Physiology international最新文献

Purpose: Chemotherapy and/or radiation are the most often delivered treatments to cancer patients. Usually during the adjuvant treatment, patients complain about fatigue. In addition, physical exercise during adjuvant treatment of cancer seems to have beneficial effects. The aim of this investigation was to assess the effects of multimodal aerobic and strength exercises programs on muscle deoxygenation of patients with breast cancer undergoing adjuvant chemotherapy treatment.

Methods: Thirty-two women with breast cancer (20 patients as the training group and 12 patients as the control group) undergoing adjuvant chemotherapy participated in the study. The training group took part in 6 weeks of supervised intermittent aerobic cycling, home-based walking, isometric and electrical muscle stimulation (EMS) exercise training programs. The Outcome measures were muscle deoxygenation (ΔHHb), Maximal Voluntary isometric Contraction (MViC) and Endurance Time (ET) before and after the training period.

Results: Compared to the control group, a significant increase in ΔHHb (P < 0.01) accompanied with an increase in ET (P < 0.01) and MViC (P < 0.01) of the quadriceps was obtained in the training group. However, no significant differences of MViC, ET and ΔHHb were observed in the control group.

Conclusion: Multimodal aerobic and strength exercise programs enhance muscle oxygen utilization, which may partly explain the improvement in muscular strength and endurance, and the reduction of muscle fatigue in patients with breast cancer during an adjuvant chemotherapy period.

Anemia is a common finding in the elderly. Approximately 10 percent of the elderly suffers from anemia. Anemia per se is an independent factor of mortality in older patients regardless its cause. Frailty is also frequent in geriatric patients. That means that there is a decreased reserve capacity to react to different stress factors including anemia. The frequent presence of heart failure and also impaired cerebrovascular circulation makes more difficult to tolerate anemia in older age. Anemia is a symptom, finding and treating the underlying cause is also important. Treatment always depends on clinical findings: the more severe the symptoms, the more important to treat them. Severity of anemia depends not only the underlying cause, degree of anemia, co-morbidities and frailty of the patients, but also the speed of its development. Sudden blood loss due to an accident is less well tolerated than the same degree of anemia due to B12 deficiency. Main causes of anemia in the elderly include nutritional deficiencies, chronic diseases, tumors, and certain hematological malignancies such as chronic lymphocytic leukemia, multiple myeloma, myelodysplastic syndrome.

Congenital hypothyroidism (CH) occurs with a relatively alarming prevalence in infants, and if not diagnosed and treated in time, it can have devastating consequences for the development of the nervous system. CH is associated with genetic changes in several genes that encode transcription factors responsible for thyroid development, including mutations in the NK2 homeobox 1 (NKX2.1) gene, which encodes the thyroid transcription factor-1 (TTF-1). Although CH is frequently observed in pediatric populations, there is still a limited understanding of the genetic factors and molecular mechanisms contributing to this disease. The sequence of the NKX2.1 gene was investigated in 75 pediatric patients with CH by polymerase chain reaction (PCR), single-stranded conformation polymorphism (SSCP), and direct DNA sequencing. Four missense heterozygous variations were identified in exon 3 of the NKX2.1 gene, including three novel missense variations, namely c.708A>G, p.Gln202Arg; c.713T>G, p.Tyr204Asp; c.833T>G, p.Tyr244Asp, and a previously reported variant rs781133468 (c.772C>G, p.His223Gln). Importantly, these variations occur in highly conserved residues of the TTF-1 DNA-binding domain and were predicted by bioinformatics analysis to alter the protein structure, with a probable alteration in the protein function. These results indicate that nucleotide changes in the NKX2.1 gene may contribute to CH pathogenesis.

Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In addition to the pulmonary manifestations, COVID-19 patients may present a wide range of neurological disorders as extrapulmonary presentations. In this view, several studies have recently documented the worsening of neurological symptoms within COVID-19 morbidity in patients previously diagnosed with neurodegenerative diseases (NDs). Moreover, several cases have also been reported in which the patients presented parkinsonian features after initial COVID-19 symptoms. These data raise a major concern about the possibility of communication between SARS-CoV-2 infection and the initiation and/or worsening of NDs. In this review, we have collected compelling evidence suggesting SARS-CoV-2, as an environmental factor, may be capable of developing NDs. In this respect, the possible links between SARS-CoV-2 infection and molecular pathways related to most NDs and the pathophysiological mechanisms of the NDs such as Alzheimer's disease, vascular dementia, frontotemporal dementia, Parkinson's disease, and amyotrophic lateral sclerosis will be explained.

