Miracle-dz/UniFAR-FTUs huggingface dataset:
Marketization, Nostalgia, and Social Connectedness: An Exploratory Study in Eastern Germany

The purpose of this paper is to uncover how East Germans reacted to product shortages following product abundance immediately after reunification and over time. The authors conduct in-depth interviews to document the stories of the individuals during this time period. Our data analysis reveals that East Germans experienced surprising trade-offs during this transition period. On the one hand, they now had access to an abundance of products. But on the other hand, something unexpected was lost. East Germans no longer needed extensive social networks to obtain products and services. As a result, the importance of maintaining social networks decreased leading to a lack of social connectedness and security. As their disenchantment with the new market system grew, Ostalgie - a form of nostalgia indigenous to the region characterized by a deep longing for the past emerged. This seems to indicate that societies based on materialism can have unforeseen consequences of feelings of insecurity. Business can use these results to fundamentally reconsider their role in the well-being of consumers. As a result, marketers that focus on creating opportunities for social connection will satisfy a fundamental human need leading to more successful business models
The impact of fluctuations in boat velocity during the rowing cycle on race time

In competitive rowing, the fluctuations in boat velocity during the rowing cycle are associated with an increased water resistance of the boat as compared with a boat moving at a constant velocity. We aimed to quantify the influence of the increased water resistance on race time using a mathematical approximation, based on the increase in physiological power being proportional to the 2nd power of boat speed. Biomechanical data (oar force, rowing angle, boat velocity, and boat acceleration) were measured when eight elite coxless pair crews performed a rowing test with a stepwise increasing stroke rate (SR: 20, 24, 28, and 32 min−1) that successively increased the mean boat speed. The results revealed a +4.59 s (SR 24.2) to +5.05 s (SR 31.5) 2000‐m race‐time difference compared with a boat hypothetically moving without velocity fluctuations. Velocity fluctuations were highly correlated with SR (r=0.93) because the accelerations of the rowers' body mass and the mass of the counteracting boat increase with SR. The possibilities to reduce velocity fluctuations and therefore race time are limited. For elite rowers, race time may be slightly reduced by a moderate reduction in SR that is compensated by an increased force output for each stroke.
Intermittent ATP release from nerve terminals elicits focal smooth muscle Ca2+ transients in mouse vas deferens

A confocal Ca2+ imaging technique has been used to detect ATP release from individual sympathetic varicosities on the same nerve terminal branch. Varicose nerve terminals and smooth muscle cells in mouse vas deferens were loaded with the Ca2+ indicator Oregon Green 488 BAPTA‐1. Field (nerve) stimulation evoked discrete, focal increases in [Ca2+] in smooth muscle cells adjacent to identified varicosities. These focal increases in [Ca2+] have been termed ‘neuroeffector Ca2+ transients’ (NCTs). NCTs were abolished by α,β‐methylene ATP (1 μM), but not by nifedipine (1 μM) or prazosin (100 nm), suggesting that NCTs are generated by Ca2+ influx through P2X receptors without a detectable contribution from L‐type Ca2+ channels or α1‐adrenoceptor‐mediated pathways. Action potential‐evoked ATP release was highly intermittent (mean probability 0.019 ± 0.002; range 0.001‐0.10) at 1 Hz stimulation, even though there was no failure of action potential propagation in the nerve terminals. Twenty‐eight per cent of varicosities failed to release transmitter following more than 500 stimuli. Spontaneous ATP release was very infrequent (0.0014 Hz). No Ca2+ transient attributable to noradrenaline release was detected even in response to 5 Hz stimulation. There was evidence of local noradrenaline release as the α2‐adrenoceptor antagonist yohimbine increased the probability of occurrence of NCTs by 55 ± 21 % during trains of stimuli at 1 Hz. Frequency‐dependent facilitation preferentially occurred at low probability release sites. The monitoring of NCTs now allows transmitter release to be detected simultaneously from each functional varicosity on an identified nerve terminal branch on an impulse‐to‐impulse basis.
Gut–Liver Axis Derangement in Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is the most frequent type of chronic liver disease in the pediatric age group, paralleling an obesity pandemic. A “multiple-hit” hypothesis has been invoked to explain its pathogenesis. The “first hit” is liver lipid accumulation in obese children with insulin resistance. In the absence of significant lifestyle modifications leading to weight loss and increased physical activity, other factors may act as “second hits” implicated in liver damage progression leading to more severe forms of inflammation and hepatic fibrosis. In this regard, the gut–liver axis (GLA) seems to play a central role. Principal players are the gut microbiota, its bacterial products, and the intestinal barrier. A derangement of GLA (namely, dysbiosis and altered intestinal permeability) may promote bacteria/bacterial product translocation into portal circulation, activation of inflammation via toll-like receptors signaling in hepatocytes, and progression from simple steatosis to non-alcoholic steato-hepatitis (NASH). Among other factors a relevant role has been attributed to the farnesoid X receptor, a nuclear transcriptional factor activated from bile acids chemically modified by gut microbiota (GM) enzymes. The individuation and elucidation of GLA derangement in NAFLD pathomechanisms is of interest at all ages and especially in pediatrics to identify new therapeutic approaches in patients recalcitrant to lifestyle changes. Specific targeting of gut microbiota via pre-/probiotic supplementation, feces transplantation, and farnesoid X receptor modulation appear promising.
Resveratrol is a Peroxidase-mediated Inactivator of COX-1 but Not COX-2

