Miracle-dz/UniFAR-FTUs huggingface dataset:
Influence of exercise intensity and duration on biochemical adaptations in skeletal muscle.

The influence of intensity and daily duration of exercise on cytochrome c concentration in the three muscle fiber types was assessed in rats that were treadmill trained for 8 wk (5 days/wk) by 1 of 19 protocols. The importance of exercise duration was determined at six running intensities (10, 20, 30, 40, 50, and 60 m/min). Daily run times resulted in a maximal adaptive change for each running intensity. The general pattern of cytochrome c change, caused by increasing daily run times, followed a first-order manner in all fiber types. The final time-independent asymptotic values were dependent on the intensity of running. In addition, as running intensity was increased, the length of daily run time required to achieve the peak adaptive response was shortened. The intensity influence was very different between fiber types. In the fast-twitch red fiber, the maximal time-independent response at each work intensity was altered by exercise intensity at only submaximal work loads (i.e., the adaptation from 19 to 29 nmol/g was not further increased at 50 and 60 m/min). In contrast, the adaptive response in the fast-twitch white fiber began at 30 m/min (approx 80% VO2max) and increased exponentially as intensity was increased (200% increase at 60 m/min). Whether this different adaptive response between fiber types is due solely to the ordered recruitment of motor units remains to be determined.
Laminin Modulates Morphogenic Properties of the Collagen XVIII Endostatin Domain*

We have shown previously that the oligomeric endostatin domain of collagen XVIII (NC1) functioned as a motility-inducing factor regulating the extracellular matrix-dependent morphogenesis of endothelial cells. This motogenic activity gave rise to structures resembling filipodia and lamellipodia and was dependent on Rac, Cdc42, and mitogen-activated protein kinase. Here, we demonstrate that these properties of endostatin are primarily mediated by laminin in the basement membrane and heparan sulfates on the cell surface. The sites of interaction between laminin and oligomeric endostain include the N-terminal regions of all three laminin chains (amino acids 204–1243 of the α chain, 932–1161 of the β chain, and 150–965 of the γ chain). A monoclonal antibody that blocks the interactions between endostatin and laminin was utilized to inhibit the motogenic activity of endostatin. In parallel, we have engineered selective point mutations and produced recombinant forms that lack binding to heparan sulfates on the cell surface. Our data are consistent with a model of endostatin with two binding sites: one mainly to laminin in the basement membrane and the other to heparan sulfates on the cell surface. The two binding domains on endostatin appear to be separate with the possibility of some overlap between the two sites.
Levels of measurement

The level of measurement refers to the relationship among the values that are assigned to the attributes for a variable. What does that mean? Begin with the idea of the variable, in this example "party affiliation. " That variable has a number of attributes. Let's assume that in this particular election context the only relevant attributes are "republican", "democrat", and "independent". For purposes of analyzing the results of this variable, we arbitrarily assign the values 1, 2 and 3 to the three attributes. The level of measurement describes the relationship among these three values. In this case, we simply are using the numbers as shorter placeholders for the lengthier text terms. We don't assume that higher values mean "more" of something and lower numbers signify "less". We don't assume the the value of 2 means that democrats are twice something that republicans are. We don't assume that republicans are in first place or have the highest priority just because they have the value of 1. In this case, we only use the values as a shorter name for the attribute. Here, we would describe the level of measurement as "nominal".
Algorithms for Model Assignment in MultiGene Phylogenetics

The maximum likelihood method is a frequently applied approach to infer phylogenetic (evolutionary) trees from genetic data. For this purpose stochastic models are applied that specify the rates at which mutations occur. Depending on the model-choice, the plausibility of phylogenies can be di erent. Therefore, one wants to assign models reasonably. Frequently only one common model is used for distinct genetic partitions for multi-gene phylogenetic inferences. However, this does not allow for gene-speci c variation of rates. In this thesis we introduce the combinatorial optimization problem of protein model assignment. This problem describes the task of appropriately specifying di erent protein models to distinct genetic partitions. That is, we strive to nd a model for each partition such that the likelihood score is maximized. The complexity of this task grows exponentially with the number of genes included in the data. Therefore, it does not to seem to be feasible to exhaustively evaluate all model to partition assignments. However, it is important to provide objective approaches to quickly determine appropriate model assignments, because of the vastly growing availability of data for whole genomes. Therefore, we also develop and evaluate heuristics to estimate partition distinct model assignments for the use in multi-gene phylogenetics.
Enzyme Degradation and Proinflammatory Activity in Arthritogenic and Nonarthritogenic Eubacterium aerofaciens Cell Walls

