Table 2 - uploaded by Bozena JemioloContent may be subject to copyright.DownloadView publicationCopy referenceCopy captionEmbed figurePrimer set sequences and amplicon information Source publication Myogenic gene expression at rest and after a bout of resistance exercise in young (18-30 yr) and old (80-89 yr) womenArticleFull-text availableAug 2006 Ulrika Raue Dustin R Slivka Bozena Jemiolo[...] Scott TrappeThe purpose of this study was to investigate mRNA expression of several key skeletal muscle myogenic controllers; myogenic differentiation factor (MyoD), muscle regulatory factor 4 (MRF4), myogenic factor 5 (Myf5), myogenin, myostatin, and myocyte enhancer factor 2 (MEF2) at rest and 4 h after a single bout of resistance exercise (RE) in young and...CiteDownload full-textContext in source publicationContext 1... reaction mix consisted of 2.5 lo f1 0 SYBRgreen real-time PCR buffer (Biosource, Camavillo, CA), 0.625 lo f1 0m Md e - oxynucleotide 5-triphosphate, 0.2 lo f5U / l Platinum Taq DNA Polymerase (Invitrogen), 1 lof10M each for forward and reverse primers in the case of the genes of interest (GOI) and 2.5 lo f1 0 primer pairs for GAPDH (Biosource, Camavillo, CA), 2.5 lo f cDNA, and RNase-free water to a final volume of 25 l. All primers used in this study were mRNA specific (on different exons and/or crossing over an intron) and designed for gene expression real-time PCR analysis using Vector NTI Advance 9 software (Invitrogen) ( Table 2). ...View in full-textSimilar publications+1 Prolonged underfeeding of sheep increases myostatin and myogenic regulatory factor Myf-5 in skeletal muscle while IGF-I and myogenin are repressedArticleFull-text availableApr 2003 Ferenc Jeanplong James Johnston Bass Heather K Smith[...] J M OldhamThe IGF axis is nutritionally sensitive in vivo and IGFs stimulate myoblast proliferation and differentiation in vitro, while myostatin inhibits these processes in vitro. We hypothesised that underfeeding would reversibly inhibit the myogenic activity of satellite cells in vivo together with decreased IGF-I and increased myostatin in muscle. Satell...View Molecular expression of myostatin and MyoD is greater in double-muscled than normal-muscled cattle fetusesArticleFull-text availableJun 2001 J M Oldham Julie Martyn M Sharma[...] James Johnston BassExcessive muscling in double-muscled cattle arises from mutations in the myostatin gene, but the role of myostatin in normal muscle development is unclear. The aim of this study was to measure the temporal relationship of myostatin and myogenic regulatory factors during muscle development in normal (NM)- and double-muscled (DM) cattle to determine...ViewCitations... In addition, FGF21 acts as a key metabolic mediator of mitochondrial adaptations under muscle mitochondrial stress conditions [36]. Thus, we presume that increased FGF21 under a hot [37][38][39]. Furthermore, myostatin gene expression in human skeletal muscle was downregulated by passive heat exposure (33 • C) for 3 h [40]. ...Myokine secretion following moderate-intensity endurance exercise under different environmental temperaturesArticleAug 2021CytokineYoshifumi Tsuchiya Kazushige GotoPurposeIn the present study, the effects of endurance exercise under different environmental temperatures on myokine responses were elucidated.MethodsSeven healthy males (age: 22.7 ± 0.4 years, height: 173.7 ± 2.7 cm, body weight: 65.2 ± 2.8 kg) performed pedaling at 60% of their maximal oxygen consumption for 60 min under three different environmental temperature conditions, cold (without shivering; 15–19 °C), moderate (24 °C), and hot (34 °C), in a counterbalanced fashion. Exercise intensity (60% maximal oxygen consumption evaluated under each condition) was relatively matched among the conditions. Venous blood samples were collected before, during, immediately after, and at 1, 2, and 3 h after exercise.ResultsExercise-induced changes in plasma irisin, interleukin-6, insulin or insulin-like growth factor-1 concentrations did not differ significantly among the conditions (P 0.05). In hot condition, exercise-induced elevation of plasma fibroblast growth factor-21 (FGF21) concentration was significantly enhanced compared with the cold condition, and the myostatin concentration was lowered compared with the moderate condition (P 0.05). Furthermore, the area under the curve for the myostatin concentration over an exercise session (including during and after exercise) was significantly lower in the hot than moderate condition (P 0.05). Notably, a positive correlation between the peak plasma FGF21 and myostatin concentrations was observed at the moderate environment, but not at the cold or hot condition (P 0.05).ConclusionIrisin and FGF21 concentrations induced by moderate-intensity endurance exercise were not enhanced under the cold environmental temperature without shivering. In contrast, exercise in the hot environmental temperature changed favorably FGF21 and myostatin concentrations compared with thermoneutral environment.View... 2 Likewise, previous literature has demonstrated that older women express higher myogenic mRNA levels of muscle regulatory factors at rest, which may reflect an attempt to preserve muscle mass and function in this group. 