Miracle-dz/UniFAR-FTUs huggingface dataset:
Assessment of Treatment Patterns and Patient Outcomes in Levodopa-Induced Dyskinesias (ASTROID): A US Chart Review Study.

BACKGROUND No curative therapy is available for Parkinson's disease; therefore, one of the main goals of treatment is to control motor symptoms, often via the use of levodopa (also known as L-dopa). However, prolonged levodopa treatment in Parkinson's disease has been associated with the development of motor fluctuations and the occurrence of levodopa-induced dyskinesias (LIDs). OBJECTIVE To gain a clear, empirical understanding of the current real-world approach to treatment and patient outcomes associated with Parkinson's disease and LIDs. METHODS This study used a mixed methodology, combining a cross-sectional survey of neurologists practicing in the United States, a retrospective chart review of patients with Parkinson's disease and LIDs, and cross-sectional surveys of health-related quality of life (QOL) and physical functioning in patients with Parkinson's disease. The surveys included the 39-item Parkinson's Disease Questionnaire, the Unified Parkinson's Disease Rating Scale, the Parkinson Disease Dyskinesia 26-item Scale, and the modified Abnormal Involuntary Movement Scale (mAIMS). Survey and chart data were collected between May 2010 and July 2011. Descriptive analyses were used to evaluate the distribution of study variables, treatment patterns, patient QOL, and patient physical functioning. RESULTS Data from 7 neurologists and from 172 patients with Parkinson's disease and LIDs were collected. Results from the physician survey indicate that prescribing patterns depend largely on the severity of LIDs, assessed via mAIMS. Most patients (88%) received pharmacologic therapy as first-line treatment for LIDs, with monotherapy favored in patients with mild LIDs and combination therapy in patients with moderate-to-severe LIDs. The mean time from the diagnosis of LID to the administration of first-line treatment for the condition was 10.7 months (standard deviation, 14.0 months). The study population reflects a mean time from levodopa initiation to the onset of LIDs of slightly more than 5 years, regardless of the levodopa dosage. Results from the chart review and the physician survey suggest a strong alignment in severity classification among the assessment scales used. CONCLUSION These findings indicate that the diagnosis and the treatment of Parkinson's disease and LIDs are not optimal, because of the length of time from diagnosis to treatment, and because of the variability in treatment selection and response. Additional real-world studies are recommended to better understand treatment patterns, compliance with guidelines, and their potential impact on patient outcomes.
A Review of Heavy Metals in Water, Sediment and Living Organisms in the Black Sea

Black Sea waters remain heavily impacted by a number of pollutants originating from different sources such as direct and indirect discharge of land based pollutants, sewage etc. The Black Sea environment is highly contaminated in many urban and industrialized areas of the many countries, resulting in severe ecotoxicological impacts. Heavy metals are toxic substances that accumulate in food chains with the increasing concentrations. In this review, heavy metal pollution in water column and sediment, with regard to aquatic organisms living in the Black Sea have been evaluated.
Expression of fnr Is Constrained by an Upstream IS5 Insertion in Certain Escherichia coli K-12 Strains

ABSTRACT FNR is a global transcriptional regulator that controls anaerobic gene expression in Escherichia coli. Through the use of a number of approaches it was shown that fnr gene expression is reduced approximately three- to fourfold in E. coli strain MC4100 compared with the results seen with strain MG1655. This reduction in fnr expression is due to the insertion of IS5 (is5F) in the regulatory region of the gene at position −41 relative to the transcription initiation site. Transcription of the fnr gene nevertheless occurs from its own promoter in strain MC4100, but transcript levels are reduced approximately fourfold compared with those seen with strain MG1655. Remarkably, in strains bearing is5F the presence of Hfq prevents IS5-dependent transcriptional silencing of fnr expression. Thus, an hfq mutant of MC4100 is devoid of FNR protein and has the phenotype of an fnr mutant. In strain MG1655, or a derivative of MC4100 lacking is5F, mutation of hfq had no effect on fnr transcript levels. This finding indicates that IS5 mediates the effect of Hfq on fnr expression in MC4100. Western blot analysis revealed that cellular levels of FNR were reduced threefold in strain MC4100 compared with strain MG1655 results. A selection of FNR-dependent genes fused to lacZ were analyzed for the effects of reduced FNR levels on anaerobic gene expression. Expression of some operons, e.g., focA-pfl and fdnGHJI, was unaffected by reduction in the level of FNR, while the expression of other genes such as ndh and nikA was clearly affected.
Barriers to treatment of infertility by in‐vitro fertilization and embryo transfer