ABSTRACT Two almost-identical strains of Eubacterium aerofaciens isolated from the normal human gut flora were used. The cell wall (CW) of one strain with a peptidoglycan (PG) type A4α induces chronic arthritis in the rat after a single intraperitoneal injection, whereas CW of the other with PG type A4β induces only a transient acute arthritis. The CW of the arthritogenic E. aerofaciens was a twofold-more-potent stimulator of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and monocyte chemoattractant protein 1 (MCP-1) than the nonarthritogenic CW. After degradation with mutanolysin, the capacity of the arthritogenic PG to stimulate production of TNF-α and MCP-1 was significantly increased, whereas that of the nonarthritogenic PG was significantly decreased. In other words, after enzyme degradation the arthritogenic PG had a four- to fivefold-stronger stimulatory capacity than that of the enzyme-treated nonarthritogenic PG. These findings indicate that the arthritogenicity of CW or a PG is not dependent on the enzyme resistance alone but also on how the PG fragments released by enzyme degradation stimulate the production of proinflammatory cytokines.
Parity-Dependent Recognition of DBL1X-3X Suggests an Important Role of the VAR2CSA High-Affinity CSA-Binding Region in the Development of the Humoral Response against Placental Malaria

ABSTRACT Plasmodium falciparum multidomain protein VAR2CSA stands today as the leading vaccine candidate against pregnancy-associated malaria (PAM). Most of the studies aiming to decrypt how naturally acquired immunity develops have assessed the immune recognition of individual VAR2CSA Duffy-binding-like (DBL) domains, thus overlooking the presence of conformational epitopes resulting from the overall folding of the full-length protein. In order to characterize the development of humoral immunity toward VAR2CSA, we made use of a large cohort of 293 Senegalese pregnant women to assess the level of recognition by plasma IgG of the full-length VAR2CSA protein of the 3D7 parasite strain (3D7-VAR2CSA), the CSA-binding multidomains 3D7-DBL1X to -DBL3X (3D7-DBL1X-3X), and the CSA nonbinding multidomains 3D7-DBL4ε to -DBL6ε (3D7-DBL4ε-6ε), as well as individual 3D7-DBL domains. Our results revealed a parity-dependent recognition of the full-length 3D7-VAR2CSA and of the CSA-binding region, 3D7-DBL1X-3X. Indeed, multigravid women possess significantly higher levels of antibodies directed against these constructs than primigravidae. Our results suggest an important role of antibodies targeting the CSA-binding region in the development of immunity against PAM, therefore providing new insights on how natural protection might be acquired and further information for the design of VAR2CSA-based vaccines.
Repair rates of R-band, G-band and C-band DNA in murine and human cultured cells

Repair of cyclobutane pyrimidine dimers (CPDs) in cultured neonatal human fibroblasts and in Mus spretus × M. castaneus F1 neonatal skin fibroblasts was analyzed after UVC-irradiation by cleavage with T4 endonuclease V cyclopyrimidine dimer glycosylase, alkaline-agarose gel electrophoresis, and Southern blotting. The blots were sequentially probed with 32P-labeled Alu, or B2, to preferentially illuminate R-band DNA, by L1 to preferentially illuminate G-band DNA, and by satellite DNA to illuminate C-band DNA. These three different DNA populations showed slightly different global nucleotide excision repair rates that are in the order of speed, R-band DNA > G-band DNA > C-band DNA. Fibroblasts from out-bred neonatal mice and humans showed similar band-specific repair rate ratios and the global repair rate of murine fibroblasts was almost as rapid as that of the human fibroblasts. The mass distribution of the human Alu-probed signal was further analyzed. Gel mobility data was fitted to a logistic equation to include all Mr values. Hypothetical distributions of DNA randomly cleaved to a particular number-average molecular weight were fit to the logistic gel mobility function to determine how such a randomly cleaved distribution of a particular cleavage frequency would be displayed along the experimental gel. This revealed a rapidly repaired kinetic fraction that represented 17% of the Alu-probed signal (R-band DNA), almost none of the L1 probed signal (G-band DNA), and reflects transcription coupled repair of active genes. The remaining Alu-probed DNA showed a random distribution of UVC-induced CPDs throughout all stages of global nucleotide excision repair. The Alu-probed CPDs disappeared with an excellent fit to first order kinetics and with a half-life of seven hours.
Mesopores inside electrode particles can change the Li-ion transport mechanism and diffusion-induced stress

