations were performed through hematoxylin and eosin staining of rat muscles. RESULTS: The MDA levels after the ingestion of RFP extracts were compared between the K2 group and the P1, P2, and P3 groups. The results showed significant differences (p < 0.05 for P1 and P2, and p < 0.01 for P3), indicating the production of free radicals and CK, with features of damaged muscle cells based on histopathology. Ingestion of the RFP extract led to improvements in soleus muscle cells, resulting in cell function repair. CONCLUSION: Levels of MDA and CK increased during exercise, which caused significant muscle damage. However, after treatment with the RFP extract, the levels of both markers decreased. Thus, strenuous exercise causes an increase in reactive oxygen species, resulting in increased free radical levels. RFP ingestion decreased oxidative stress levels, thus repairing mitochondrial cell function.

S3211 Outcomes of Patients Admitted With Concurrent Pancreatitis and Rhabdomyolysis: An NIS Database Study

Introduction: There have been numerous studies on acute pancreatitis; however, the effect of acute pancreatitis and rhabdomyolysis have yet to be studied. Here, we aim to assess rhabdomyolysis in patients hospitalized with acute pancreatitis. Methods: Data between 2008 and 2016 from the Nationwide Inpatient Sample database was extracted. Inclusion criteria for both groups included patients over the age of 17 with a primary diagnosis of acute pancreatitis using International Classification of Diseases, 9th and 10th revision codes. Exclusion criteria included all ICD-9 and ICD-10 codes for chronic pancreatitis and malignant pancreatico-biliary disorders and indeterminate rhabdomyolysis status. The study group consisted of patients with a primary diagnosis of acute pancreatitis and a concurrent diagnosis of rhabdomyolysis. Other co-morbidities were then compared between the two groups. Univariate and multivariate analyses were used to generate odds ratios. Results: There were a total of 1,946,591 patients in the control group, and 5,421 patients in the study group. In univariate analysis, there was a statistically significant increase in severe sepsis, respiratory failure, septic shock, calculus and HIV, but not pseudocyst in the study group. In multivariate analysis with rhabdomyolysis as the dependent variable, the odds ratio was highest for respiratory failure (OR=7.749, p < 0.001), followed by HIV (OR = 2.070, p < 0.001), septic shock (OR = 1.586, p < 0.001) and severe sepsis (OR = 1.532, p < 0.001). Calculus had an odds ratio of 0.470 (p < 0.001), suggesting a negative association with rhabdomyolysis. A multivariate analysis with patient morbidity as a dependent variable showed that patients with respiratory failure and septic shock are most likely to die in the hospital, with respiratory failure having an odds ratio of 8.292 (p < 0.001) and septic shock having an odds ratio of 3.729 (P = 0.01431). Conclusion: Rhabdomyolysis appears to confer elevated risk to patients with acute pancreatitis. Patients that are admitted with acute pancreatitis along with rhabdomyolysis also have a high rate of other conditions such as respiratory failure, HIV, septic shock and severe sepsis. Of these, respiratory failure and septic shock are the most dangerous, as they are tied to the highest mortality among patients that have both acute pancreatitis and rhabdomyolysis. We suspect the additional mortality may be due to respiratory muscle weakness and the release of intracellular substances from damaged muscle cells.

Investigation on the Effect of Cyclic Stretch and Hypoxia on Recovery of Damaged Skeletal Muscle Cells Using Microfluidic System

AbstractTo develop an effective treatment for muscle recovery, costimuli effect of cyclic stretch and hypoxia on the recovery of oxidative damaged skeletal muscle cells is investigated. C2C12 myoblast cells are differentiated into myotube in culture dish followed by seeding the myotubes in the microfluidic device for further growth. Hydrogen peroxide is used to induce oxidative stress on myotubes for mimicking intracellular muscle damage. Afterward, the damaged myotubes are recovered in either normoxia or hypoxia environment with or without cyclic stretch, to elucidate the effect of the stretch and hypoxia on recovery. For analysis, reactive oxygen species, 8‐hydroxydeoxyguanosine, and myosin heavy chain are chosen as recovery indicators and it is shown that cyclic stretch and hypoxia facilitate the recovery of muscle to the greatest extent when both cyclic stretch and hypoxia are applied. To investigate the mechanism of the stretch and hypoxia intervened recovery, hypoxia inducible factor‐1α (HIF‐1α), peroxiredoxin 2, glutathione peroxidase 1, and catalase are selected as candidates for the key factor of recovery acceleration. There is evidence that HIF‐1α and antioxidants contributed to stretch‐/hypoxia‐induced recovery, and HIF‐1α is speculated to play the most important role. Hence, the stretch and hypoxia triggered pathways of cellular recovery are suggested.

