Search

Psoriasis continues to affect a large percentage of patients worldwide and strongly appears to be a systematic disease. Efforts are being made to understand its etiology, which have led to research extended to genomic analysis with a focus on the role of pro-inflammatory cytokines, which play a major role in the pathogenesis of the disease. Plasma proteomic analysis in various diseases has provided promising results for choosing the right treatment for psoriasis, suggesting that it could play a key role in the prevention, prognosis, and treatment of the disease by individualizing treatment choices based on the proteomic profile of each patient. In this review, we focus on existing data in the bibliography on proteomic analysis in psoriasis and relevant approaches to future targeted therapies. [ABSTRACT FROM AUTHOR]

Infertility patients are willing to travel abroad to receive the medical treatment of choice. A 2010 study reported that approximately 25,000 couples travel abroad annually seeking infertility treatment. The purpose of this review is to analyze the criteria and risks related to cross-border reproductive care (CBRC) from the perspective of the patients and explore the issues raised regarding the country of origin and the destination country. A computerized search was performed in PubMed employing respective keywords. The total number of published articles provided by our PubMed search was 1905. Criteria for selecting the destination country include: the economic status, legislation, quality of care and anonymity. Despite the fact that CBRC is becoming a familiar concept, it raises concerns for the practitioner and issues of a social and bioethical nature. Most of them stem from the fact that health care acquires a commercialization aspect. Medical tourism entails several risks, such as misconceptions regarding the destination country, and legal issues arising from differences in the judiciary systems. Larger studies evaluating all aspects of CBRC are imperative. Quality assurance, a consensus and a common platform of practice, along with a system of international governance based on human rights, are a necessity for CBRC patients.

Endometriosis is a benign, estrogen-dependent gynecological condition with an uncertain exact pathogenetic mechanism. The aim of this study was to evaluate the potential differential expression of Insulin Growth Factor 1 (IGF-1) isoforms in deeply infiltrating endometriotic (DIE) lesions, in ovarian endometriomas, and in the eutopic endometrium of the same endometriosis patients and to compare their expression with that in the eutopic endometrium of women without endometriosis. A total of 39 patients were included: 28 with endometriosis, of whom 15 had endometriomas only, 7 had DIE nodules only, and 6 had both DIE and endometriomas, and 11 without endometriosis served as controls. We noticed a similar pattern of expression between IGF-1Ea and IGF-1Ec, which differed from that of the IGF-1Eb isoform, possibly implying differential biological actions of different isoforms in DIE subtypes. We observed a tendency of lower expression of IGF-1Ea and IGF-1Ec in endometriomas without DIE compared to endometriomas with concurrent DIE or in DIE nodules. In conclusion, differential expression of IGF-1 isoforms may indicate that DIE with its associated ovarian lesions and simple ovarian endometriosis should be considered as two forms of the disease developing under different molecular pathways. [ABSTRACT FROM AUTHOR]

Background/Aim: To investigate the effects of an exercise training program on physical and cognitive function in older patients with dementia. Patients and Methods: Thirtyeight patients with early-middle dementia (31 females and seven males), aged 80.6±6.9 years, residents in an Elderly Care Unit, either completed a 36-week structured exercise program (Intervention Group, IG; n=19), or received the usual medical care (Control Group, CG; n=19). Before and after the 36-week intervention, cognitive function was evaluated in both groups by Mini-Mental State Examination (MMSE) and depression by Geriatric Depression Scale (GDS); physical function was assessed using handgrip test, Timed Up to Go (TUG), Berg Balance Scale (BBS) and Chair-Stand Test (CST), and daily living functionality by Functional Rating Scale for Symptoms of Dementia (FRSSD). Results: As a result of exercise intervention, participants scored better in all functional and cognitive test assessments compared to the control group, as reflected by absolute and relative (%) differences in all metrics after the 36-week exercise program (p<0.001). Conclusion: A 36-week supervised exercise training program was found to result in significant improvements in physical and cognitive function of elderly patients in early to middle stages of dementia at an Elderly Care Unit. The promising results of this study shed more light on the adaptability of elderly patients with early and mild dementia to long-term exercise training and verified the feasibility of applying such programs in this clinical population. [ABSTRACT FROM AUTHOR]

