Miracle-dz/UniFAR-FTUs huggingface dataset:
Thrombospondin-1 Gene Deficiency Worsens the Neurological Outcomes of Traumatic Brain Injury in Mice

Background: Thrombospondin-1 (TSP-1) is an extracellular matrix protein that plays multiple physiological and pathophysiological roles in the brain. Experimental reports suggest that TSP-1 may have an adverse role in neuronal function recovery under certain injury conditions. However, the roles of TSP-1 in traumatic brain injury (TBI) have not been elucidated. In this study we for the first time investigated the roles of TSP-1 in a controlled cortical impact (CCI) model of TBI in TSP-1 knockout (TSP-1 KO) and wild type (WT) mice. Methods: We examined blood brain-barrier (BBB) damage using at 1 day post-TBI by measuring Evans Blue leakage, and neurological functional recovery at 3 weeks post-TBI by measuring neurological severity score (NSS), wire gripping, corner test and Morris Water Maze (MWM). Mechanistically, we quantified pro-angiogenic biomarkers including cerebral vessel density, vascular endothelial growth factors (VEGF) and angiopoietin-1 (Ang-1) protein expression, synaptic biomarker synaptophysin, and synaptogenesis marker brain-derived neurotrophic factor (BDNF) protein expression in contralateral and ipsilateral (peri-lesion) cortex at 21 days after TBI using immunohistochemistry and Western Blot. Results: TSP-1 is upregulated at early phase of TBI in WT mice. Compared to WT mice, TSP-1 KO (1) significantly worsened TBI-induced BBB leakage at 1 day after TBI; (2) had similar lesion size as WT mice at 3 weeks after TBI; (3) exhibited a significantly worse neurological deficits in motor and cognitive functions; (4) had no significant difference in cerebral vessel density, but significant increase of VEGF and Ang-1 protein expressions in peri-lesion cortex; (5) significantly increased BDNF but not synaptophysin protein level in peri-lesion cortex compared to sham, but both synaptophysin and BDNF expressions were significantly decreased in contralateral cortex compared to WT. Conclusion: Our results suggest that TSP-1 may be beneficial for maintaining BBB integrity in the early phase and functional recovery in late phase after TBI. The molecular mechanisms of TSP-1 in early BBB pathophysiology, and long-term neurological function recovery after TBI need to be further investigated.
Comparative Study Regarding the Colorimetric Changes of Two Composite Resins after Immersion in Several Beverages and One Antibacterial Mouthwash

The aim of the study was to assess the colorimetric changes of two composite resins immersed in five solutions as follows: saliva (control), saliva and coffee, saliva and red wine, saliva and coca-cola, saliva and Corsodyl. The study group included 200 samples of composite resins, divided in two groups (Filtek Ultimate and Filtek Z250, 3M ESPE Dental Products, St. Paul, USA), each sample with 20mm diameter and 1,5mm thickness. The pH of immersion solutions was assessed. The samples were divided in five study groups, each sample was immersed in one of the immersion solutions, at 37 o C. For each group, 10 specimens have been immersed for 24 h in the storage solution and the other ten specimens have been stored for seven days. The colorimetric measurements were performed, using Lovibond Reflectance Tintometer RT, Lovibond Brand UK. The colorimetric differences (ΔE) defined by system CIE L*a*b*, between the control group and the study group, were assessed for each immersion period. The test U Mann-Whitney was applied to compare the study groups with the control group, and test Kruskal Wallis was applied for ΔE values. The assessment of colorimetric changes (ΔE) have shown differences between the control group (saliva) and the study groups as follows: Control 1). The test U Mann-Whitney showed statistically significant differences (p = 0.0001) between the control group and the study groups for both composite resins. The test Kruskal Wallis also showed statistically significant differences for values ΔE (p< 0.05). The composite resins Filtek Ultimate and Filtek Z250 presented visible colorimetric changes after immersion in tested solutions. The most obvious changes were observed after immersion in Coca cola, coffee and red wine. Filtek Ultimate was more stable comparing with Filtek Z250 regarding colorimetric changes.
Predicting medication non-adherence in severe affective disorders