Role of acetaminophen in reducing risk of kidney injury from Rhabdomyolysis: A Narrative Review

Background: Rhabdomyolysis is a clinical syndrome that results in releasing myoglobin content from damaged muscle cells into circulation and often causes acute kidney injury (1). Different mechanisms are considered to be responsible in rhabdomyolysis and renal failure. However, free radical generation is the most important mechanism resulting in kidney injury. Thus, the effect of various antioxidants has been investigated. Acetaminophen, with antioxidant ability in therapeutic dose, has shown a considerable protective effect on kidney after muscle injury. The investigations have shown that acetaminophen enhances renal function, decreases renal damage and reduces oxidant injury. The aim of this review was to summarize proven evidences for etiology to renal injury and abilities of acetaminophen in reducing it. Methods: Articles published from 2010 to 2017 in PubMed and Google Scholar were covered in this review. The articles investigating the role of free radical in renal injury following Rhabdomylosis were searched using the keywords Rhabdomyolysis, kidney and oxidative stress. The keywords used to find articles regarding antioxidant ability of acetaminophen were antioxidant and acetaminophen. Conclusion: With assessment of evidences form antioxidant capacity of acetaminophen and mechanism of renal failure in Rhabdomyolysis, this drug can be useful for prevention and treatment of kidney injury especially following rhabdomyolysis.

Isobavachalcone attenuates myotube atrophy induced by TNF-α through muscle atrophy F-box signaling and the nuclear factor erythroid 2-related factor 2 cascade.

Skeletal muscle atrophy is a condition characterized by damaged muscle fibers and reduced numbers of muscle cells due to various causes. Muscle atrophy is associated with chronic diseases, such as heart failure, diabetes, and aging-related diseases. Isobavachalcone (IBC) is a flavonoid found in various foods and natural products, and studies have investigated its diverse effects, including its neuroprotective and anticancer effects. However, no studies have evaluated the effects of IBC on muscle atrophy. Thus, in this study, we assessed the effects of IBC on prevention of muscle atrophy. To evaluate the preventive effects of IBC on muscle atrophy, we used C2C12 myoblasts and induced muscle atrophy by tumor necrosis factor (TNF)-α. IBC regulated the expression levels of muscle atrophy F-box and muscle RING finger-1 in response to damaged muscle cells, thereby restoring the expression of myosin heavy chain and myogenin. Moreover, IBC regulated the phosphorylation of the nuclear factor-κB and p38 and upregulated the expression of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1, which are involved in regulating oxidative stress. Our results indicated that IBC acted to relieve TNF-α-induced skeletal muscle atrophy by regulating the factors related to inflammation and oxidative stress.

ЕНДОГЕННА ІНТОКСИКАЦІЯ ОРГАНІЗМУ ПІДДОСЛІДНИХ ТВАРИН ПРИ УРАЖЕННІ ПОРОЖНЬОЇ КИШКИ ЗА УМОВ ПОСТРЕЗЕКЦІЙНОЇ ПОРТАЛЬНОЇ ГІПЕРТЕНЗІЇ