25 Hence, despite having a multifactorial etiology, hormones may play a major role in the potentially poorer musculoskeletal health presented in postmenopausal women in comparison to younger women. In fact, postmenopausal women users of HRT showed higher 1RM than their nonuser counterparts. ...... 7 This suggests that estrogen may not exert a significant influence on the degree of muscle damage experienced after resistance exercise in resistance-trained women. On the contrary, other investigations indicated that postmenopausal participants not using HRT showed higher amount of DNA damage in their muscles 25 and slower strength and power recovery after damage-inducing exercise 30 relative to younger women, which may be related to damage-induced impairments in excitation-contraction coupling and cross-bridge function. 7,24 Nevertheless, the postmenopausal participants in those previous studies seem older that our postmenopausal group and some studies are not recent. ...Exercise-Induced Muscle Damage in Postmenopausal Well-Trained WomenArticleMay 2021Nuria Romero-ParraCristina Maestre-Cascales Nuria Marín-Jiménez Beatriz RaelAna B PeinadoBackground: Sex hormone deprivation derived from menopause may affect exercise-induced muscle damage (EIMD). No studies have previously evaluated this response between postmpenopausal and premenopausal eumenorrheic women over the menstrual cycle.Hypothesis: Postmenopausal women will present higher EIMD markers than premenopausal women, especially in comparison with the menstrual cycle phases where sex hormone concentrations are higher.Study design: Cross-sectional study.Level of evidence: Level 3.Methods: Thirteen postmenopausal and 19 eumenorrheic women, all of them resistance-trained, performed an eccentric squat-based exercise. The postmenopausal group performed 1 bout of exercise, while the eumenorrheic group performed 3 bouts coinciding with the early follicular, late follicular, and mid-luteal phases ot their menstrual cycle. Muscle soreness, countermovement jump, creatine kinase (CK), myoglobin, lactate dehydrogenase, interleukin-6, tumor necrosis factor-α, and C-reactive protein were evaluated before and postexercise.Results: The expected differences in sex hormones were observed between groups (P 0.001) according to their reproductive status. Postexercise increases in CK, myoglobin, and muscle soreness (168.2 ± 45.5 U/L, 123.1 ± 41.5 µg/L, and 20.7 ± 21.3 mm, respectively) were observed in comparison with baseline (136.2 ± 45.5 U/L, 76.9 ± 13.8 µg/L, and 2.7 ± 4.2 mm, respectively). Myoglobin values at baseline in postmenopausal women were higher compared with premenopausal women in the aforementioned menstrual cycle phases, respectively (62.8 ± 8.2, 60.4 ± 7.2, and 60.1 ± 10.6 µg/L; P 0.001 for all comparisons), which was supported by large effect sizes (0.72-1.08 standardized d units). No postexercise differences were observed between groups in any markers (P 0.05).Conclusion: Despite higher resting levels of myoglobin and lower strength values in postmenopausal than in premenopausal women, EIMD was similar between both reproductive profiles. This suggests a potential benefit of being physically active despite aging and sex hormone deprivation.Clinical relevance: Sex hormone deprivation derived from menopause seems not to influence muscle damage reponse to eccentric exercise in resistance-trained postmenopausal women.View... This is in contrast to findings of myostatin levels declining on ageing in men both measured by ELISA [38] and immunoplexed liquid chromatography with tandem mass spectrometry [39]. A smaller study of eight young and six elderly women showed higher levels of myostatin mRNA in muscle biopsies of the older group [40]. Various groups have sought to determine the use of myostatin as a potential biomarker for muscle wasting but the conclusions have been ambiguous [41][42][43]. ...... The effect of age on the expression of not only myostatin but also other promyogenic muscle regulatory factors (MRF) following exercise was examined by Raue et al. They found that at rest, there is a relative upregulation of both MRF and myostatin prior to exercise in elderly women compared to younger ones, but that the postexercise