Resveratrol (3,4′,5-trihydroxy-trans-stilbene) is a phytoalexin found in grapes that has anti-inflammatory, cardiovascular protective, and cancer chemopreventive properties. It has been shown to target prostaglandin H2 synthase (COX)-1 and COX-2, which catalyze the first committed step in the synthesis of prostaglandins via sequential cyclooxygenase and peroxidase reactions. Resveratrol discriminates between both COX isoforms. It is a potent inhibitor of both catalytic activities of COX-1, the desired drug target for the prevention of cardiovascular disease, but only a weak inhibitor of the peroxidase activity of COX-2, the isoform target for nonsteroidal anti-inflammatory drugs. We have investigated the unique inhibitory properties of resveratrol. We find that it is a potent peroxidase-mediated mechanism-based inactivator of COX-1 only (kinact = 0.069 ± 0.004 s-1, Ki(inact) = 1.52 ± 0.15 μm), with a calculated partition ratio of 22. Inactivation of COX-1 was time- and concentration-dependent, it had an absolute requirement for a peroxide substrate, and it was accompanied by a concomitant oxidation of resveratrol. Resveratrol-inactivated COX-1 was devoid of both the cyclooxygenase and peroxidase activities, neither of which could be restored upon gel-filtration chromatography. Inactivation of COX-1 by [3H]resveratrol was not accompanied by stable covalent modification as evident by both SDS-PAGE and reverse phase-high performance liquid chromatography analysis. Structure activity relationships on methoxy-resveratrol analogs showed that the m-hydroquinone moiety was essential for irreversible inactivation of COX-1. We propose that resveratrol inactivates COX-1 by a “hit-and-run” mechanism, and offers a basis for the design of selective COX-1 inactivators that work through a mechanism-based event at the peroxidase active site.
Prognostic indicators and outcome prediction model for severe traumatic brain injury.