Simple Summary: Sarcopenia is a serious clinical condition experienced by many oncology patients as a disease and/or treatment-related adverse event that threatens their quality of life and survival. However, the assessment of body composition has not been incorporated into daily clinical practice and sarcopenia is either underdiagnosed or diagnosed at an advanced stage. Physical exercise offers significant benefits against sarcopenia, in terms of both prevention and treatment. In this review, the ways of assessing sarcopenia and sarcopenic obesity, their prognostic value, and their relation to the toxicity of the anticancer treatments are discussed. We also describe mechanisms by which exercise can counteract sarcopenia, and the potential role of myokines in the preservation of muscle mass. One of the most common adverse effects of cancer and its therapeutic strategies is sarcopenia, a condition which is characterised by excess muscle wasting and muscle strength loss due to the disrupted muscle homeostasis. Moreover, cancer-related sarcopenia may be combined with the increased deposition of fat mass, a syndrome called cancer-associated sarcopenic obesity. Both clinical conditions have significant clinical importance and can predict disease progression and survival. A growing body of evidence supports the claim that physical exercise is a safe and effective complementary therapy for oncology patients which can limit the cancer- and its treatment-related muscle catabolism and promote the maintenance of muscle mass. Moreover, even after the onset of sarcopenia, exercise interventions can counterbalance the muscle mass loss and improve the clinical appearance and quality of life of cancer patients. The aim of this narrative review was to describe the various pathophysiological mechanisms, such as protein synthesis, mitochondrial function, inflammatory response, and the hypothalamic–pituitary–adrenal axis, which are regulated by exercise and contribute to the management of sarcopenia and sarcopenic obesity. Moreover, myokines, factors produced by and released from exercising muscles, are being discussed as they appear to play an important role in mediating the beneficial effects of exercise against sarcopenia. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is a very common liver disease associated with obesity, unhealthy diet, and lack of physical exercise. Short-term aerobic or resistance exercise has been shown to result in reduced liver fat in patients with NAFLD; however, the impact of the combination of these types of exercise has received less attention. This study investigated the effect of a short-term (7 days) concurrent exercise training program performed daily on liver steatosis indices, as well as the glycemic and lipidemic profile of overweight/obese sedentary volunteers. Twenty adult patients (age: 47.3 ± 12.3 yrs, body mass index: 32.4 ± 3.4 kg/m2) with NAFLD, detected by ultrasound and hematological indices, participated in the study. Pre- and post-exercise intervention assessment included body weight (BW), waist circumference (WC), hip/waist ratio (H/W), Homeostasis Model Assessment Insulin Resistance (HOMA-IR), blood lipids, and steatosis indices. Fatty Liver Index, Lipid Accumulation Index, WC, H/W, triglycerides, and total cholesterol were improved (p < 0.05) post-exercise, while no differences (p > 0.05) were observed in BW, HOMA-IR, HDL, LDL, Hepatic Steatosis Index, and Framingham Steatosis Index compared to pre-exercise values. It is concluded that a 7-day combined exercise program can have beneficial effects on hepatic steatosis and central adiposity indices, independently of weight loss, in patients with NAFLD. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the industrialized world and in the future is expected to be the number one killer worldwide. The main cause underlying CVD is atherosclerosis. A key event in atherosclerosis initiation and progression is oxidative stress through the production of reactive oxygen species as well as endothelial dysfunction. Several pro- inflammatory and anti-inflammatory cytokines and proteins are involved in this process, complemented by activation of adhesion molecules that promote leukocyte rolling, tethering and infiltration into the sub-endothelial space. Statins represent the agent of choice since numerous clinical trials have verified that their pharmacological action extends beyond lipid lowering. Statins demonstrate direct anti-oxidant effects by scavenging free radicals and stimulating anti-oxidant enzymes while acting as regulators for cytokine, protein and adhesion molecule expression, all of which are involved in the atherosclerotic process. Statin use is considered one of the most efficient currently used interventions in managing CVD with the likely hood of remaining so in the near future.