downregulation of myostatin is not hampered by age [40]. A study in healthy and sarcopenic elderly men demonstrated that resistance training or a combination of resistance and endurance training caused a decrease in myostatin [44,45]. ...Antimyostatin Treatment in Health and Disease: The Story of Great Expectations and Limited SuccessArticleFull-text availableMar 2021Tue L. NielsenJohn Vissing Thomas O. KragIn the past 20 years, myostatin, a negative regulator of muscle mass, has attracted attention as a potential therapeutic target in muscular dystrophies and other conditions. Preclinical studies have shown potential for increasing muscular mass and ameliorating the pathological features of dystrophic muscle by the inhibition of myostatin in various ways. However, hardly any clinical trials have proven to translate the promising results from the animal models into patient populations. We present the background for myostatin regulation, clinical and preclinical results and discuss why translation from animal models to patients is difficult. Based on this, we put the clinical relevance of future antimyostatin treatment into perspective.View... Ageing appears to upregulate myostatin expression independent of adiposity, which if translated to increased myostatin protein secretion could contribute to sarcopenia by promoting atrophic and inhibiting hypertrophic pathways via canonical TGF-β signalling. Muscle myostatin mRNA and protein expression was 2.0fold and 1.4-fold higher, respectively, in older than younger males [224] and myostatin mRNA expression was 56% greater in elderly than young women [74]. Older males matched with younger males for total-and lean-body mass and body fat percentage tended to have higher basal muscle myostatin mRNA expression and significantly greater muscle myostatin protein content [75]. ...Recent advances and future avenues in understanding the role of adipose tissue cross talk in mediating skeletal muscle mass and function with ageingArticleFull-text availableFeb 2021 Andrew Wilhelmsen Kostas Tsintzas Simon W JonesSarcopenia, broadly defined as the age-related decline in skeletal muscle mass, quality, and function, is associated with chronic low-grade inflammation and an increased likelihood of adverse health outcomes. The regulation of skeletal muscle mass with ageing is complex and necessitates a delicate balance between muscle protein synthesis and degradation. The secretion and transfer of cytokines, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), both discretely and within extracellular vesicles, have emerged as important communication channels between tissues. Some of these factors have been implicated in regulating skeletal muscle mass, function, and pathologies and may be perturbed by excessive adiposity. Indeed, adipose tissue participates in a broad spectrum of inter-organ communication and obesity promotes the accumulation of macrophages, cellular senescence, and the production and secretion of pro-inflammatory factors. Pertinently, age-related sarcopenia has been reported to be more prevalent in obesity; however, such effects are confounded by comorbidities and physical activity level. In this review , we provide evidence that adiposity may exacerbate age-related sarcopenia and outline some emerging concepts of adipose-skeletal muscle communication including the secretion and processing of novel myokines and adipokines and the role of ex-tracellular vesicles in mediating inter-tissue cross talk via lncRNAs and miRNAs in the context of sarcopenia, ageing, and obesity. Further research using advances in proteomics, transcriptomics, and techniques to investigate extracellular vesicles, with an emphasis on translational, longitudinal human studies, is required to better understand the physiological significance of these factors, the impact of obesity upon them, and their potential as therapeutic targets in combating muscle wasting.View... In this regard, acute resistance exercise has been indicating to attenuate myostatin expression in young adults 4 h [47] and 24 h after exercise [44]. ...Effect of different muscle contraction mode on the expression of Myostatin, IGF-1, and PGC-1 alpha family members in human Vastus Lateralis muscleArticleFull-text availableDec 2020Mol Biol RepPejman Taghibeikzadehbadr Sadegh Shirian Mostafa SabouriMuscle contraction stimulates a transient change of myogenic factors, partly related to the mode of contractions. Here, we assessed the response of IGF-1Ea, IGF-1Eb, IGF-1Ec, PGC1α-1, PGC1α-4, and myostatin to the eccentric Vs. the concentric contraction in human skeletal muscle. Ten healthy males were performed an acute eccentric and concentric exercise bout (n = 5 per group). For each contraction