Abstract Objective This study explored the utility of the Health Belief Models (HBM) in explaining medication adherence in subjects with severe affective disorders. Method Well established measuring instruments, with confirmed reliability and validity, were used to assess each component of two HBMs and adherence with mood stabilising medication in 104 subjects with bipolar (n=82), unipolar (n=18) or schizo-affective (n=4) disorders. Results Highly adherent and partially adherent subjects differed significantly in the stability of the level and the overall serum level of drug acheived. Subject's beliefs about themselves and their illness and their control over the disorder were more important than side-effects in predicting medication adherence. There were marked differences in the primary reasons for non-adherence identified by patients and their clinicians. Conclusion Although the study has a number of methodological limitations, the results suggest that clinical assessment of components of HBMs may improve the detection of patients at risk of non-adherence with mood stabilising medication.
Expression of Nitric Oxide Synthase Isoforms and Nitric Oxide Production in Acute Pancreatitis and Associated Lung Injury

Background/Aims: The role of nitric oxide (NO) has been increasingly implicated in the pathophysiology of acute pancreatitis (AP). Studies have shown increased NO production in AP although not all are agreeable on whether NO is beneficial or detrimental in AP. This study aims to profile NO production and NO synthase (NOS) expression in the pancreas and lungs in the progression of AP in mice to gain insights to the role played by different NOS isoforms. Methods: AP was induced in mice by hourly administration of cerulein. NO production was determined by measuring the total nitrite and nitrate (NOx) content while NOS expression was measured by Western blot. Results: Pancreatic NO production increased sharply and was sustained throughout AP. iNOS expression was greatly increased while eNOS was downregulated at the later stages. In the lungs, there was an unexpected early increase in the constitutive NOS expression; however iNOS was also significantly overexpressed at the later time point along with a significant increase in NO. Acinar cells were found to overproduce NO in response to cerulein hyperstimulation with iNOS again being the major contributor. Conclusion: These data show that NO production and NOS expression are differentially regulated temporally and in magnitude in the pancreas and lungs in response to cerulein hyperstimulation which suggests differing roles for each NOS isoform.
Comparison of the histological changes in the skin of DBA/2 and C57BL/6 mice following exposure to various promoting agents.

The effects of multiple applications of 12-O-tetradecanoyl-phorbol-13-acetate (TPA, 6.8 nmol), teleocidin (6.8 nmol), 1,8-dihydroxy-3-methyl-9-anthrone (chrysarobin, 220 nmol), mezerein (6.8 nmol), 4-O-Methyl-TPA (4-O-Me-TPA, 150 micrograms) and benzoyl peroxide (BzP, 20 mg) on the skin of DBA/2 and C57BL/6 mice were studied histologically. After four applications of TPA given over a 2-week period, the epidermis of DBA/2 mice showed a marked epidermal hyperplasia and the presence of a much greater number of dark basal keratinocytes (DCs) 48 h after the last treatment compared with C57BL/6 mice treated with a similar dose and protocol. A marked dermal infiltration of polymorphonuclear leukocytes (PMNs) was observed in DBA/2 mice 48 h after the last application of TPA, whereas little PMN infiltration was observed in skin of C57BL/6 mice. At 96 h after the last application of TPA, DBA/2 mice still showed a much greater degree of epidermal hyperplasia than C57BL/6 mice. PMNs were virtually absent in the dermis of both DBA/2 and C57BL/6 mice by 96 h after the last TPA treatment. Interestingly, treatment of both strains of mice with multiple applications of teleocidin induced a marked epidermal hyperplasia, a high percentage of DCs and a high labeling index (LI), similar to that observed in DBA/2 mice 48 h after the last treatment. Chrysarobin (given once-weekly for 4 weeks) induced a moderate sustained hyperplasia and DC response 48 h after the last treatment in both DBA/2 and C57BL/6 mice; however, C57BL/6 mice showed a greater epidermal hyperplasia than DBA/2 mice. Chrysarobin induced a significant infiltration of PMNs into the dermis of DBA/2 mice whereas in C57BL/6 mice there was only a slight dermal infiltration of PMNs. Mezerein (given twice-weekly for 2 weeks) induced a moderate epidermal hyperplasia, DC response and LI of similar magnitude in both DBA/2 and C57BL/6 mice, but did not induce PMN infiltration in either strain. BzP and 4-O-Me-TPA (given twice-weekly for 2 weeks) induced only a weak sustained epidermal hyperplasia, DC response and LI of similar magnitude in both strains of mice, and there was little, if any, dermal infiltration of PMNs either 48 or 96 h after the last treatment. Examination of the relationship between the extent of induced hyperplasia and the DC response showed an excellent linear correlation whereas the extent of PMN infiltration into the dermis was not well correlated with either parameter. (ABSTRACT TRUNCATED AT 400 WORDS)
Distinct Domains in the SHP-2 Phosphatase Differentially Regulate Epidermal Growth Factor Receptor/NF-κB Activation through Gab1 in Glioblastoma Cells