Вступ. Видалення великих об’ємів паренхіми печінки може супроводжуватися виникненням пострезекційної портальної гіпертензії. Остання призводить до морфологічної перебудови органів басейну ворітної печінкової вени, ураження їх структур, зростання ендогенної інтоксикації, яку при пошкодженнях порожньої кишки у названих патологічних умовах досліджено недостатньо. &#x0D; Мета дослідження – вивчити особливості ендогенної інтоксикації організму піддослідних тварин при ураженні порожньої кишки за умов пострезекційної портальної гіпертензії. &#x0D; Методи дослідження. Дослідження проведено на 60 білих щурах-самцях, яких поділили на 4 групи: 1-ша нараховувала 15 інтактних тварин; 2-га – 15 щурів, у яких було видалено 31,5 % паренхіми печінки; 3-тя – 15 тварин, в яких видалили 42 % паренхіми печінки; 4-та – 15 щурів після резекції 58,1 % паренхіми печінки. Евтаназію піддослідних тварин здійснювали шляхом кровопускання за умов тіопенталового наркозу через місяць від початку експерименту. Стан ендогенної інтоксикації оцінювали за концентрацією в сироватці крові ТБК-активних продуктів, визначенням окисної модифікації білків, вмістом молекул середньої маси. Гістологічні препарати з порожньої кишки фарбували гематоксилін-еозином, за ван-Гізон, Маллорі, Вейгертом, толуїдиновим синім. Гістостереометрично визначали відносні об’єми пошкоджених епітеліоцитів, м’язових клітин, ендотеліоцитів. Кількісні величини обробляли статистично. &#x0D; Результати й обговорення. У щурів через місяць після резекції 42 та 58,1 % паренхіми печінки спостерігали розширення печінкової ворітної вени, повнокров’я і розширення брижових вен та видимого венозного русла тонкої і товстої кишок. Виявлені зміни свідчили про наявність портальної гіпертензії. Слизова оболонка порожньої кишки повнокровна, набрякла, з поодинокими осередками точкових крововиливів. У стінці порожньої кишки виявили дистрофію, некробіоз епітеліоцитів, міоцитів, ендотеліоцитів, стромальних структур, інфільтративні та склеротичні процеси, які були більш виражені при резекції 58,1 % паренхіми печінки. Відносні об’єми пошкоджених досліджуваних структур значно зросли через місяць після резекції 42 % паренхіми печінки і найбільших величин досягли при видаленні 58,1 % об’єму даного органа, вказуючи на виражене ураження порожньої кишки в змодельованих експериментальних умовах. При виявленому ураженні порожньої кишки суттєво зросла ендогенна інтоксикація організму, що підтверджувалося достовірним (р&lt;0,05) збільшенням вмісту молекул середньої маси в сироватці крові, ТБК-активних продуктів, окисномодифікованих білків. Ступінь ендогенної інтоксикації організму при пострезекційній портальній гіпертензії залежав від вираження ураження порожньої кишки. &#x0D; Висновки. Резекція великих об’ємів паренхіми печінки призводить до розвитку пострезекційної портальної гіпертензії, пошкоджень структур порожньої кишки та ендогенної інтоксикації організму, яка супроводжується збільшенням вмісту молекул середньої маси, окисномодифікованих білків, активацією пероксидного окиснення ліпідів. Ступінь ендогенної інтоксикації організму залежить від видаленого об’єму паренхіми печінки та вираження пошкоджень структур порожньої кишки.

Heterotopic Ossification - Complication or Chance?

So far, there has been no clear explanation of the pathophysiological relationships in the development of HO. There is little experimental data dealing with the post-traumatic inflammatory response in terms of a balance between the repair of damaged muscle cells and the opposite response in its development. There are numerous indications regarding possible predisposing factors, such as existence of surrounding tissue hypoxia or the function of pro-angiogenic (VEGF e.g.) and osteoinductive (BMP e.g.) factors. These different scientific approaches offer the opportunity to clinically intervene. In our opinion, early intervention seems to make the most sense in terms of effectiveness and recurrence of HO. An important pathomechanism seems to be chronic inflammation. Currently, non-steroidal anti-inflammatory drugs are the most commonly prescribed prophylaxis drugs. The effectiveness and efficacy of non-steroidal anti-inflammatory drugs is limited by the time-limited release and the side effect potential. Therefore, it is interesting to focus future research towards the cross-talks between immunosuppressive downregulation of the inflammatory response and its effect on the balance between muscle regeneration and the development of HO.

Reduction of Real-Time Imaging of M1 Macrophage Chemotaxis toward Damaged Muscle Cells is PI3K-Dependent.