Vitamin D is a steroid hormone with potent immune-modulating properties. It has been shown to stimulate innate immunity and induce immune tolerance. Extensive research efforts have shown that vitamin D deficiency may be related to the development of autoimmune diseases. Vitamin D deficiency has been observed in patients with rheumatoid arthritis (RA) and has been shown to be inversely related to disease activity. Moreover, vitamin D deficiency may be implicated in the pathogenesis of the disease. Vitamin D deficiency has also been observed in patients with systemic lupus erythematosus (SLE). It has been found to be inversely related to disease activity and renal involvement. In addition, vitamin D receptor polymorphisms have been studied in SLE. Vitamin D levels have been studied in patients with Sjogren's syndrome, and vitamin D deficiency may be related to neuropathy and the development of lymphoma in the context of Sjogren's syndrome. Vitamin D deficiency has been observed in ankylosing spondylitis, psoriatic arthritis (PsA), and idiopathic inflammatory myopathies. Vitamin D deficiency has also been observed in systemic sclerosis. Vitamin D deficiency may be implicated in the pathogenesis of autoimmunity, and it may be administered to prevent autoimmune disease and reduce pain in the context of autoimmune rheumatic disorders. [ABSTRACT FROM AUTHOR]

Mitochondria are cellular organelles that play an essential role in generating the chemical energy needed for the biochemical reactions in cells. Mitochondrial biogenesis, i.e., de novo mitochondria formation, results in enhanced cellular respiration, metabolic processes, and ATP generation, while autophagic clearance of mitochondria (mitophagy) is required to remove damaged or useless mitochondria. The balance between the opposing processes of mitochondrial biogenesis and mitophagy is highly regulated and crucial for the maintenance of the number and function of mitochondria as well as for the cellular homeostasis and adaptations to metabolic demands and extracellular stimuli. In skeletal muscle, mitochondria are essential for maintaining energy homeostasis, and the mitochondrial network exhibits complex behaviors and undergoes dynamic remodeling in response to various conditions and pathologies characterized by changes in muscle cell structure and metabolism, such as exercise, muscle damage, and myopathies. In particular, the involvement of mitochondrial remodeling in mediating skeletal muscle regeneration following damage has received increased attention, as modifications in mitophagy-related signals arise from exercise, while variations in mitochondrial restructuring pathways can lead to partial regeneration and impaired muscle function. Muscle regeneration (through myogenesis) following exercise-induced damage is characterized by a highly regulated, rapid turnover of poor-functioning mitochondria, permitting the synthesis of better-functioning mitochondria to occur. Nevertheless, essential aspects of mitochondrial remodeling during muscle regeneration remain poorly understood and warrant further characterization. In this review, we focus on the critical role of mitophagy for proper muscle cell regeneration following damage, highlighting the molecular mechanisms of the mitophagy-associated mitochondrial dynamics and network reformation. [ABSTRACT FROM AUTHOR]

Background: Peripheral myopathy consists a hallmark of heart failure (HF) and has been associated with poor prognosis. Inflammation has been suggested to dominate this pathology, while exercise training is typically associated with the induction of anti-inflammatory mechanisms. However, the current knowledge regarding the involvement of inflammation-related genes in the exercise training-induced muscle adaptations in HF patients is very limited. Given that high-intensity interval training (HIIT) alone or combined with strength training (COM) has gained ground in HF cardiac rehabilitation, this study aimed to investigate the local muscle expression of inflammatory and tissue remodeling factors in HF patients, who underwent 3 months of these training schemes. In addition, we examined whether these exercise training-induced gene expression responses are associated with changes in exercise capacity in those patients. Methods: Thirteen male patients with chronic HF (age: 51 ± 13 y; body mass index (BMI): 27 ± 4 kg/m2) were randomly assigned to a 3-month exercise program consisted of either HIIT (N = 6) or COM training (N = 7). Muscle tissue biopsies were obtained from vastus lateralis pre- and post-training and transcriptional changes in interleukin 6 (IL-6), interleukin 8 (IL-8), tumor necrosis factor-1 alpha (TNF-1a), urokinase-type plasminogen activator (uPA), urokinase-type plasminogen activator receptor (uPAR), and transforming growth factor-beta 1 (TGF-ß1) were quantified by RT-PCR. Results: An overall increase in the expression levels of selected inflammatory (IL-8, TNF-1a) and remodeling factors (uPAR) was found post-training (p < 0.05), while IL-6, uPA and TGF-ß1 gene expression remained unchanged (p > 0.05). The observed alterations did not differ between training groups. Additionally, IL-8 changes were found to be correlated with the improvement in exercise capacity post-training (p < 0.05). Conclusions: This is the first study demonstrating an increase in intramuscular inflammatory and remodeling key factors induced by HIIT or COM training in HF patients. Combining these observations with our previous findings of improved muscle hypertrophy and capillarization post-training in these patients, the findings of the present study may suggest that inflammatory responses are part of an ongoing remodeling process in the exercising skeletal muscle. Clinical Trial Registration: NCT02387411. [ABSTRACT FROM AUTHOR]