A survey was made of 121 patients who withdrew from an in‐vitro fertilization and embryo transfer programme, and the reasons leading to withdrawal were solicited by a questionnaire. The most common reasons stated by the 91 patients who returned the survey questionnaires were the heavy financial burden and psychosocial stresses that accompanied treatment. Seventy per cent of these patients expressed a desire to re‐enter the programme at a later date.
Modulation of human aorta smooth muscle cell phenotype: a study of muscle-specific variants of vinculin, caldesmon, and actin expression.

Vinculin- and caldesmon-immunoreactive forms and actin isoform patterns were studied in samples of normal and atherosclerotic human aorta. After removal of adventitia and endothelium, the remaining tissue was divided into three layers: media, muscular-elastic (adjacent to media) intima, and subendothelial (juxtaluminal) intima. In media of normal aorta, meta-vinculin accounted for 41.0 +/- 0.9% (mean +/- SEM) of total immunoreactive vinculin (meta-vinculin + vinculin); 150-kDa caldesmon accounted for 78.2 +/- 5.1% of immunoreactive caldesmon (150-kDa + 70-kDa); the fractional contents of alpha-smooth muscle actin, beta-nonmuscle, and gamma-isoactins were 49.0 +/- 0.6%, 30.4 +/- 0.6%, and 20.8 +/- 0.8%, respectively. Muscular-elastic intima was very similar to media by these criteria. In subendothelial intima, the fractional content of meta-vinculin and 150-kDa caldesmon was significantly lower (6.9 +/- 1.5% and 32.7 +/- 7.0%, respectively) than in muscular-elastic intima and media, whereas the isoactin pattern was identical to that in adjacent layers, demonstrating the smooth muscle origin of subendothelial intima cells. In atherosclerotic fibrous plaque, the fractional content of alpha-actin was decreased in subendothelial intima, rather than in media and muscular-elastic intima. Additionally, the proportion of subendothelial intima cells [i.e., the cells that express low amounts of smooth muscle phenotype markers (meta-vinculin, 150-kDa caldesmon, and alpha-actin)] in the total intima cell population increased dramatically in atherosclerotic fibrous plaque. The results suggest that changes in the relative content of meta-vinculin and 150-kDa caldesmon as well as alpha-actin in human aortic intima are associated with atherosclerosis although, in subendothelial intima of normal aorta, a certain smooth muscle cell population exists that expresses reduced amounts of "contractile" phenotype markers, even in the absence of the disease.
Integrin-associated Lyn Kinase Promotes Cell Survival by Suppressing Acid Sphingomyelinase Activity*

Integrins govern cellular adhesion and transmit signals leading to activation of intracellular signaling pathways aimed to prevent apoptosis. Herein we report that attachment of oligodendrocytes (OLs) to fibronectin via αvβ3 integrin receptors rendered the cells more resistant to apoptosis than the cells attached to laminin via α6β1 integrins. Investigation of molecular mechanisms involved in αvβ3 integrin-mediated cell survival revealed that ligation of the integrin with fibronectin results in higher expression of activated Lyn kinase. Both in OLs and in the mouse brain, Lyn selectively associates with αvβ3 integrin, not with αvβ5 integrin, leading to suppression of acid sphingomyelinase activity and preventing ceramide-mediated apoptosis. In OLs, knockdown of Lyn with small interfering RNA resulted in OL apoptosis with concomitant accumulation of C16-ceramide due to activation of acid sphingomyelinase (ASMase) and sphingomyelin hydrolysis. Knocking down ASMase partially protected OLs from apoptosis. In the brain, ischemia/reperfusion (IR) triggered rearrangements in the αvβ3 integrin-Lyn kinase complex leading to disruption of Lyn kinase-mediated suppression of ASMase activity. Thus, co-immunoprecipitation studies revealed an increased association of αvβ3 integrin-Lyn kinase complex with ionotropic glutamate receptor subunits, GluR2 and GluR4, after cerebral IR. Sphingolipid analysis of the brain demonstrated significant accumulation of ceramide and sphingomyelin hydrolysis. The data suggest a novel mechanism for regulation of ASMase activity during cell adhesion in which Lyn acts as a key upstream kinase that may play a critical role in cerebral IR injury.
Modelagem Espacial de Florestas Estacionais do Domínio do Cerrado no Estado de Minas Gerais

