scholarly journals Reduced muscle strength in ether lipid-deficient mice is accompanied by altered development and function of the neuromuscular junction

2017 ◽  
Vol 143 (5) ◽  
pp. 569-583 ◽  
Author(s):  
Fabian Dorninger ◽  
Ruth Herbst ◽  
Bojana Kravic ◽  
Bahar Z. Camurdanoglu ◽  
Igor Macinkovic ◽  
...  
Keyword(s):  
Muscle Strength ◽  
Neuromuscular Junction ◽  
Ether Lipid ◽  
And Function ◽  
Deficient Mice

scholarly journals The Effectiveness Of Quadriceps Strengthening Exercises Combined With Neuromuscular Electrical Stimulation on Patellofemoral Pain Syndrome

2017 ◽  
Vol 5 (2_suppl2) ◽  
pp. 2325967117S0010
Author(s):  
Sezen Karabörklü Argut ◽  
Nilgün Türker ◽  
Derya Çelik ◽  
Önder İsmet Kılıçoğlu
Keyword(s):  
Electrical Stimulation ◽  
Muscle Strength ◽  
Neuromuscular Electrical Stimulation ◽  
Pain Syndrome ◽  
Quadriceps Strength ◽  
Patellofemoral Pain ◽  
Group I ◽  
Strengthening Exercises ◽  
Group Ii ◽  
And Function

Objective: The weakness of the quadriceps strength in patellofemoral pain syndrome (PFPS) is very evident. Therefore, quadriceps strengthening exercises are very important part of the rehabilitation program. Neuromuscular Electrical Stimulation (NMES) is considered one of the methods for increasing quadriceps muscle strength. To evaluate the effectiveness of combined NMES and strengthening exercises to improve the recovery of quadriceps strength and function in patients with PFPS. Methods: This study was planned as a randomized controlled pilot study. A total of 27 patients (mean age=38.9±10.8 years, range=20-60 years; 16 females) with PFPS were assessed and randomly assigned into 2 groups. Group I received a standard program (quadriceps strengthening, hip strengthening and hamstring stretching) and NMES combined with quadriceps strengthening exercises simultaneously. Group II received the same standard program without NMES. Both groups were enrolled 3 times per week for 40 minutes per day in 6 weeks. Patients were assessed at the baseline, 3 rd, 6th, and 12th weeks of treatment. Quadriceps strength was evaluated by isokinetic dynamometer. The range of motion at testing was set between 0 for extension to 90 for flexion. The test was performed at 60 degrees/sn and concentric maximum peak torque value was recorded. Kujala and Lysholm scores were used for functional assessments. The data were analyzed using the SPSS 20.0. Shapiro-Wilk test was used to assess the distribution of data. The changes in dependent variables before treatment, 3 rd, 6th, and 12th weeks were analyzed using a 2 by 4 mixed-model analysis of variance (ANOVA). Pairwise comparisons with paired t test were used to determine whether the Group I or Group II, has changed over time. An intention- to- treat analysis was performed to impute values for missing data. An alpha level of 0.05 was established. Results: The study was completed with 20 patients. Group I (n=10; mean age=39.4±8.5 years; 7 females) and group II (n=10; mean age=43.2±11.7 years; 5 females) had no differences in pre-operative measures (p>.05). There was significant improvements in within groups statistics of all parameters for both groups (p<.05). No differences in quadriceps strength, Kujala and Lysholm scores between groups were found at the different time points (F= 0.86; p = 0.12, F=0,001; p =0.97, F=0.12; p=0.73, respectively) Conclusion: NMES combined with quadriceps strengthening exercises has no additional effect on PFPS patients’ on muscle strength and function. When considering these results, we believe that there is no need to continue the study in progress. [Table: see text]

scholarly journals Physical and functional performance assessment in pediatric oncology: a systematic review

2021 ◽  
Author(s):  
Regine Söntgerath ◽  
Julia Däggelmann ◽  
Sabine V. Kesting ◽  
Corina S. Rueegg ◽  
Torge-Christian Wittke ◽  
...  
Keyword(s):  
Systematic Review ◽  
Muscle Strength ◽  
Physical Performance ◽  
Cardiorespiratory Fitness ◽  
Pediatric Cancer ◽  
Motor Performance ◽  
Performance Test ◽  
Functional Mobility ◽  
Cancer Type ◽  
And Function