ABSTRACT The transcription factor nuclear factor κB (NF-κB) plays an important role in inflammation and cancer, is activated by a variety of stimuli including tumor necrosis factor alpha, interleukin-1, UV irradiation, and viruses, as well as receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR). Although previous studies suggest that EGFR can induce NF-κB, the mechanism of this activation remains unknown. In this study, we identify the components of the EGFR-induced signalosome in human glioblastoma cells required to regulate NF-κB activation. Immunoprecipitation analyses with ErbB-modulated cells indicate that association between SHP-2 and Grb2-associated binder 1 (Gab1) is the critical step in the formation of the signalosome linking EGFR to NF-κB activation. We also show that EGFR-induced NF-κB activation is mediated by the PI3-kinase/Akt activation loop. Overexpression of SHP-2, Gab1, and myristoylated Akt significantly upregulated NF-κB transcriptional activity and DNA binding activity in glioblastoma cells. Interestingly, overexpression of either one of the two SH2 domain mutants of SHP-2, R32E or R138E, slightly reduced NF-κB activity relative to that of wild-type SHP-2, indicating that the SH2 domains of SHP-2 are required for EGFR-induced NF-κB activation. On the other hand, ectopic overexpression of either a Gab1 mutant incapable of binding to SHP-2 (Y627F) or a phosphatase-inactive SHP-2 mutant (C459S) caused a significant increase in NF-κB activity. Moreover, SHP-2 C459S-expressing cells displayed higher Gab1 phosphotyrosine content, suggesting that SHP-2 regulates Gab1 phosphorylation through its phosphatase domain, which confers a negative regulatory effect on NF-κB activity. These results indicate that SHP-2/Gab1 association is critical for linking EGFR to NF-κB transcriptional activity via the PI3-kinase/Akt signaling axis in glioblastoma cells and that SHP-2 acts as a dual regulator of NF-κB activation.
The mass function of hydrogen-rich white dwarfs: robust observational evidence for a distinctive high-mass excess near 1 M⊙

The mass function of hydrogen-rich atmosphere white dwarfs has been frequently found to reveal a distinctive high-mass excess near 1 M-circle dot. However, a significant excess of massive white dwarfs has not been detected in the mass function of the largest white dwarf catalogue to date from the Sloan Digital Sky Survey (SDSS). Hence, whether a high-mass excess exists or not has remained an open question. In this work, we build the mass function of the latest catalogue of data release ten SDSS hydrogen-rich white dwarfs, including the cool and faint population (i.e. effective temperatures 6000 less than or similar to T-eff less than or similar to 12 000 K, equivalent to 12 mag less than or similar to M-bol less than or similar to 13 mag). We show that the high-mass excess is clearly present in our mass function, and that it disappears only if the hottest (brightest) white dwarfs (those with T-eff greater than or similar to 12 000 K, M-bol less than or similar to 12 mag) are considered. This naturally explains why previous SDSS mass functions failed at detecting a significant excess of high-mass white dwarfs. Thus, our results provide additional and robust observational evidence for the existence of a distinctive high-mass excess near 1 M-circle dot. We investigate possible origins of this feature and argue that the most plausible scenario that may lead to an observed excess of massive white dwarfs is the merger of the degenerate core of a giant star with a main-sequence or a white dwarf companion during or shortly after a common envelope event.
Heme Oxygenase Activity as a Determinant of the Renal Hemodynamic Response to Low Dose Angiotensin II