There is provided a sewage treatment apparatus particularly intended for marine use where the apparatus is subject to tilting as a result of pitching and rolling of the ship. The apparatus includes an oxidation tank having a sewage liquor outlet incorporating a discharge weir. This weir is disposed at the center of a horizontal plane across the interior of the tank and containing the discharge weir, so that the above tilting of the tank substantially does not affect the rate of sewage liquor discharge and therefore substantially does not result in surging in the flow of sewage liquor from the oxidation tank to a settlement chamber. Such surging could adversely affect the maintenance of quiescent conditions in the settlement chamber. The settlement chamber is substantially fully enclosed and has a clarified liquid outlet incorporating an upstanding discharge weir presented coaxially by a top wall of the chamber. The chamber is operatively maintained substantially full, and since the free surface area of the sewage liquor in the chamber is minimized the above tilting of the chamber likewise does not adversely affect the maintenance of substantially quiescent conditions within the chamber.
Dietary cholecalciferol and phosphorus influence intestinal mucosa phytase activity in broiler chicks

1. The role of cholecalciferol and phosphorus in the regulation of intestinal mucosa phytase was investigated in broiler chicks. 2. A total of 144 7-d-old male broiler chicks were grouped by weight into 6 blocks of 4 cages with 6 broiler chicks per cage. Four maize–soybean meal-based mash diets were randomly assigned to cages within each block. The 4 diets consisted of cholecalciferol at 0 or 75 µg/kg and total phosphorus at 3·6 or 7·0 g/kg in a 2 × 2 factorial arrangement. The birds were given the experimental diets for 12 d under conditions which excluded ultraviolet light. 3. Broiler chicks fed on diets with the higher concentration of cholecalciferol had higher V max and K m of the mucosa phytase, weight gain, feed intake, feed efficiency and percentage tibia ash, higher ileal digestibility of dry matter, energy, phosphorus (P) and calcium (Ca), and increased retention of dry matter, nitrogen, P, Ca and energy. 4. Broiler chicks receiving diets with the higher P concentration showed lower V max and K m of the intestinal mucosa phytase but greater weight gain, feed intake, feed efficiency and percentage tibia ash, higher ileal digestibility of dry matter, energy, P and nitrogen, and increased retention of dry matter, energy, nitrogen and Ca. 5. In conclusion, both dietary P and cholecalciferol influenced the activity of intestinal mucosa phytase.
JMR EARLY CAREER SCHOLARS IN MATERIALS SCIENCE ANNUAL ISSUE: REVIEW How to improve the stability and rate performance of lithium-ion batteries with transition metal oxide anodes

Sufeng Wei Key Laboratory of Advanced Structural Materials, Changchun University of Technology, Changchun 130012, People’s Republic of China Yan Liu Key Laboratory of Bionic Engineering (Ministry of Education), Jilin University, Changchun 130022, People’s Republic of China Jianshe Lian and Qing Jiang Key Laboratory of Automobile Materials, Department of Materials Science and Engineering, Jilin University, Changchun 130025, People’s Republic of China
CYP2U1 activity is altered by missense mutations in hereditary spastic paraplegia 56

Hereditary spastic paraplegia (HSP) is an inherited disorder of the central nervous system mainly characterized by gradual spasticity and weakness of the lower limbs. SPG56 is a rare autosomal recessive early onset complicated form of HSP caused by mutations in CYP2U1. The CYP2U1 enzyme was shown to catalyze the hydroxylation of arachidonic acid. Here, we report two further SPG56 families carrying three novel CYP2U1 missense variants and the development of an in vitro biochemical assay to determine the pathogenicity of missense variants of uncertain clinical significance. We compared spectroscopic, enzymatic, and structural (from a 3D model) characteristics of the over expressed wild‐type or mutated CYP2U1 in HEK293T cells. Our findings demonstrated that most of the tested missense variants in CYP2U1 were functionally inactive because of a loss of proper heme binding or destabilization of the protein structure. We also showed that functional data do not necessarily correlate with in silico predictions of variants pathogenicity, using different bioinformatic phenotype prediction tools. Our results therefore highlight the importance to use biological tools, such as the enzymatic test set up in this study, to evaluate the effects of newly identified variants in clinical settings.
Applying Telepresence to Incident Management: The Virtual Incident Command Center

