Physiology international最新文献

Introduction: The COVID-19 pandemic has impacted many aspects of acute myocardial infarction. Based on literature data, the prognosis of COVID+, STEMI patients is significantly worse than that of COVID- STEMI patients. On the other hand, physicians report fewer acute coronary syndrome (ACS) patients presenting to hospitals in countries severely affected by the pandemic. It is concerning that patients with life-threatening illness can suffer more complications or die due to their myocardial infarction. We aimed to investigate the changes in myocardial infarction care in the country's biggest PCI-center and to compare total 30-day mortality in COVID+ and COVID-patients with acute myocardial infarction treated at the Semmelweis University Heart and Vascular Center, and to investigate risk factors and complications in these two groups.

Methods: Between 8 October 2020 and 30 April 2021, 43 COVID+, in 2018-2019, 397 COVID-patients with acute myocardial infarction were admitted. Total admission rates pre- and during the pandemic were compared.

Results: Within 30 days, 8 of 43 patients in the COVID+ group (18.60%), and 40 of the 397 patients in the control group (10.07%) died (P = 0.01). Regarding the comorbidities, more than half of COVID+ patients had a significantly reduced ejection fraction (EF≤ 40%), and the prevalence of heart failure was significantly higher in this group (51.16% vs. 27.84%, P = 0.0329). There was no significant difference between the two patient groups in the incidence of STEMI and NSTEMI. Although there was no significant difference, VF (11.63% vs. 6.82%), resuscitation (23.26% vs. 10.08%), and ECMO implantation (2.38% vs. 1.26%) were more common in the COVID+ group. The mean age was 68.8 years in the COVID+ group and 67.6 years in the control group. The max. Troponin also did not differ significantly between the two groups (1,620 vs. 1,470 ng/L). There was a significant decline in admission rates in the first as well as in the second wave of the pandemic.

Conclusions: The 30-day total mortality of COVID+ patients was significantly higher, and a more severe proceeding of acute myocardial infarction and a higher incidence of complications can be observed. As the secondary negative effect of the pandemic serious decline in admission rates can be detected.

Acute respiratory distress syndrome (ARDS) refers to the injury of alveolar epithelial cells and capillary endothelial cells due to various injury factors. Research on the pathogenesis of ARDS has made great progress, but the exact pathogenesis of ARDS has not been fully elucidated. Up to now, the prevention and treatment of ARDS is still an important scientific problem that needs to be solved urgently. In this work, we analyzed the effect of uridine on ARDS. An ARDS model was successfully constructed by lipopolysaccharide (LPS) stimulation. Western-blotting, IFA, ELISA, RT-PCT and CLSM were conducted to investigate the effect of uridine on ARDS and insulin resistance, and the results showed that lung histopathological alterations were significantly attenuated by uridine treatment. Further work showed that the levels of proinflammatory cytokines were significantly down-regulated in the lung tissue after treatment with uridine. Additionally, the numbers of total cells and neutrophils in the bronchoalveolar lavage fluid (BALF) were also decreased in the uridine-treated ARDS mice. We further explored the potential mechanism by which uridine could treat ARDS, and the results indicated that NF-κB signaling was down-regulated by uridine treatment. Next, we studied insulin sensitivity in the ARDS mice, and found that insulin signaling was significantly down-regulated, and uridine could enhance insulin sensitivity in the ARDS mice model. Furthermore, we found that the levels of inflammation and oxidative stress were decreased by uridine treatment, which may be the potential mechanism by which uridine could improve insulin sensitivity. Taken together, the current work provides evidence that uridine can serve as a potential drug to treat ARDS and insulin resistance.

Background: Regular sport has favourable influence on the physical and mental state. Our aim was to analyse the relationship between regular sport activities, body parameters, cortisol level, perceived stress and the frequency of psychosomatic symptoms in male and female university students.

Methods: Subjects were university students (N = 200). They were divided in sporting (more than 7 h week-1: 56 males (sm), 50 females (sf)) and non-sporting (less than 3 h week-1: 44 males (nsm) and 50 females (nsf)) groups. Body composition was estimated by Inbody720-analyser. Stress levels were measured by (1) free cortisol level in saliva measured by using IBL-ELISA kits and (2) questionnaires about psychosomatic symptoms and perceived stress scale.

Results: There were significant subgroup' differences in body composition (fat%:sm:12.1 ± 6.0 vs. nsm:17.9 ± 6.8; sf:20.8 ± 5.5 vs. nsf:25.4 ± 5.7; muscle%:sm:50.3 ± 3.6 vs. nsm:47.6 ± 3.9; sf:43.8 ± 3.2 vs. nsf:41.7 ± 3.3), and in stress level (total scores:sm:21.0 ± 5.7 vs. nsm:23.3 ± 7.2; sf:25.5 ± 7.0 vs. nsf:28.0 ± 9.7). There were gender differences in the psychosomatic symptoms' frequency (total scores: sm: 14.6 ± 6.3 vs. sf: 20.4 ± 7.4; nsm: 14.9 ± 6.1 vs. nsf: 19.6 ± 8.2). The sporting students had larger muscle, smaller fat percentages, and lower level of stress. Basic level of salivary cortisol revealed significant relation with physical activity: sporting students had lower level of cortisol. This relation was reflected in higher percentage of students with low level of cortisol in the physically active subgroups (s/ns males: 29% vs. 15%; s/ns females: 18% vs. 5%) and in the higher percentage of female students with high level of cortisol in the non-sporting subgroup (27% vs. 11%).

Conclusion: Regular sport activity is positively related with lower stress levels in university students.

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.