The Effects Of A Single Exercise Bout On Plasma Leptin Concentration In Obese Males

Recent findings suggest that leptin may be regulated in response to abrupt changes in energy homeostasis. Therefore, it is conceivable that transient changes in energy balance induced by exercise may also regulate leptin synthesis and secretion. As such, we hypothesized that acute increases energy expenditure (i.e. exercise), may regulate leptin concentrations in obese individuals. Fifteen healthy obese males underwent either a single exercise session of moderate intensity (58.4 % ± 4.0 of VO2max) for 60 min (n=8), or served as controls (n=7). The exercise session elicited an energy expenditure of 567±80 Kcal. No significant changes in plasma leptin (pre 23.5± 30.2; post 24.3± 34.3; 24h-post 34.9± 66.6; 48h-post 33.8±64.0 ng/ml), or insulin levels (pre 16.1± 9.2 vs. post 8.1± 9.1; 24h-post 14.3± 9.9; 48h-post 13.8± 10.2 ?U/ml) were detected immediately after the intervention. Baseline plasma leptin levels were positively correlated with BMI (r=0.65; p\u3c0.01), body weight (r=0.64; p\u3c0.01), % body fat (r=0.90; p\u3c0.01) and were negatively correlated with VO2max (r=-0.82; p\u3c0.01). The results of the present study suggest that acute exercise of moderate intensity and duration may not affect leptin concentration

Inversion of noisy Radon transform by SVD based needlet

A linear method for inverting noisy observations of the Radon transform is developed based on decomposition systems (needlets) with rapidly decaying elements induced by the Radon transform SVD basis. Upper bounds of the risk of the estimator are established in $L^p$ ($1\le p\le \infty$) norms for functions with Besov space smoothness. A practical implementation of the method is given and several examples are discussed

The Endocytic Protein Numb Regulates App Metabolism And Notch Signaling: Implications For Alzheimer\u27s Disease

Increased production of amyloid beta (A-beta) peptide, via altered proteolytic cleavage of amyloid protein precursor (APP), and abnormalities in neuronal calcium homeostasis play central roles in the pathogenesis of Alzheimer\u27s disease (AD). Notch1, a membrane receptor that controls cell fate decisions during development of the nervous system, has been linked to AD because it is a substrate for the gamma-secretase protein complex in which mutations cause early-onset inherited AD. Numb is an evolutionarily conserved endocytic adapter involved in the internalization of transmembrane receptors. Mammals produce four Numb isoforms that differ in two functional domains, a phosphotyrosine-binding domain (PTB) and a proline-rich region (PRR). Recent studies showed that the PTB domain of Numb interacts with the cytoplasmic tails of APP and Notch but the functional relevance of these interactions with respect to AD pathogenesis is not clear. In the current studies, we proposed to investigate the biological consequences of the interaction of the Numb proteins with APP and Notch in neural cells stably overexpressing each of the four human Numb proteins. In the first part of our studies, we found that expression of the Numb isoforms lacking the insert in the PTB (SPTB-Numb) caused the abnormal accumulation of cellular APP in the early endosomes, and increased the levels of C-terminal APP fragments and A-beta. By contrast, expression of the Numb isoforms with the insert in PTB (LPTB-Numb) leads to the depletion of cellular APP and coincides with significantly lower production of APP derivatives and A-beta. The contrasting effects of the Numb isoforms on APP metabolism were not attributed to differences in the expression of APP nor the activities of the various APP-processing secretases. In the second part of our studies, we found that expression of SPTB-Numb protein enhances neuronal vulnerability to serum deprivation-induced cell death by a mechanism involving the dysregulation of cellular calcium homeostasis. Neural cells expressing SPTB-Numb exhibited enhanced Notch activity, which markedly upregulated the expression of transient receptor potential canonical 6 (TRPC6) channels enhancing calcium entry in response to store depletion. We also found that serum deprivation increased TRPC6 expression, mediating the serum deprivation-induced death in neural cells. Interestingly, expression of LPTB-Numb protein suppressed serum deprivation-induced activation of Notch and the subsequent upregulation of TRPC6 and cell death. Finally, we showed that the Numb proteins differentially impact Notch activation by altering the endocytic trafficking and processing of Notch. Taken together, these studies demonstrate that aberrant expression of the Numb proteins may influence APP metabolism and Notch-mediated cellular responses to injury by altering their endocytic trafficking and processing

Serum leptin and tumor necrosis factor - alpha levels and maximal exercise performance in patients with chronic obstructive pulmonary disease

Systemic inflammation plays an important role in skeletal muscle dysfunction in patients with Chronic Obstructive Pulmonary Disease (COPD). The aim of this study is to determine whether serum leptin and tumor necrosis factor- alpha (TNF-a) levels, as markers of systemic inflammation, affect the maximal exercise performance of COPD patients.Methods: Thirty male COPD patients underwent pulmonary function and progressive exercise testing for maximal exercise and for VO2max determination. Fat Free Mass (FFM), Fat Mass (FM) and Thigh Muscle Area (TMA) were estimated by measuring skinfold thickness. Serum leptin and TNF-a levels were determined in morning blood samples.Results: Significant correlations were found between serum leptin levels and Body Mass Index (BMI) (r = 0.421, p < 0.02), FM (r = 0.551, p < 0.01) and TNF-a (r = 0.521, p < 0.001). Exercise performance, expressed as VO2max, correlated significantly with % FEV1 (r = 0.563, p < 0.001), BMI (r = 0.636, p < 0.001), FFM (r = 0.415, p < 0.02), TMA (r = 0.651, p < 0.001), but not with serum leptin or TNF-a levels. By stepwise regression analysis TMA appeared to be a significant predictor of VO2max in COPD patients.Conclusion: Serum leptin and TNF-a levels were poor predictors of maximal exercise capacity (VO2max) in COPD patients. The best predictors of VO2max during exercise were airflow limitation (%FEV1) and thigh muscle mass expressed by TMA.Results: Significant correlations were found between serum leptin levels and Body Mass Index (BMI) (r = 0.421, p < 0.02)