This paper describes an application of telepresence technology to the incident management domain. The system combines national guidelines for incident management with many aspects of collaborative virtual environments to enable effective communication between first responders in the field and remotely located command personnel. A brief overview of existing incident management systems is given, followed by a set of requirements for future systems. We then describe our virtual incident command center (VICC) prototype, explain how it addresses the requirements, and outline our future plans. Finally, we report feedback from ongoing demonstrations of the prototype system that supports our contention that VICC represents a unique solution to the incident management problem.
Polymer-MEMS-Based Optoelectronic Display

In this paper, a novel all-polymer integrated microsystem, which realizes a 2-D display by integrating a 1-D array of polymer light-emitting diodes (PLEDs) with a polymer scanner of microelectromechanical system (MEMS), is presented. Electronic modulation of PLEDs forms the first dimension of the display (fast scan), and the scanner actuation orthogonal to the direction of PLED lineup forms the second one (slow scan). MEMS scanner (actuator) is fabricated on a polymer composite (FR4 material) with a double-sided process using lithography to pattern copper lines and laser micromachining to cut the scanner outline. PLEDs are fabricated on polyethylene terephthalate sheets. They have a thin-film structure of indium tin oxide, poly (3,4-ethylenedioxythiophene) poly (styrenesulfonate), poly [2-methoxy-5-(2'-ethyl-hexyloxy)-1,4-phenylene vinylene], and aluminum. The scanner is actuated electromagnetically in its slow-scan resonance mode at 49 Hz, generating a maximum displacement of 3.5 mm at a drive power of 84 mW with the help of a mini permanent magnet attached to the tip of the scanner and an off-chip energizing coil. Turn-on voltage of a PLED is 7.5 V, and each one generate a luminance of 0.3 cd/m2 at 13 V, consuming 1.1-mA current. Successful operation of the integrated-display system is shown by forming a checker box image with a resolution of 20 × 7 and a size of 9 mm by 3.4 mm.
The Process Model of Family Functioning *

The Process Model of Family Functioning differs from the McMaster Model of Family Functioning and their common source, the Family Categories Schema, by its increased emphasis on the dynamic interaction between the major dimensions of family functioning, and by its stress on the interface between intrapsychic subsystems and the interpersonal dimensions of the family system. A model of family process rather than family structure, it defines six universal criteria of family functioning. It describes the processes involved in each along with the content components and the critical aspects of each. A self-report test developed from the model (FAM-III) is being widely used both as a research tool and as a clinical adjunct. Tests to define its validity and reliability continue.
Deficient Smad7 expression: A putative molecular defect in scleroderma

Scleroderma is a chronic systemic disease that leads to fibrosis of affected organs. Transforming growth factor (TGF) β has been implicated in the pathogenesis of scleroderma. Smad proteins are signaling transducers downstream from TGF-β receptors. Three families of Smads have been identified: (i) receptor-regulated Smad2 and -3 (R-Smads); (ii) common partner Smad4 (Co-Smad); and (iii) inhibitory Smad6 and -7 (I-Smads, part of a negative feedback loop). We have investigated the signaling components for the TGF-β pathway and TGF-β activity in scleroderma lesions in vivo and in scleroderma fibroblasts in vitro. Basal level and TGF-β-inducible expression of Smad7 are selectively decreased, whereas Smad3 expression is increased both in scleroderma skin and in explanted scleroderma fibroblasts in culture. TGF-β signaling events, including phosphorylation of Smad2 and -3, and transcription of the PAI-1 gene are increased in scleroderma fibroblasts, relative to normal fibroblasts. In vitro adenoviral gene transfer with Smad7 restores normal TGF-β signaling in scleroderma fibroblasts. These results suggest that alterations in the Smad pathway, including marked Smad7 deficiency and Smad3 up-regulation, may be responsible for TGF-β hyperresponsiveness observed in scleroderma.
Preventive effect of pre-dive hydration on bubble formation in divers