BACKGROUND Although some predictive models for patient outcomes after severe traumatic brain injury have been proposed, a mathematical model with high predictive value has not been established. The purpose of the present study was to analyze the most important indicators of prognosis and to develop the best outcome prediction model. METHODS One hundred eleven consecutive patients with a Glasgow Coma Scale score of <9 were examined and 14 factors were evaluated. Intracranial pressure and cerebral perfusion pressure were recorded at admission to the intensive care unit. The absence of the basal cisterns, presence of extensive subarachnoid hemorrhage, and degree of midline shift were evaluated by means of computed tomography within 24 hours after injury. Multivariate logistic regression analysis was used to identify independent risk factors for a poor prognosis and to develop the best prediction model. RESULTS The best model included the following variables: age (p < 0.01), light reflex (p = 0.01), extensive subarachnoid hemorrhage (p = 0.01), intracranial pressure (p = 0.04), and midline shift (p = 0.12). Positive predictive value of the model was 97.3%, negative predictive value was 87.1%, and overall predictive value was 94.2%. The area under the receiver operating characteristic curve was 0.977, and the p value for the Hosmer-Lemeshow goodness-of-fit was 0.866. CONCLUSIONS Our predictive model based on age, absence of light reflex, presence of extensive subarachnoid hemorrhage, intracranial pressure, and midline shift was shown to have high predictive value and will be useful for decision making, review of treatment, and family counseling in case of traumatic brain injury.
Chemoselection as a strategy for organ preservation in patients with T4 laryngeal squamous cell carcinoma with cartilage invasion

High rates of overall survival (OS) and laryngeal preservation were achieved in two sequential phase II clinical trials in patients with stage III/IV laryngeal squamous cell carcinoma (SCC). Patients were treated with chemoradiation after a >50% primary tumor response to one cycle of neoadjuvant chemotherapy (IC). We analyzed outcomes for T4 patients with cartilage invasion from both studies.
Functionally and morphologically distinct populations of extracellular vesicles produced by human neutrophilic granulocytes

EVs in the microvesicle size range released during spontaneous death of human neutrophils were characterized and their properties compared with previously described EVs with antibacterial effect (aEVs, generated on specific activation) or produced spontaneously (sEVs). The 3 vesicle populations overlapped in size and in part of the constituent proteins were stained with annexin V and were impermeable to PI. However, none of them produced superoxide. In contrast, remarkable differences were observed in the morphology, abundance of proteins, and antibacterial function. EVs formed spontaneously in 30 min (sEVs) were more similar to EVs released during spontaneous death in 1–3 d than to EVs formed in 30 min on stimulation of opsonin receptors (aEVs). Spontaneously generated EVs had no antibacterial effect despite their large number and protein content. We hypothesized 2 parallel mechanisms: one that proceeds spontaneously and produces EVs without antibacterial effect and another process that is triggered by opsonin receptors and results in differential sorting of proteins into EVs with antibacterial capacity. Our results call attention to the functional and morphologic heterogeneity within the microvesicle/ectosome fraction of EVs.
Significance of the transcription factor KLF5 in cardiovascular remodeling

Summary. Structural remodeling of the heart and blood vessels is an important pathologic process in the development of many cardiovascular diseases. However, transcriptional regulation of altered gene expression during cardiovascular remodeling is not well understood. We previously isolated KLF5/basic transcription element‐binding (BTEB)2, a Krüppel‐like factor, as a transcription factor that binds the promoter of the embryonic smooth muscle myosin heavy chain gene (SMemb). KLF5 activates many genes inducible during cardiovascular remodeling, such as platelet‐derived growth factor (PDGF)‐A/B, Egr‐1, plasminogen activator inhibitor‐1 (PAI‐1), inducible nitric oxide synthase (iNOS), and vascular endothelial growth factor (VEGF) receptors. KLF5 is abundantly expressed in embryonic smooth muscles and is down‐regulated with vascular development, but reinduced in proliferative neointimal smooth muscles in response to vascular injury. In KLF5 gene‐targeted mice, homozygotes die at an early embryonic stage whereas heterozygotes are apparently normal. However, in response to external stress, arteries of heterozygotes exhibit diminished levels of smooth muscle and adventitial cell activation. Furthermore, angiotensin II‐induced cardiac hypertrophy and fibrosis are attenuated in heterozygotes. KLF5 activities are regulated by many transcriptional regulators and nuclear receptors, such as retinoic acid receptor‐α (RARα), NF‐κB, PPARγ, p300, and SET. Interestingly, RARα agonist suppresses KLF5 and cardiovascular remodeling, whereas RARα antagonist activates KLF5 and induces angiogenesis. These results indicate that KLF5 is an essential transcription factor in cardiovascular remodeling and a potential therapeutic target for cardiovascular disease.
Transabdominal coelocentesis as early source of fetal DNA for chromosomal and molecular diagnosis