Following earlier work of Huggins and Nix [ Ionics 6 , 57 (2000)], several recent theoretical studies have used the shrinking core model to predict intraparticle Li concentration profiles and associated stress fields. A goal of such efforts is to understand and predict particle fracture, which is sometimes observed in degraded electrodes. In this paper we present experimental data on LiCoO_2 and graphite active particles, consistent with previously published data, showing the presence of numerous internal pores or cracks in both positive and negative active electrode particles. New calculations presented here show that the presence of free surfaces, from even small internal cracks or pores, both quantitatively and qualitatively alters the internal stress distributions such that particles are prone to internal cracking rather than to the surface cracking that had been predicted previously. Thus, the fracture strength of particles depends largely on the internal microstructure of particles, about which little is known, rather than on the intrinsic mechanical properties of the particle materials. The validity of the shrinking core model for explaining either stress maps or transport is questioned for particles with internal structure, which includes most, if not all, secondary electrode particles.
Exercise modulates circulating adipokine levels in hypertrophic cardiomyopathy.

INTRODUCTION Studies conducted so far have shown that patients with left ventricular hypertrophy have increased adiponectin levels; however, these studies were performed only in resting condition. OBJECTIVES The aim of the study was to compare adiponectin, resistin, and leptin levels (at rest and after exercise) between patients with hypertrophic cardiomyopathy (HCM) and healthy controls. Additionally, we examined potential relationships between the levels of the 3 adipokines and the left ventricular outflow tract (LVOT) gradient both at rest and at peak exercise. PATIENTS AND METHODS We studied 29 patients with HCM (mean age 42.7 ±11.9 years, 16 men and 13 women). The control group included 19 healthy subjects matched for age-, sex-, and the body mass index. After echocardiographic examination in a supine position, all patients were placed in an upright position and treadmill exercise test was performed with simultaneous continuous echocardiographic monitoring of the LVOT gradient. Adiponectin, resistin, and leptin levels were measured immediately prior to exercise in a supine position and at peak exercise in an upright position. RESULTS At baseline (at rest), adiponectin levels tended to be increased in patients with HCM (P = 0.09), while resistin and leptin levels were significantly higher in patients with HCM than in healthy controls. In HCM patients, exercise induced an increase in adiponectin (20.74 ±7.95 vs. 22.52 ±8.10 μg/ml, P <0.05), a decrease in leptin (22.78 ±6.08 vs. 20.63 ±5.57 ng/ml, P <0.05), and no significant effect on resistin. In the control group, all biomarkers mildly decreased at peak exercise (adiponectin 19.23 ±5.43 vs. 18.66 ±5.31 μg/ml P = 0.044), resistin 14.80 ±1.87 vs. 13.87 ±1.21 ng/ml, P = 0.030), (leptin 14.34 ±4.74 vs. 13.50 ±3.98 ng/ml, P = 0.045). In HCM patients, neither resting nor peak exercise values of the LVOT gradient correlated with any levels of adipokines. CONCLUSIONS In patients with HCM, but not in healthy individuals, moderate exercise induced an increase in adiponectin levels and a decrease in leptin levels independent of a rise in the LVOT gradient. The potential cardioprotective role of adiponectin during exercise stress in HCM requires further studies.
Cardiovascular Disease and Hypertension Risk in Living Kidney Donors: An Analysis of Health Administrative Data in Ontario, Canada