Background: During aging, muscle cell apoptosis increases and myogenesis gradually declines. The impaired myogenic and survival potential of the aged skeletal muscle can be ameliorated by its mechanical loading. However, the molecular responses of aged muscle cells to mechanical loading remain unclear. This study examined the effect of mechanical loading of aged, proliferating, and differentiated myoblasts on the gene expression and signaling responses associated with their myogenic lineage progression and survival. Methods: Control and aged C2C12 cells were cultured on elastic membranes and underwent passive stretching for 12 h at a low frequency (0.25 Hz) and different elongations, varying the strain on days 0 and 10 of myoblast differentiation. Activation of ERK1/2 and Akt, and the expression of focal adhesion kinase (FAK) and key myogenic regulatory factors (MRFs), MyoD and Myogenin, were determined by immunoblotting of the cell lysates derived from stretched and non-stretched myoblasts. Changes in the expression levels of the MRFs, muscle growth, atrophy, and pro-apoptotic factors in response to mechanical loading of the aged and control cells were quantified by real-time qRT-PCR. Results: Mechanical stretching applied on myoblasts resulted in the upregulation of FAK both in proliferating (day 0) and differentiated (day 10) cells, as well as in increased phosphorylation of ERK1/2 in both control and aged cells. Moreover, Akt activation and the expression of early differentiation factor MyoD increased significantly after stretching only in the control myoblasts, while the late differentiation factor Myogenin was upregulated in both the control and aged myoblasts. At the transcriptional level, mechanical loading of the proliferating myoblasts led to an increased expression of IGF-1 isoforms and MRFs, and to downregulation of muscle atrophy factors mainly in control cells, as well as in the upregulation of pro-apoptotic factors both in control and aged cells. In differentiated cells, mechanical loading resulted in an increased expression of the IGF-1Ea isoform and Myogenin, and in the downregulation of atrophy and pro-apoptotic factors in both the control and aged cells. Conclusions: This study revealed a diminished beneficial effect of mechanical loading on the myogenic and survival ability of the senescent muscle cells compared with the controls, with a low strain (2%) loading being most effective in upregulating myogenic/anabolic factors and downregulating atrophy and pro-apoptotic genes mainly in the aged myotubes. [ABSTRACT FROM AUTHOR]

Simple Summary: The benefits of physical exercise against cancer onset and progression, as well as the adverse effects of physical inactivity have changed the way that we utilize exercise for cancer patients. Nevertheless, although guidelines of various scientific societies and organizations propose exercise as a complementary intervention during cancer therapies, the exact cellular and molecular mechanisms by which exercise acts against cancer have not yet been elucidated. In the present review, we analyze the factors which either are secreted from skeletal muscle or are regulated by exercise and can restrain cancer evolution. We also describe the exercise-induced factors that counteract severe side effects of cancer treatment, as well as the ways that muscle-derived factors are delivered to the target cells. A growing body of in vitro and in vivo studies suggests that physical activity offers important benefits against cancer, in terms of both prevention and treatment. However, the exact mechanisms implicated in the anticancer effects of exercise remain to be further elucidated. Muscle-secreted factors in response to contraction have been proposed to mediate the physical exercise-induced beneficial effects and be responsible for the inter-tissue communications. Specifically, myokines and microRNAs (miRNAs) constitute the most studied components of the skeletal muscle secretome that appear to affect the malignancy, either directly by possessing antioncogenic properties, or indirectly by mobilizing the antitumor immune responses. Moreover, some of these factors are capable of mitigating serious, disease-associated adverse effects that deteriorate patients' quality of life and prognosis. The present review summarizes the myokines and miRNAs that may have potent anticancer properties and the expression of which is induced by physical exercise, while the mechanisms of secretion and intercellular transportation of these factors are also discussed. [ABSTRACT FROM AUTHOR]