Atomic and molecular decomposition of homogeneous spaces of distributions associated to non-negative self-adjoint operators

We deal with homogeneous Besov and Triebel-Lizorkin spaces in the setting of a doubling metric measure space in the presence of a non-negative self-adjoint operator whose heat kernel has Gaussian localization and the Markov property. The class of almost diagonal operators on the associated sequence spaces is developed and it is shown that this class is an algebra. The boundedness of almost diagonal operators is utilized for establishing smooth molecular and atomic decompositions for the above homogeneous Besov and Triebel-Lizorkin spaces. Spectral multipliers for these spaces are established as well

Batch and Streaming Data Ingestion towards Creating Holistic Health Records

The healthcare sector has been moving toward Electronic Health Record (EHR) systems that produce enormous amounts of healthcare data due to the increased emphasis on getting the appropriate information to the right person, wherever they are, at any time. This highlights the need for a holistic approach to ingest, exploit, and manage these huge amounts of data for achieving better health management and promotion in general. This manuscript proposes such an approach, providing a mechanism allowing all health ecosystem entities to obtain actionable knowledge from heterogeneous data in a multimodal way. The mechanism includes diverse techniques for automatically ingesting healthcare-related information from heterogeneous sources that produce batch/streaming data, managing, fusing, and aggregating this data into new data structures (i.e., Holistic Health Records (HHRs)). The latter enable the aggregation of data coming from different sources, such as Internet of Medical Things (IoMT) devices, online/offline platforms, while to effectively construct the HHRs, the mechanism develops various data management techniques covering the overall data path, from data acquisition and cleaning to data integration, modelling, and interpretation. The mechanism has been evaluated upon different healthcare scenarios, ranging from hospital-retrieved data to patient platforms, combined with data obtained from IoMT devices, having produced useful insights towards its successful and wide adaptation in this domain. In order to implement a paradigm shift from heterogeneous and independent data sources, limited data exploitation, and health records, the mechanism has combined multidisciplinary technologies toward HHRs. Doi: 10.28991/ESJ-2023-07-02-03 Full Text: PD

The Homocysteine-inducible Endoplasmic Reticulum Stress Protein Counteracts Calcium Store Depletion and Induction of CCAAT Enhancer-binding Protein Homologous Protein in a Neurotoxin Model of Parkinson Disease

The endoplasmic reticulum (ER) is a key organelle regulating intracellular Ca(2+) homeostasis. Oxidants and mitochondria-derived free radicals can target ER-based Ca(2+) regulatory proteins and cause uncontrolled Ca(2+) release that may contribute to protracted ER stress and apoptosis. Several ER stress proteins have been suggested to counteract the deregulation of ER Ca(2+) homeostasis and ER stress. Here we showed that knockdown of Herp, an ubiquitin-like domain containing ER stress protein, renders PC12 and MN9D cells vulnerable to 1-methyl-4-phenylpyridinium-induced cytotoxic cell death by a mechanism involving up-regulation of CHOP expression and ER Ca(2+) depletion. Conversely, Herp overexpression confers protection by blocking 1-methyl-4-phenylpyridinium-induced CHOP upregulation, ER Ca(2+) store depletion, and mitochondrial Ca(2+) accumulation in a manner dependent on a functional ubiquitin-proteasomal protein degradation pathway. Deletion of the ubiquitin-like domain of Herp or treatment with a proteasomal inhibitor abolished the central function of Herp in ER Ca(2+) homeostasis. Thus, elucidating the underlying molecular mechanism(s) whereby Herp counteracts Ca(2+) disturbances will provide insights into the molecular cascade of cell death in dopaminergic neurons and may uncover novel therapeutic strategies to prevent and ameliorate Parkinson disease progression

Risk Factors of Pancreatic Cancer: A Literature Review

Objective: To identify and compare current modifiable and non-modifiable risk factors for pancreatic cancer (PaCa) that may have potential application in PaCa risk stratification, prevention, and early detection. / Material: All articles in this literature review were identified through systematic searches of PubMed, Medline, and Embase databases. All articles were published in the English language, between January 2000 to December 2021 and with an abstract. In this review study, we judge the evidence level of different PaCa risk factors through the criteria of grading evidence for cancer prevention. / Results: The modifiable risk factors identified included cigarette smoking, heavy alcohol consumption, increased Body Mass Index (BMI) and abdominal obesity, chronic pancreatitis, diabetes, hepatitis B virus (HBV) infection, periodontal disease, cholecystectomy and chemicals and asbestos exposure. The non-modifiable risk factors included age, gender, ethnicity, blood type, family history, inherited syndromes, germline mutation, and single nucleotide polymorphisms (SNPs). However, there are still some ambiguous risk factors for which the current evidence is inconclusive such as low physical activity, increased consumption of red/processed meat and dairy products, vitamin D insufficiency, and some medical-related conditions including gut microbiota such as Helicobacter Pylori infection, long-term usage of Proton-pump inhibitors (PPI), and Systemic Lupus Erythematosus (SLE) history. / Conclusions: This literature review summarizes the modifiable and non-modifiable risk factors of PaCa with strong evidence, which could be used to further establish PaCa predictive model as an application of PaCa risk stratification, raise public awareness and educate the public as a prevention program. Further studies are needed to investigate other potential risk factors