Macrophages migrate and invade into damaged muscle rapidly and are important for muscle repair and subsequent regeneration. The exact cellular and biological events that cause macrophage migration toward injured muscle are not completely understood. In this study, the effect of macrophage differentiation on the chemotactic capability to invade local damaged muscle was investigated using an in vitro model of muscle injury. We used C2C12 cell myoblasts and J774 cell macrophages, and the “killed-C2C12” cells were combined with live C2C12 cells as a partially damaged muscle model. The cultured J774 cells, with or without lipopolysaccharide (LPS), were treated with Ly294002 (Ly), which is an inhibitor of phosphoinositide 3-kinase (PI3K). In order to evaluate the polarization effect of LPS stimulation on J774 cells, expression of cell surface Toll-like receptor 4 (TLR4), CD11c and CCR2, and expression of F-actin intensity, were analyzed by flow cytometry. The real-time horizontal chemotaxis assay of J774 cells was tested using the TAXIScan device. The expressions of TLR4, CD11c, and F-actin intensity in LPS-treated cells were significantly higher than those in Ctrl cells. In LPS-treated cells, the chemotactic activity toward damaged muscle cells completely disappeared. Moreover, the reduced chemotaxis depended far more on directionality than velocity. However, Ly treatment reversed the reduced chemotactic activity of the LPS-treated cells. In addition, cell-adhesion and F-actin intensity, but not CCR2 expression, in LPS-treated cells, was significantly reduced by Ly treatment. Taken together, our results suggest that the PI3K/Akt activation state drives migration behavior towards damaged muscle cells.

Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury.

Rhabdomyolysis is a serious syndrome caused by skeletal muscle injury and the subsequent release of breakdown products from damaged muscle cells into systemic circulation. The muscle damage most often results from strenuous exercise, muscle hypoxia, medications, or drug abuse and can lead to life-threatening complications, such as acute kidney injury (AKI). Rhabdomyolysis and the AKI complication can also occur during crush syndrome, an emergency condition that commonly occurs in victims of natural disasters, such as earthquakes, and man-made disasters, such as wars and terrorism. Myoglobin released from damaged muscle is believed to trigger renal dysfunction in this form of AKI. Recently, macrophages were implicated in the disease pathogenesis of rhabdomyolysis-induced AKI, but the precise molecular mechanism remains unclear. In the present study, we show that macrophages released extracellular traps (ETs) comprising DNA fibers and granule proteins in a mouse model of rhabdomyolysis. Heme-activated platelets released from necrotic muscle cells during rhabdomyolysis enhanced the production of macrophage extracellular traps (METs) through increasing intracellular reactive oxygen species generation and histone citrullination. Here we report, for the first time to our knowledge, this unanticipated role for METs and platelets as a sensor of myoglobin-derived heme in rhabdomyolysis-induced AKI. This previously unknown mechanism might be targeted for treatment of the disease. Finally, we found a new therapeutic tool for prevention of AKI after rhabdomyolysis, which might rescue some sufferers of this pathology.

Tomatidine enhances lifespan and healthspan in C. elegans through mitophagy induction via the SKN-1/Nrf2 pathway

Aging is a major international concern that brings formidable socioeconomic and healthcare challenges. Small molecules capable of improving the health of older individuals are being explored. Small molecules that enhance cellular stress resistance are a promising avenue to alleviate declines seen in human aging. Tomatidine, a natural compound abundant in unripe tomatoes, inhibits age-related skeletal muscle atrophy in mice. Here we show that tomatidine extends lifespan and healthspan in C. elegans, an animal model of aging which shares many major longevity pathways with mammals. Tomatidine improves many C. elegans behaviors related to healthspan and muscle health, including increased pharyngeal pumping, swimming movement, and reduced percentage of severely damaged muscle cells. Microarray, imaging, and behavioral analyses reveal that tomatidine maintains mitochondrial homeostasis by modulating mitochondrial biogenesis and PINK-1/DCT-1-dependent mitophagy. Mechanistically, tomatidine induces mitochondrial hormesis by mildly inducing ROS production, which in turn activates the SKN-1/Nrf2 pathway and possibly other cellular antioxidant response pathways, followed by increased mitophagy. This mechanism occurs in C. elegans, primary rat neurons, and human cells. Our data suggest that tomatidine may delay some physiological aspects of aging, and points to new approaches for pharmacological interventions for diseases of aging.

Effects of Biowastes Released by Mechanically Damaged Muscle Cells on the Propagation of Deep Tissue Injury: A Multiphysics Study.