Background. Knowledge of any harm associated with living kidney donation guides informed consent and living donor follow-up. Risk estimates in the literature are variable, and most studies did not use a healthy control group to assess outcomes attributable to donation. Methods. We observed a retrospective cohort using health administrative data for donations which occurred in Ontario, Canada between the years 1993 and 2005. There were a total of 1278 living donors and 6359 healthy adults who acted as a control group. Individuals were followed for a mean of 6.2 years (range, 1-13 years) after donation. The primary outcome was a composite of time to death or first cardiovascular event (myocardial infarction, stroke, angioplasty, and bypass surgery). The secondary outcome was time to a diagnosis of hypertension. Results. There was no significant difference in death or cardiovascular events between donors and controls (1.3% vs. 1.7%; hazard ratio 0.7, 95% confidence interval 0.4-1.2). Donors were more frequently diagnosed with hypertension than controls (16.3% vs. 11.9%, hazard ratio 1.4, 95% confidence interval 1.2-1.7) but were also seen more often by their primary care physicians (median [interquartile range] 3.6 [1.9-6.1] vs. 2.6 [1.4-4.3] visits per person year, P<0.001). Conclusions. Based on administrative data, the risk of cardiovascular disease was unchanged in the first decade after kidney donation. The observed increase in diagnosed hypertension may be due to nephrectomy or more blood pressure measurements received by donors in follow-up and requires prospective study.
Spinal Muscular Atrophy With Respiratory Distress Type 1 (SMARD1)

Autosomal recessive spinal muscular atrophy with respiratory distress type 1 (SMARD1), recently referred to as distal spinal muscular atrophy 1 (DSMA1; MIM#604320) and also known as distal hereditary motor neuropathy type 6 (dHMN6 or HMN6), results from mutations in the IGHMBP2 gene on chromosome 11q13.3 encoding the immunoglobulin µ-binding protein 2. In contrast to the infantile spinal muscular atrophy type 1 (SMA1; Werdnig-Hoffmann disease) with weakness predominantly of proximal muscles and bell-shaped thorax deformities due to intercostal muscle atrophy, infants with distal spinal muscular atrophy 1 usually present with distal muscle weakness, foot deformities, and sudden respiratory failure due to diaphragmatic paralysis that often requires urgent intubation. In this article, the authors review the clinical, neuropathological, and genetic aspects of distal spinal muscular atrophy 1 and discuss differential diagnoses.
Pre-Trained AlexNet Architecture with Pyramid Pooling and Supervision for High Spatial Resolution Remote Sensing Image Scene Classification

The rapid development of high spatial resolution (HSR) remote sensing imagery techniques not only provide a considerable amount of datasets for scene classification tasks but also request an appropriate scene classification choice when facing with finite labeled samples. AlexNet, as a relatively simple convolutional neural network (CNN) architecture, has obtained great success in scene classification tasks and has been proven to be an excellent foundational hierarchical and automatic scene classification technique. However, current HSR remote sensing imagery scene classification datasets always have the characteristics of small quantities and simple categories, where the limited annotated labeling samples easily cause non-convergence. For HSR remote sensing imagery, multi-scale information of the same scenes can represent the scene semantics to a certain extent but lacks an efficient fusion expression manner. Meanwhile, the current pre-trained AlexNet architecture lacks a kind of appropriate supervision for enhancing the performance of this model, which easily causes overfitting. In this paper, an improved pre-trained AlexNet architecture named pre-trained AlexNet-SPP-SS has been proposed, which incorporates the scale pooling—spatial pyramid pooling (SPP) and side supervision (SS) to improve the above two situations. Extensive experimental results conducted on the UC Merced dataset and the Google Image dataset of SIRI-WHU have demonstrated that the proposed pre-trained AlexNet-SPP-SS model is superior to the original AlexNet architecture as well as the traditional scene classification methods.
Dihydropteroate Synthase and Novel Dihydrofolate Reductase Gene Mutations in Strains of Pneumocystis jirovecii from South Africa