Objective: To investigate whether prehydration 90 min before a dive could decrease bubble formation, and to evaluate the consequent adjustments in plasma volume (PV), water balance and plasma surface tension (ST). Methods: Eight military divers participated in a crossover trial of pre-dive hydration using saline–glucose beverage (protocol 1) and a control dive with no prehydration (protocol 2). Drink volume was 1300 ml (osmolality 324 mOsm/l) and drinking time was 50–60 min. The diving protocol consisted of an open sea field air dive at 30 msw depth for 30 min followed by a 9 min stop at 3 msw. Haemodynamic parameters, body weight measurements, urine volume and blood samples were taken before/after fluid intake and after the dive. Decompression bubbles were examined by a precordial pulsed Doppler. Results: Bubble activity was significantly lower for protocol 1 than for protocol 2. PV increased after fluid ingestion by 3.5% and returned toward baseline after diving for protocol 1, whereas it decreased by 2.2% after diving for protocol 2. Differences in post-dive PV between the two conditions were highly significant. Body weight loss before/after diving and post-dive urine volume after diving were significant in both protocols, but the relative decline in weight remained lower for protocol 1 than for protocol 2, with reduction of negative water balance due to higher fluid retention. There were no differences in ST after fluid intake and after diving for the two protocols. Conclusion: Pre-dive oral hydration decreases circulatory bubbles, thus offering a relatively easy means of reducing decompression sickness risk. The prehydration condition allowed attenuation of dehydration and prevention of hypovolaemia induced by the diving session. Hydration and diving did not change plasma surface tension in this study.
Identification of a human cDNA encoding a novel protein kinase with two repeats of the LIM/double zinc finger motif.

By low-stringency screening of a human hepatoma HepG2 cell cDNA library, using the genomic fragment of chick c-sea receptor tyrosine kinase as a probe, we isolated overlapping cDNAs encoding a novel protein kinase, which we termed LIM-kinase (LIMK). * The predicted open reading frame encodes a 647-amino-acid polypeptide containing a putative protein kinase structure in the C-terminal half. In addition, LIMK has two repeats of cysteine-rich LIM/double zinc finger motif at the most N-terminus. To our knowledge, this is the first protein kinase seen to contain the LIM motif(s) in the molecule. Although the protein kinase domain of LIMK has highly conserved sequence elements of protein kinases, phylogenetic analysis revealed that LIMK cannot be classified into any subfamily of known protein kinases. Northern blot analysis revealed that the single species of LIMK mRNA of 3.3 kb was expressed in various human epithelial and hematopoietic cell lines. In rat tissues, LIMK mRNA was expressed in the brain, at the highest level. LIM is suggested to be involved in protein-protein interactions by binding to another LIM motif. As the LIM domain is frequently present in the homeodomain-containing transcriptional regulators and oncogenic nuclear proteins, LIMK may be involved in developmental or oncogenic processes through interactions with these LIM-containing proteins.
Leptin in obesity

Obesity runs in families, mainly due to genetic factors.1 Several different mendelian inherited, monogenic forms of obesity exist in rodents, but they are rare in humans.1 Analysis of the distribution of fatness in families suggests that a few major genes may act on a polygenic and environmental background, but it remains unclear which genes are involved.1 The identification and sequencing of the mouse obese (ob) gene by Friedman's group in 19942 opened important new avenues in obesity research and have already led to overwhelming research activity.3 In homozygous ob/ob mice, the mutation of the ob gene results in increased food intake, reduced energy expenditure, elevated insulin and cortisol levels, and subsequently, in massive obesity and non-insulin dependent diabetes mellitus.2 The ob gene encodes a protein, leptin, which is produced only in fat cells and secreted into the blood. There are two different strains of ob/ob mice: one with a mutation that establishes a stop codon within the ob gene, resulting in the production of a truncated, inactive protein; the other with a mutation that produces no protein at all.2 Administration of leptin corrects the multiple metabolic disturbances.4 The finding of a human homologue of …