type, participants performed 12 sets of 10 repetitions knee extension by the dominant leg. Baseline and post-exercise muscle biopsy were taken 4 weeks before and immediately after experimental sessions from Vastus Lateralis muscle. Genes expression was measured by real-time PCR technique. There was a significant increase in PGC1α-1, PGC1α-4, IGF-1Ea and, IGF-1Eb mRNA after concentric contraction (p ≤ 0.05), while the PGC1α-4 and IGF-1Ec significantly increased after eccentric contraction (p ≤ 0.05). It is intriguing to highlight that; no significant differences between groups were evident for changes in any variables following exercise bouts (p ≥ 0.05). Our results found that concentric and eccentric contractions presented different responses in PGC1α-1, IGF-1Ea, IGF-1Eb, and IGF-1Ec mRNA. However, a similar significant increase in mRNA content was observed in PGC1α-4. Further, no apparent differences could be found between the response of genes to eccentric and concentric contraction.View... Differences in MRFs between young and elderly could be crucial mechanisms behind differences in muscle mass and strength [22,23,30] and in the response to resistance training and deconditioning. Previous studies found elevated levels of MyoD, myogenin, and IGF-I-R mRNA in elderly both at rest [17,[31][32][33][34] and in response to one bout of resistance exercise [11]. Moreover, 16 weeks of resistance training increased muscle myoD mRNA levels to a similar extent in young and elderly, whereas the training-induced increase in mRNA levels of myogenin was impaired in the elderly [17]. ...... With the same levels of MRFs in elderly compared to young persons in the present study, our findings contrast the majority of previous studies measuring on mRNA levels. Previous studies found elevated levels of MyoD, myogenin, and IGF-I-R mRNA in elderly both at rest [17,[31][32][33][34] and in response to exercise training compared to younger individuals [17,[47][48][49][50]. This suggests that the increase in MRF mRNA levels represented a continuous compensatory mechanism to preserve muscle protein and mass with aging [17]. ...Preserved Capacity for Adaptations in Strength and Muscle Regulatory Factors in Elderly in Response to Resistance Exercise Training and DeconditioningArticleFull-text availableJul 2020 Andreas Mæchel Fritzen Frank D. ThøgersenKhaled Abdul Nasser Qadri Thomas KragTina D. JeppesenAging is related to an inevitable loss of muscle mass and strength. The mechanisms behind age-related loss of muscle tissue are not fully understood but may, among other things, be induced by age-related differences in myogenic regulatory factors. Resistance exercise training and deconditioning offers a model to investigate differences in myogenic regulatory factors that may be important for age-related loss of muscle mass and strength. Nine elderly (82 ± 7 years old) and nine young, healthy persons (22 ± 2 years old) participated in the study. Exercise consisted of six weeks of resistance training of the quadriceps muscle followed by eight weeks of deconditioning. Muscle biopsy samples before and after training and during the deconditioning period were analyzed for MyoD, myogenin, insulin-like growth-factor I receptor, activin receptor IIB, smad2, porin, and citrate synthase. Muscle strength improved with resistance training by 78% (95.0 ± 22.0 kg) in the elderly to a similar extent as in the young participants (83.5%; 178.2 ± 44.2 kg) and returned to baseline in both groups after eight weeks of deconditioning. No difference was seen in expression of muscle regulatory factors between elderly and young in response to exercise training and deconditioning. In conclusion, the capacity to gain muscle strength with resistance exercise training in elderly was not impaired, highlighting this as a potent tool to combat age-related loss of muscle function, possibly due to preserved regulation of myogenic factors in elderly compared with young muscle.View... However, MRF4 has been shown to inhibit muscle growth by repressing myocyte enhancer factor 2 transcriptional activity (28). Regular resistance training sessions, mainly composed of coupled concentric-eccentric contractions, are known to induce increases in MyoD, myogenin, and MRF4 mRNA levels within 2-24 h after exercise (3,37,38,51). Our results showed that MyoD, myogenin, and MRF4 mRNA levels increased after the first eccentric cycling bout and remained elevated 2 wk later. ...... We speculate that MRF4 increase may be a counter-regulatory effect against muscle growth because of the inhibitory effect on protein synthesis (28). Similarly to our results, small or no changes in Myf-5 mRNA levels have been reported 4 h after resistance exercise (38,51). However, maximal eccentric isokinetic contractions induced increases in MyoD, myogenin, MRF4, and Myf-5 mRNA levels 4 h after exercise in postmenopausal women (8). ...Activation of Protein Synthesis, Regeneration and MAPK Signaling Pathways Following Repeated Bouts of Eccentric CyclingArticleFull-text availableOct 2019AM J PHYSIOL-ENDOC M Denisse Valladares-Ide Luis Peñailillo Nicolás CollaoHugo Marambio Hermann Zbinden-FonceaThe aim of this study was to examine the activation of skeletal muscle signaling pathways related to protein synthesis and the gene expression of regeneration/degradation markers following repeated bouts of eccentric cycling. Nine untrained men (25.4 ± 1.9 y) performed two 30-min eccentric cycling bouts (ECC1, ECC2) at 85% of maximal concentric workload, separated by 2 weeks. Muscle biopsies were taken from the vastus lateralis before and 2h after each bout. Indirect markers of muscle damage were assessed before and 24-48h after exercise. Changes in the Akt/mTOR/S6K1/rpS6 and MAPK signaling pathways were measured by western blot and changes in mRNA expression of IL-6, IL-1β and myogenic regulatory factors (MRF) were measured by real time PCR. ECC1 induced greater increases in indirect markers of muscle damage compared to ECC2. Phosphorylation of S6K1 and rpS6 increased after both exercise bouts, while phosphorylation of mTOR increased after ECC2 only. Atrogin-1 mRNA expression decreased after ECC1 and ECC2, without changes in MuRF-1 mRNA. Basal mRNA levels of MyoD, MRF4 and Myogenin were higher two weeks after ECC1. MRF4 mRNA increased after ECC1 and ECC2, while MyoD mRNA expression increased only after ECC1. Phosphorylation of JNK and p38 MAPK increased after both exercise bouts similar to IL-6 and IL-1β mRNA expression. All together, these results suggest that differential regulation of the mTOR pathway and MRF expression could mediate the repeated bout effect observed between an initial and a second bout of eccentric exercise.View... During ageing there is a decrease in Notch signalling (Carey et al. 2007) and a switch from the canonical Wnt signalling to non-canonical Wnt signalling, this results in the prevention of the self-renewal ability of satellite cells that is seen in the aged satellite cell (Florian et al. 2013). Key genes which regulate skeletal muscle development, MyoD and Myf5 are also increased in the aged muscle in humans, mouse and rats (Hameed et al. 2003;Raue et al. 2006;Chakkalakal et al. 2012). ...Age-related changes in skeletal muscle: changes to life-style as a therapyArticleFull-text availableDec 2018Biogerontology Rachel McCormick Aphrodite VasilakiAs we age, there is an age-related loss in skeletal muscle mass and strength, known as sarcopenia. Sarcopenia results in a decrease in mobility and independence, as well as an increase in the risk of other morbidities and mortality. Sarcopenia is therefore a major socio-economical problem. The mechanisms behind sarcopenia are unclear and it is likely that it is a multifactorial condition with changes in numerous important mechanisms all contributing to the structural and functional deterioration. Here, we review the major proposed changes which occur in skeletal muscle during ageing and highlight evidence for changes in physical activity and nutrition as therapeutic approaches to combat age-related skeletal muscle wasting.View... Aberrant MstnPP processing could also play a role during aging. Interestingly, several studies suggest that muscle MstnPP mRNA levels increase with age [75][76][77]. In a cohort of old cattle showing signs of sarcopenia, age-related myopathic features reminiscent of sIBM, including Congo Red positive deposits and protein accumulations immunoreactive with anti-APP antibody 6E10 or anti-Mstn-C antibody, have been observed [78]. ...... Indeed, arimoclomol, a drug activating the cellular heat shock response and reducing ER stress ameliorated disease pathology and improved muscle function in an animal model with sIBM pathology [20]. Recent studies argue that serum level of Mstn GF decrease with age in humans and other mammals [81][82][83][84][85], even though MstnPP mRNA might be upregulated [75][76][77]. As proteolytic processing of MstnPP and complex posttranslational regulation control the liberation of biologically active Mstn GF, careful evaluation of Mstn processing and secretion is required, using immunoreagents that do not cross-react with other TGF-β GFs or immunoglobins [84]. ...Endoplasmic Reticulum Stress Induces Myostatin High Molecular Weight Aggregates and Impairs Mature Myostatin SecretionArticleFull-text availableNov 2018MOL NEUROBIOLRishibha SachdevKarin Kappes-HornLydia Paulsen Yvonne Duernberger Ina VorbergSporadic inclusion body