Abstract Background Research indicates reduced physical performance from diagnosis into survivorship of pediatric cancer patients. However, there is no systematic information or guideline available on the methods to assess physical performance and function in this population. The purpose was to systematically compile and describe assessments of physical performance and function in patients and survivors of pediatric cancer, including cardiorespiratory fitness, muscle strength, speed, balance, flexibility, functional mobility, gait and motor performance test batteries. Methods We searched the databases PubMed, SPORTDiscus, and Cochrane Database and performed abstract and full-text selection of 2619 articles according to the Cochrane Handbook of Systematic Reviews. Information on patients characteristics, assessments, information on validity and reliability, and relevant references was extracted. Results In summary, 63 different assessments were found in 149 studies including 11639 participants. Most studies evaluated cardiorespiratory fitness and muscle strength with the majority conducted off treatment. Some outcomes (e.g. speed) and diagnoses (e.g. neuroblastoma) were severely underrepresented. With the exception of gait, leukemia patients represented the largest group of individuals tested. Conclusions Insufficient data and patient heterogeneity complicate uniform recommendations for assessments. Our results support researchers and practitioners in selecting appropriate assessment to meet their specific research questions or individual daily practice needs. Impact This systematic review includes 149 studies and provides a comprehensive summary of 63 assessments to evaluate cardiorespiratory fitness, muscle strength, speed, balance, flexibility, functional mobility, gait or motor performance test batteries in patients and survivors of pediatric cancer. We present the most studied fields within the pediatric cancer population, which are cardiorespiratory fitness and muscle strength, off treatment phase, and leukemia patients. We propose research priorities by identification of subgroups in terms of cancer type, phase of treatment, and outcome of interest that are underrepresented in studies currently available.

NKR-P1B Receptor Expression and Function in the Different Innate Lymphoid Cells of the Lung

2021 ◽  
Author(s):  
Lucas Vajko
Keyword(s):  
Nk Cell ◽  
Γδ T Cells ◽  
Bronchial Epithelium ◽  
Lung Parenchyma ◽  
Recognition System ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Receptor Expression ◽  
And Function ◽  
Deficient Mice

Group 2 innate lymphoid cells (ILC2) are the majority of ILCs in murine lungs at steady state. ILC2s are the main producer of type-2-cytokines, IL-4, IL-5, IL-9, IL-13, and amphiregulin, playing key roles in lung tissue homeostasis, airway responses to pathogens and allergens, and in cancer-related defenses. ILC functions are regulated by cell surface receptors. NKR-P1B is an inhibitory receptor, which recognizes C-type lectin-related protein (Clr-b) as its ligand. NKR-P1B is expressed on subsets of natural killer cells, ILC2, ILC3, γδ T cells, macrophages and dendritic cells in a tissue-specific manner and regulates NK cell and ILC3 functions in the gut. Expression and function of NKR-P1B in the lung ILC populations is unexplored. Moreover, Clr-b, the ligand for NKR-P1B, is expressed in the bronchial epithelium, endothelial cells and in lung parenchyma, but its role in immune regulation in the lung is unknown. We hypothesize that ILC2s in the lung express NKR-P1B, and their function is regulated by the NKR-P1B:Clr-b recognition system. Using wild-type (WT) and NKR-P1B-deficient mice, we study the expression of NKR-P1B on lung ILC2, and the function of NKR-P1B:Clr-b recognition system in ILC2 development and function. We compare the phenotype, frequency, numbers and cytokine production by ILC2s upon stimulation between WT and NKR-P1B-deficient mice using antibody staining and flow cytometry analysis. This study will reveal the role of NKR-P1B as a model system for its human homolog, NKR-P1A, in the regulation of ILC development and function, advancing our understanding of how immune responses in the lung are regulated.

Abstract 3: Il-10 Regulated Mir-375 Enhances Endothelial Progenitor Cell Mediated Myocardial Repair And Survival After Myocardial Infarction.

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Venkata N Garikipati ◽  
Prasanna Krishnamurthy ◽  
Suresh K Verma ◽  
Alexandra R Mackie ◽  
Erin E Vaughan ◽  
...  
Keyword(s):  
Capillary Density ◽  
Tube Formation ◽  
Lv Function ◽  
Myocardial Repair ◽  
Knock Down ◽  
Cardiac Functions ◽  
Dependent Protein ◽  
And Function ◽  
Deficient Mice

We hypothesized that IL-10 regulates miR-375 signaling in EPCs to enhance their survival and function in ischemic myocardium after MI. miR-375 knock down EPC were transplanted intramyocardially after induction of MI. Mice receiving EPC treated with miR-375 inhibitor showed increased number of GFP+EPCs retention that was associated with reduced EPC apoptosis in the myocardium. The engraftment of EPC into the vascular structures and the associated capillary density was significantly higher in miR-375-treated mice. The above findings further correlated with reduced infarct size, fibrosis and enhanced LV function (echocardiography) in miR-375 knock down EPC group as compared to scrambled EPC. Our in vitro studies revealed that the knockdown of miR-375 enhanced EPC proliferation, migration; tube formation ability and inhibited cell apoptosis, while the up-regulation of miR-375 with the mimic had the opposite effects. In addition, we found that miR-375 negatively regulates the expression of 3-phosphoinositide-dependent protein kinase 1 (PDK1) by directly targeting the 3'UTR of the PDK1 transcript. Interestingly, EPC isolated from IL-10-deficient mice has elevated basal levels of miR-375 and exhibited poor proliferation and tube formation ability where as miR-375 knock down in EPC isolated from IL-10 deficient mice attenuated these effects. Furthermore, transplantation of miR-375 knock down IL-10 deficient EPC after MI resulted in attenuated cardiac functions compared to scramble IL-10 deficient EPCs. Taken together, our studies suggest that IL-10 regulated miR-375 enhances EPC survival and function, associated with efficient myocardial repair via activation of PDK-1/AKT signaling cascades.