COVID-19 has become a great burden of the world in respect of health care, social, and economical reason. Several million people died worldwide so far and more and more mutants are generated and spread. Older people with co-morbidities and frailty syndrome have a significantly higher risk to get the infection and also higher the risk of a more serious disease process. Mortality of COVID-19 is also higher in case of geriatric patients. In this review we attempted to summarize the factors of the higher susceptibility for more serious disease, what actions need to be taken for defending older patients and also special aspects of clinical presentation including ophthalmic symptoms.

Podocyte calcium (Ca2+) signaling plays important roles in the (patho)physiology of the glomerular filtration barrier. Overactivation of podocyte transient receptor potential canonical (TRPC) channels including TRPC6 and purinergic signaling via P2 receptors that are known mechanosensors can increase podocyte intracellular Ca2+ levels ([Ca2+]i) and cause cell injury, proteinuria and glomerular disease including in diabetes. However, important mechanistic details of the trigger and activation of these pathways in vivo in the intact glomerular environment are lacking. Here we show direct visual evidence that podocytes can sense mechanical overload (increased glomerular capillary pressure) and metabolic alterations (increased plasma glucose) via TRPC6 and purinergic receptors including P2Y2. Multiphoton microscopy of podocyte [Ca2+]i was performed in vivo using wild-type and TRPC6 or P2Y2 knockout (KO) mice expressing the calcium reporter GCaMP3/5 only in podocytes and in vitro using freshly dissected microperfused glomeruli. Single-nephron intra-glomerular capillary pressure elevations induced by obstructing the efferent arteriole lumen with laser-induced microthrombus in vivo and by a micropipette in vitro triggered >2-fold increases in podocyte [Ca2+]i. These responses were blocked in TRPC6 and P2Y2 KO mice. Acute elevations of plasma glucose caused >4-fold increases in podocyte [Ca2+]i that were abolished by pharmacological inhibition of TRPC6 or P2 receptors using SAR7334 or suramin treatment, respectively. This study established the role of Ca2+ signaling via TRPC6 channels and P2 receptors in mechanical and metabolic sensing of podocytes in vivo, which are promising therapeutic targets in conditions with high intra-glomerular capillary pressure and plasma glucose, such as diabetic and hypertensive nephropathy.

In this study, the ability of microRNA-1906 (miR-1906) to attenuate bone loss in osteoporosis was evaluated by measuring the effects of a miR-1906 mimic and inhibitor on the cellular toxicity and cell viability of MC3T3-E1 cells. Bone marrow-derived macrophage (BMM) cells were isolated from female mice, and tartrate-resistant acid phosphatase signalling was performed in miR-1906 mimic-treated, receptor-activated nuclear factor kappa-B (NF-κB) ligand (RANKL)-induced osteoclasts. In-vivo, osteoporosis was induced by ovariectomy (OVX). Rats were treated with 500 nmol/kg of the miR-1906 mimic via intrathecal administration for 10 consecutive days following surgery. The effect of the miR-1906 mimic on bone mineral density (BMD) in OVX rats was observed in the whole body, lumbar vertebrae and femur. Levels of biochemical parameters and cytokines in the serum of miR-1906 mimic-treated OVX rats were analysed. The mRNA expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), p-38 and NF-κB in tibias of osteoporotic rats (induced by ovariectomy) was observed using quantitative reverse-transcription polymerase chain reaction. Treatment with the miR-1906 mimic reduced cellular toxicity and enhanced the cell viability of MC3T3-E1 cells. Furthermore, osteoclastogenesis in miR-1906 mimic-treated, RANKL-induced osteoclast cells was reduced, whereas the BMD in the miR-1906 mimic-treated group was higher than in the OVX group of rats. Treatment with the miR-1906 mimic also increased levels of biochemical parameters and cytokines in the serum of ovariectomised rats. Finally, mRNA expression levels of TLR4, MyD88, p-38 and NF-κB were lower in the tibias of miR-1906 mimic-treated rats than in those of OVX rats. In conclusion, the miR-1906 mimic reduces bone loss in rats with ovariectomy-induced osteoporosis by regulating the TLR4/MyD88/NF-κB pathway.