Angiotensin II causes renal injury through hemodynamic and other effects, and pressor doses of angiotensin II induce heme oxygenase-1 (HO-1) as a protective response. The present studies examined the hemodynamic effects of more clinically relevant, lower doses of angiotensin II, and the role of HO activity in influencing these effects. Under euvolemic conditions, angiotensin II increased arterial pressure and renal vascular resistance. Angiotensin II did not induce oxidative stress, inflammation/injury-related gene expression, or proteinuria, and did not alter extrarenal vascular reactivity. At these doses angiotensin II failed to increase HO-1 or HO-2 mRNA expression, or HO activity. Inhibiting HO activity in angiotensin IItreated rats by tin mesoporphyrin (SnMP) further increased renal vascular resistances, decreased renal blood flow, and blunted the rise in arterial pressure, without inducing oxidative stress or altering expression of selected vasoactive/injury/inflammation-related genes; SnMP did not alter vasorelaxation of mesenteric resistor vessels. We conclude that, in this model, renal vasoconstriction occurs without the recognized adverse effects of angiotensin II on GFR, renal blood flow, oxidative stress, vascular reactivity, proteinuria, and injury-related gene expression; renal HO activity is essential in preserving perfusion of the angiotensin II-exposed kidney. These findings represent an uncommon example wherein function of a “stressed” organ (by angiotensin II), but not that of the “unstressed” organ, requires intact renal HO activity, even when the imposed stress neither induces HO-1 nor HO activity. These findings may be germane to conditions attended by heightened angiotensin II levels, “ineffective” renal perfusion, and susceptibility to acute kidney injury. Running Head: Renal Effects of Angiotensin II 3
Cellular Mechanisms Contributing to Response Variability of Cortical Neurons In Vivo

Cortical neurons recorded in vivo exhibit highly variable responses to the repeated presentation of the same stimulus. To further understand the cellular mechanisms underlying this phenomenon, we performed intracellular recordings from neurons in cat striate cortex in vivo and examined the relationships between spontaneous activity and visually evoked responses. Activity was assessed on a trial-by-trial basis by measuring the membrane potential (Vm) fluctuations and spike activity during brief epochs immediately before and after the onset of an evoked response. We found that the response magnitude, expressed as a change in Vm relative to baseline, was linearly correlated with the preceding spontaneousVm. This correlation was enhanced when the cells were hyperpolarized to reduce the activation of voltage-gated conductances. The output of the cells, expressed as spike counts and latencies, was only moderately correlated with fluctuations in the preceding spontaneous Vm. Spike-triggered averaging of Vm revealed that visually evoked action potentials arise from transient depolarizations having a rise time of ∼10 msec. Consistent with this, evoked spike count was found to be linearly correlated with the magnitude ofVm fluctuations in the γ (20–70 Hz) frequency band. We also found that the threshold of visually evoked action potentials varied over a range of ∼10 mV. Examination of simultaneously recorded intracellular and extracellular activity revealed a correlation between Vmdepolarization and spike discharges in adjacent cells. Together these results demonstrate that response variability is attributable largely to coherent fluctuations in cortical activity preceding the onset of a stimulus, but also to variations in action potential threshold and the magnitude of high-frequency fluctuations evoked by the stimulus.
Adult Stem Cells, Lung Biology, and Lung Disease

University of Vermont College of Medicine, Burlington, Vermont; Will Rogers Institute Pulmonary Research Center, University of Southern California, Los Angeles, California; Division of Lung Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health; and the Cystic Fibrosis Foundation, Bethesda, Maryland; Children’s Hospital of Pittsburgh Center for Gene Therapy, Pittsburgh, Pennsylvania; and Tulane University Health Sciences Center, New Orleans, Louisiana
Design of fractional order PID controller for boost converter based on Multi-Objective optimization