Surfactant metabolism in transgenic mice after granulocyte macrophage-colony stimulating factor ablation

1996 ◽  
Vol 270 (4) ◽  
pp. L650-L658 ◽  
Author(s):  
M. Ikegami ◽  
T. Ueda ◽  
W. Hull ◽  
J. A. Whitsett ◽  
R. C. Mulligan ◽  
...  
Keyword(s):  
Protein A ◽  
Surfactant Protein ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
And Function ◽  
Stimulating Factor ◽  
Deficient Mice ◽  
Surfactant Metabolism

Mice made granulocyte macrophage-colony stimulating factor (GM-CSF)-deficient by homologous recombination maintain normal steady-state hematopoiesis but have an alveolar accumulation of surfactant lipids and protein that is similar to pulmonary alveolar proteinosis in humans. We asked how GM-CSF deficiency alters surfactant metabolism and function in mice. Alveolar and lung tissue saturated phosphatidylcholine (Sat PC) were increased six- to eightfold in 7- to 9-wk-old GM-CSF-deficient mice relative to controls. Incorporation of radiolabeled palmitate and choline into Sat PC was higher in GM-CSF deficient mice than control mice, and no loss of labeled Sat PC occurred from the lungs of GM-CSF-deficient mice. Secretion of radiolabeled Sat PC to the alveolus was similar in GM-CSF-deficient and control mice. Labeled Sat PC and surfactant protein A (SP-A) given by tracheal instillation were cleared rapidly in control mice, but there was no measurable loss from the lungs of GM-CSF-deficient mice. The function of the surfactant from GM-CSF-deficient mice was normal when tested in preterm surfactant-deficient rabbits. GM-CSF deficiency results in a catabolic defect for Sat PC and SP-A.

Treadmill running causes significant fiber damage in skeletal muscle of KATP channel-deficient mice

2005 ◽  
Vol 22 (2) ◽  
pp. 204-212 ◽  
Author(s):  
M. Thabet ◽  
T. Miki ◽  
S. Seino ◽  
J.-M. Renaud
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Treadmill Running ◽  
Wild Type ◽  
Connective Tissues ◽  
Fiber Damage ◽  
Hindlimb Muscles ◽  
Skeletal Muscle Fibers ◽  
And Function ◽  
Deficient Mice

Although it has been suggested that the ATP-sensitive K+ (KATP) channel protects muscle against function impairment, most studies have so far given little evidence for significant perturbation in the integrity and function of skeletal muscle fibers from inactive mice that lack KATP channel activity in their cell membrane. The objective was, therefore, to test the hypothesis that KATP channel-deficient skeletal muscle fibers become damaged when mice are subjected to stress. Wild-type and KATP channel-deficient mice (Kir6.2−/− mice) were subjected to 4–5 wk of treadmill running at either 20 m/min with 0° inclination or at 24 m/min with 20° uphill inclination. Muscles of all wild-type mice and of nonexercised Kir6.2−/− mice had very few fibers with internal nuclei. After 4–5 wk of treadmill running, there was little evidence for connective tissues and mononucleated cells in Kir6.2−/− hindlimb muscles, whereas the number of fibers with internal nuclei, which appear when damaged fibers are regenerated by satellite cells, was significantly higher in Kir6.2−/− than wild-type mice. Between 5% and 25% of the total number of fibers in Kir6.2−/− extensor digitum longus, plantaris, and tibialis muscles had internal nuclei, and most of such fibers were type IIB fibers. Contrary to hindlimb muscles, diaphragms of Kir6.2−/− mice that had run at 24 m/min had few fibers with internal nuclei, but mild to severe fiber damage was observed. In conclusion, the study provides for the first time evidence 1) that the KATP channels of skeletal muscle are essential to prevent fiber damage, and thus muscle dysfunction; and 2) that the extent of fiber damage is greater and the capacity of fiber regeneration is less in Kir6.2−/− diaphragm muscles compared with hindlimb muscles.

Understanding and Addressing Muscle Strength, Mass, and Function in Older Persons

2019 ◽  
Vol 20 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Philip D. Sloane ◽  
Emanuele Marzetti ◽  
Francesco Landi ◽  
Sheryl Zimmerman
Keyword(s):  
Muscle Strength ◽  
Older Persons ◽  
And Function
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