myositis (sIBM) is the most prevalent acquired muscle disorder in the elderly with no defined etiology or effective therapy. Endoplasmic reticulum stress and deposition of myostatin, a secreted negative regulator of muscle growth, have been implicated in disease pathology. The myostatin signaling pathway has emerged as a major target for symptomatic treatment of muscle atrophy. Here, we systematically analyzed the maturation and secretion of myostatin precursor MstnPP and its metabolites in a human muscle cell line. We find that increased MsntPP protein levels induce ER stress. MstnPP metabolites were predominantly retained within the endoplasmic reticulum (ER), also evident in sIBM histology. MstnPP cleavage products formed insoluble high molecular weight aggregates, a process that was aggravated by experimental ER stress. Importantly, ER stress also impaired secretion of mature myostatin. Reduced secretion and aggregation of MstnPP metabolites were not simply caused by overexpression, as both events were also observed in wildtype cells under ER stress. It is tempting to speculate that reduced circulating myostatin growth factor could be one explanation for the poor clinical efficacy of drugs targeting the myostatin pathway in sIBM.Electronic supplementary materialThe online version of this article (10.1007/s12035-018-0997-9) contains supplementary material, which is available to authorized users.View... Hyperplasia and hypertrophy mechanisms in muscle growth are controlled by the sequential expression of MRFs [223]. Both acute and chronic exercise is effective in reducing myostatin while subsequently up-regulating myogenin and myogenic differentiation factor D (MyoD) [224,225,223,226,31]. Furthermore, 16 weeks of resistance training, three days/week, resulted in increased skeletal muscle mass, myogenin, and MyoD in healthy men and women [227]. ...The Role of Systemic Inflammation in Cancer-Associated Muscle Wasting and Rationale for Exercise as a Therapeutic InterventionArticleFull-text availableSep 2018 Calvin Lloyd Cole Ian R. KlecknerAminah JatoiEdward M SchwarzRichard F. DunneProgressive skeletal muscle wasting in cancer cachexia involves a process of dysregulated protein synthesis and breakdown. This catabolism may be the result of mal-nutrition, and an upregulation of both pro-inflammatory cytokines and the ubiquitin proteasome pathway (UPP), which can subsequently increase myostatin and activin A release. The skeletal muscle wasting associated with cancer cachexia is clinically significant, it can contribute to treatment toxicity or the premature discontinuation of treatments resulting in increases in morbidity and mortality. Thus, there is a need for further investigation into the pathophysiology of muscle wasting in cancer cachexia to develop effective prophylactic and therapeutic interventions. Several studies have identified a central role for chronic-systemic inflammation in initiating and perpetuating muscle wasting in patients with cancer. Interestingly, while exercise has shown efficacy in improving muscle quality, only recently have investigators begun to assess the impact that exercise has on chronic-systemic inflammation. To put this new information into context with established paradigms, here we review several biological pathways (e.g. dysfunctional inflammatory response, hypothalamus pituitary adrenal axis, and increased myostatin/activin A activity) that may be responsible for the muscle wasting in patients with cancer. Additionally, we discuss the potential impact that exercise has on these pathways in the treatment of cancer cachexia. Exercise is an attractive intervention for muscle wasting in this population, partially because it disrupts chronic-systemic inflammation mediated catabolism. Most importantly, exercise is a potent stimulator of muscle synthesis, and therefore this therapy may reverse muscle damage caused by cancer cachexia.ViewShow moreGet access to 30 million figuresJoin ResearchGate to access over 30 million figures and 135+ million publications – all in one place.Join for freeAdvertisementJoin ResearchGate to find the people and research you need to help your work.20+ million members135+ million publications700k+ research projectsJoin for free orDiscover by subject areaRecruit researchersJoin for freeLoginEmail Tip: Most researchers use their institutional email address as their ResearchGate loginPasswordForgot password? Keep me logged inLog inorContinue with GoogleWelcome back! Please log in.Email · HintTip: Most researchers use their institutional email address as their ResearchGate loginPasswordForgot password? Keep me logged inLog inorContinue with GoogleNo account? 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