ABSTRACT Dihydropteroate synthase (DHPS) gene mutations have raised concerns about emerging sulfonamide resistance in Pneumocystis jirovecii. DHPS and dihydrofolate reductase (DHFR) gene products were amplified in clinical specimens from South African patients. One of 53 DHPS genes sequenced contained the double mutation Thr55Ala Pro57Ser. DHFR gene mutations detected were Ala67Val and the new mutations Arg59Gly and C278T.
No Evidence for Axonal Atrophy in Human Diabetic Polyneuropathy

In rats with streptozin-induced diabetes mellitus, the caliber of distal myelinated fiber (MF) axons in relation to the number of myelin lamellae is smaller than in controls. This finding usually has been attributed to axonal atrophy, but shrinkage or maldevelopment has also been considered. For human diabetic polyneuropathy (DP), axonal atrophy has been assumed by some investigators, but convincing evidence has not been demonstrated. We morphometrically evaluated transverse sections of 33 sural nerves from carefully evaluated diabetic patients ≥ 30 years old without (8 patients) or with (25 patients) DP and compared them with 24 nerves from healthy subjects ≥ 30 years old. Nerves from diabetic patients and controls were obtained under identical conditions and processed and evaluated in the same way, using an observer blind to the disease condition. Using computer digitization of electron micrographs, we evaluated the axonal area, perimeter, index of circularity, number of myelin lamellae, and frequency of adaxonal sequestration of 50.4 (mean) ± 5.8 (SD) MF per sural nerve for healthy subjects and diabetic patients ≥ 30 years old. The regression lines of the natural log (In) of axonal area on number of myelin lamellae of diabetic patients (with or without DP) were not significantly different from the regression lines of nerves of healthy subjects for large MFs—the most reliable group in which to recognize atrophy. Likewise, the regression lines of index of circularity (IC) (an index that is decreased with atrophy or shrinkage) on number of myelin lamellae for large fibers was not significantly different between the disease and control groups. The rate of adaxonal sequestration was not significantly higher in DP than in healthy subjects. These results do not support the hypothesis that axonal atrophy occurs in human DP. For small MF. or all MF. some significant differences in regression lines of In axonal area or IC on number of lamellae were found, but these changes are probably explained by events of remyelination and axonal regeneration, which can affect these relationships and are known to occur in DP.
INVESTIGATION OF NEUROPROTECTIVE EFFECT OF DEXAMETHASONE BY USING NITRIC OXIDE AND LEUKOCYTE LEVELS IN EXPERIMENTAL HEAD TRAUMA

The objective of the present study was to determine the levels of nitric oxide (NO) and white blood cells (WBCs), which are assumed to play a role in secondary cerebral damage by increasing to pathological levels during cranial trauma, and to investigate the neuroprotective effect of dexamethasone on NO and WBC levels in experimental cranial trauma. For this purpose, adult Sprague-Dawley male rats were used. Blood NO and WBC levels were investigated in one group of non-trauma rats (control group, n = 10) after 6 h; in a group of rats with experimental post-cranial trauma (trauma group, n = 10) after 6 and 24 h; and in a third group of rats with experimental cranial trauma, intraperitoneally injected with 10 mg/kg dexamethasone after 1 and 12 h (trauma + dexamethasone group, n = 10), WBC and NO levels were measured after 6 and 24 h. Determination of NO levels was carried out by assaying serum nitrite and nitrate levels. The increases in post-trauma serum NO (nitrite and nitrate) and WBC levels were statistically significant for the trauma and trauma + dexamethasone groups compared to controls. There was no significant difference between serum NO and WBC levels in rats in the trauma + dexamethasone and those in the trauma group. The study demonstrated no significant inhibition of NO and WBC levels by dexamethasone, a drug used for its anti-edema and anti-inflammatory effects and its influence on membrane stabilization and in avoiding oscillation stress. In the present study, dexamethasone was found to be ineffective in decreasing NO and WBC levels to avoid secondary cerebral damage after cranial trauma.