Deep tissue injuries occur in muscle tissues around bony prominences under mechanical loading leading to severe pressure ulcers. Tissue compression can potentially compromise lymphatic transport and cause accumulation of metabolic biowastes, which may cause further cell damage under continuous mechanical loading. In this study, we hypothesized that biowastes released by mechanically damaged muscle cells could be toxic to the surrounding muscle cells and could compromise the capability of the surrounding muscle cells to withstand further mechanical loadings. In vitro, we applied prolonged low compressive stress (PLCS) and short-term high compressive stress to myoblasts to cause cell damage and collected the biowastes released by the damaged cells under the respective loading scenarios. In silico, we used COMSOL to simulate the compressive stress distribution and the diffusion of biowastes in a semi-3D buttock finite element model. In vitro results showed that biowastes collected from cells damaged under PLCS were more toxic and could compromise the capability of normal myoblasts to resist compressive damage. In silico results showed that higher biowastes diffusion coefficient, higher biowastes release rate, lower biowastes tolerance threshold and earlier timeline of releasing biowastes would cause faster propagation of tissue damage. This study highlighted the importance of biowastes in the development of deep tissue injury to clinical pressure ulcers under prolonged skeletal compression.

Change in viability of C2C12 myoblasts under compression, shear and oxidative challenges

Skeletal and epidermal loadings can damage muscle cells and contribute to the development of deep tissue injury (DTI) – a severe kind of pressure ulcers affecting many people with disability. Important predisposing factors include the multiaxial stress and strain fields in the internal tissues, particularly the vulnerable muscles around bony prominences. A careful study of the mechanical damage thresholds for muscle cell death is critical not only to the understanding of the formation of DTI, but also to the design of various body support surfaces for prevention. In this paper, we measured the mechanical damage thresholds of C2C12 myoblasts under prescribed compressive strains (15% and 30%) and shear strains (from 0% to 100%), and studied how oxidative stress, as caused potentially by reperfusion or inflammation, may affect such damage thresholds. A flat plate was used to apply a uniform compressive strain and a radially increasing shear strain on disks of Gelatin–methacrylate (GelMA) hydrogel with myoblasts encapsulated within. The percentages of cell death were estimated with propidium iodide (PI) and calcein AM staining. Results suggested that cell death depended on both the level and duration of the applied strain. There seemed to be a non-linear coupling between compression and shear. Muscle cells often need to function biomechanically in challenging oxidative environments. To study how oxidative stress may affect the mechanical damage thresholds of myoblasts, cell viability under compressive and shear strains was also studied after the cells were pre-treated for different durations (1h and 20h) with different concentrations (0.1mM and 0.5mM) of hydrogen peroxide (H2O2). Oxidative stress can either compromise or enhance the cellular resistance to shear damage, depending on the level and duration of the oxidative exposure.

Saturated Fatty Acids Differentially Affects Adipocytes and Muscle Cells

Obesity and obesity related type 2 diabetes have become serious health issues in the US and worldwide. It is certain that the human genetic coding cannot been changed so dramatically by evolution during such a short period of time. Environmental factors including diets may play an important role in developing obesity/type 2 diabetes. Since adipose and muscle tissues are significantly affected in individuals with obesity, adipocytes and muscle cells were cultured in the conditions to mimic hyperlipidemia situations that happen during the development of obesity. We have observed that saturated fatty acids at high concentrations differentially affects adipocytes and muscle cells. The saturated fatty acid palmitic acid damages muscle cells and induces muscle cell death while causing more lipid accumulation in adipocytes. Polyunsaturated fatty acid linoleic acid also causes more lipid accumulation in adipocytes but it does not damage muscle cells. A few new candidate genes that are regulated by a saturated fatty acid in muscle cells have been identified by cDNA microarray. Further studies will be conducted to explore the mechanisms at the molecular level.

Low-Intensity Repetitive Exercise Induced Rhabdomyolysis.

Rhabdomyolysis is a rare condition caused by the proteins of damaged muscle cells entering the bloodstream and damaging the kidneys. Common symptoms of rhabdomyolysis are muscle pain and fatigue in conjunction with dark urine; kidney damage is a common symptom among these patients. We present a case of a 23-year-old woman who displayed myalgia in the upper extremities caused by low-intensity and high-repetition exercise. She was successfully diagnosed and treated for exertional rhabdomyolysis. This patient had no significant medical history that would induce this condition. We urge the emergency medical community to observe and monitor patients that complain of myalgia to ensure they are not suffering from rhabdomyolysis even in atypical cases.

Real-time Imaging of Macrophage Chemotaxis Toward Damaged Muscle Cells Is PI3K-dependent

Real-time Imaging of Macrophage Chemotaxis Toward Damaged Muscle Cells Is PI3K-dependent