Objective: The aim of the present study was to analyse the relationships between creatine kinase (CK) concentration, an indirect marker of muscle damage, and global positioning system (GPS)-derived metrics of a continuous two-week-long preseason training period in elite football.

Design: Twenty-one elite male professional soccer players were assessed during a 14-day preseason preparatory period. CK concentrations were determined each morning, and a GPS system was used to quantify the external load. A generalized estimating equation (GEE) model was established to determine the extent to which the external load parameter explained post-training CK levels.

Results: The GEE model found that higher numbers of decelerations (χ 2 = 7.83, P = 0.005) were most strongly associated with the post-training CK level. Decelerations and accelerations accounted for 62% and 11% of the post-training CK level, respectively, and considerable interindividual variability existed in the data.

Conclusion: The use of GPS to predict muscle damage could be of use to coaches and practitioners in prescribing recovery practices. Based on GPS data, more individualized strategies could be devised and could potentially result in better subsequent performance.

Aim: Limited investigations on metabolic responses to exercise training in female adolescent volleyball athletes exist. The aim of this study was to obtain serum and urine metabolite markers in female adolescent volleyball athletes within 2-week strength-endurance training using a metabolomics approach coupled with biochemical analysis, which would be potential biomarkers for evaluating the physiological state of athletes.

Methods: Twelve female adolescent volleyball athletes were recruited for 2-week strength-endurance training. Differential serum and urine metabolic profiles between the pre- and post-training group were obtained on gas chromatography coupled to mass spectrometry (GC-MS) and data subsequently underwent orthogonal partial least-squares analysis (OPLS).

Results: Strength-endurance training exerted a significant influence on the athletes' serum and urine metabolic profiles. The changed metabolites were primarily involved in energy metabolism, lipid metabolism and amino acids metabolism. Results support the hypothesis that female athletes displayed an increased propensity to oxidize lipids as the major energy source. Exposure to strength-endurance training also led to a significant increase in cortisol, but a decrease in testosterone, indicating disordered hormone adjustment. Exercise-induced oxidative stress occurred, as was evidenced by the decrease in reduced glutathione, and increases in blood malondialdehyde and oxidized glutathione. Since the muscle damage markers creatine kinase and lactate dehydrogenase did not show significant changes, the training might not cause cell membrane damage and the athletes did not cross the adaptive injury level.

Conclusion: By measurement of endogenous metabolites, the metabolomics study has the potential to reveal the global physiological changes in response to exercise training.

Based on the current literature, the link between Achilles tendon moment arm length and running economy is not well understood. Therefore, the aim of this study was to further investigate the connection between Achilles tendon moment arm and running economy and the influence of Achilles tendon moment arm on the function of the plantarflexor muscle-tendon unit during running.Ten male competitive marathon runners volunteered for this study. The participants ran on a treadmill at two running speeds: 3 and 3.5 m s-1. During running the oxygen consumption, lower leg kinematics, electrical activity of plantar flexor muscles, and fascicle behavior of the lateral gastrocnemius were measured simultaneously. On the second occasion, an MRI scan of the right leg was taken and used to estimate the Achilles tendon moment arm length.There was a negative correlation between running economy and the body height normalized moment arm length at both selected speeds (r = -0.68, P = 0.014 and r = -0.70, P = 0.01). In addition, Achilles tendon moment arm length correlated with the amplitude of the ankle flexion at both speeds (r = -0.59, P = 0.03 and r = -0.60, P = 0.03) and with the electrical activity of the medial gastrocnemius muscle at 3 m s-1 speed (r = -0.62, P = 0.02). Our finding supports the concept that a longer moment arm could be beneficial for distance runners.