This paper proposes the theory and application of a new designing method of the Fractional Order PID (FOPID) controller for boost converters. FOPID is a PID where the derivation and integration orders are of fractional order rather than integer. A FOPID is an extension to classic integer order PID controllers, that potentially promises better results. The method is based on the use of a Multi-Objective optimization evolutionary algorithm called Strength Pareto Evolutionary Algorithm (SPEA). Other controller methods cannot guarantee a good start-up response but the proposed method can provide an excellent start-up response besides desired dynamic response. The optimum fractional order PID coefficients for the desired control objectives are included and designers can implement each of them based on objective functions priority. A comparison between the optimum integer order PID controller and optimum fractional order PID controller is presented in the paper. The simulation and some experimental results prove the superiority of the fractional controllers over the integer controllers.
Synthesis, processing, and transport of Pseudomonas aeruginosa elastase

Three cell-associated elastase precursors with approximate molecular weights of 60,000 (P), 56,000 (Pro I), and 36,000 (Pro II) were identified in Pseudomonas aeruginosa cells by pulse-labeling with [35S]methionine and immunoprecipitation. In the absence of inhibitors, cells of a wild-type strain as well as those of the secretion-defective mutant PAKS 18 accumulated Pro II as the only elastase-related radioactive protein. EDTA but not EGTA [ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] inhibited the formation of Pro II, and this inhibition was accompanied by the accumulation of Pro I. P accumulated in cells labeled in the presence of ethanol (with or without EDTA), dinitrophenol plus EDTA, or carbonyl cyanide m-chlorophenyl hydrazone plus EDTA. Pro I and Pro II were localized to the periplasm, and as evident from pulse-chase experiments, Pro I was converted to the mature extracellular enzyme with Pro II as an intermediate of the reaction. P was located to the membrane fraction. Pro I but not Pro II was immunoprecipitated by antibodies specific to a protein of about 20,000 molecular weight (P20), which, as we showed before (Kessler and Safrin, J. Bacteriol. 170:1215-1219, 1988), forms a complex with an inactive periplasmic elastase precursor of about 36,000 molecular weight. Our results suggest that the elastase is made by the cells as a preproenzyme (P), containing a signal sequence of about 4,000 molecular weight and a "pro" sequence of about 20,000 molecular weight. Processing and export of the preproenzyme involve the formation of two periplasmic proenzyme species: proelastase I (56 kilodaltons [kDa]) and proelastase II (36 kDa). The former is short-lived, whereas proelastase II accumulates temporarily in the periplasm, most likely as a complex with the 20-kDa propeptide released from proelastase I upon conversion to proelastase II. The final step in elastase secretion seems to required both the proteolytic removal of a small peptide from proelastase II and dissociation of the latter from P20.
Understanding and modeling AC BTI

We present a model for AC NBTI which is based on capture and emission of charges in and out of oxide border traps. Capture and emission time constants of these traps are widely distributed from &#60;µs to >105s and have been experimentally determined. The model gives a good quantitative understanding of experimental data from alternating stress / recovery sequences. It also provides a physical understanding of all the special features seen in AC NBTI independently of technology parameters.
ET(B) receptor protects the tubulointerstitium in experimental thrombotic microangiopathy.

BACKGROUND The characteristic features of thrombotic microangiopathy (TMA) include glomerular and peritubular capillary endothelial cell injury with thrombus formation and subsequent ischemic tubulointerstitial damage. The endothelin ET(B) receptor has been shown to mediate both endothelial cell proliferation and vasodilation, and we therefore hypothesized that blockade of this receptor might promote more severe injury in this model. METHODS TMA was induced in recently established transgenic rats that lack expression of ET(B) receptor in the kidney; these animals were compared to control rats with TMA both in the short-term (days 1 and 3) when acute glomerular injury was most manifest, and the long-term (day 17) when glomeruli have recovered but tubulointerstitial injury is still present. Renal damage was assessed by histological analysis and blood urea nitrogen (BUN) measurements. RESULTS No difference in the TMA model was observed between rats with and without ET(B) receptor on days 1 or 3. At day 17, however, rats without the ET(B) receptor showed more severe tubulointerstitial injury compared with those with ET(B) receptor, which was associated with higher BUN levels. The tubulointerstitial damage was associated with a more severe loss of peritubular capillaries. CONCLUSIONS These findings suggest that the ET(B) receptor may protect peritubular capillaries under the ischemic insult, and serve a defensive role in the tubulointerstitium induced by renal microvascular injury.