Abstract This study reports a comparative analysis between results of transabdominal coelocentesis and traditional invasive procedure in order to assess the usefulness of coelocentesis as a source of fetal DNA for molecular and chromosomal analysis. A number of 28 women were included in the study. A successful sampling of coelomic fluid was obtained in 25 women by transabdominal procedure. A positive amplification of DNA with QF-PCR techniques was obtained in 90% of cases, while 10% of cases failed to reveal interpretable results. Although all samples were cultured, the growth rate was not sufficient to determine karyotypes within 2 weeks. Five samples were selected to be analyzed by array-based comparative genomic hybridization (a-CGH) but the interpretation of these results was difficult and ambiguous. Our results suggest that transabdominal coelocentesis is suitable for the detection of single DNA variation and for QF-PCR analysis, while further experiments are needed to develop optimized protocols for traditional karyotyping and array-analysis.
Native mitochondrial RNA-binding complexes in kinetoplastid RNA editing differ in guide RNA composition

Many mitochondrial mRNAs in trypanosomes are subject to extensive RNA editing involving both insertion and deletion of blocks of uridine residues. This paper examines the RNA constituents of distinct protein complexes known as mitochondrial RNA-binding complexes or MRBs. The evidence supports the existence of multiple subcomplexes of MRBs containing different RNA/protein composites.
Replication Origin of Mitochondrial DNA in Insects

The precise position of the replication origin (OR) of mtDNA was determined for insect species belonging to four different orders (four species of Drosophila, Bombyx mori, Triborium castaneum, and Locusta migratoria, which belong to Diptera, Lepidoptera, Coleoptera, and Orthoptera, respectively). Since the free 5′ ends of the DNA strands of mtDNA are interpreted as the OR, their positions were mapped at 1-nucleotide resolution within the A + T-rich region by using the ligation-mediated PCR method. In all species examined, the free 5′ ends were found within a very narrow range of several nucleotides in the A + T-rich region. For four species of Drosophila, B. mori, and T. castaneum, which belong to holometabolous insects, although the OR's were located at different positions, they were located immediately downstream of a series of thymine nucleotides, the so-called T-stretch. These results strongly indicate that the T-stretch is involved in the recognition of the OR of mtDNA at least among holometabolous insects. For L. migratoria (hemimetabolous insect), on the other hand, none of the long stretches of T's was found in the upstream portion of the OR, suggesting that the regulatory sequences involved in the replication initiation process have changed through insect evolution.
Merit aid as a predictor variable of undergraduate student enrollment

OF DISSERTATION Merit-based financial aid has long been utilized by college and university enrollment managers to attract the most academically qualified applicants for admission. Considerable research has been done to illustrate the impact of statebased merit aid programs and other scholarly pursuits have drawn attention to the consequences of merit aid on institutional investments in need-based aid. Less is known about the efficacy of merit aid to achieve college student enrollment objectives. The purpose of this study was to evaluate the relationship between merit aid values and the likelihood of undergraduate student enrollment yield on offers of admission. The primary research question to be answered was: What is the relationship between the amount of merit aid students receive from a college or university and their enrollment decisions? The sample comprised 2,770 students at three private higher education institutions in the United States. Binary logistic regression and a forward selection process were used to test a range of possible predictors (e.g., sex, race, ethnicity, in-state residency, distance from home, academic qualifications, merit aid awards, and information from the financial aid applications of those offered admission) to determine the relative strength of merit aid in the prediction of student enrollment yield on offers of admission. The amount of merit aid offered was positively related to the likelihood of a student to enroll, even when academic qualifications and other student characteristics were controlled.
Effects of Typical and Atypical Antipsychotics on the Prepulse Inhibition of the Startle Reflex in Patients With Schizophrenia

Patients with schizophrenia show a loss of sensory (motor) gating, which is reflected in a reduced prepulse inhibition (PPI) of the startle reflex. Furthermore, patients with schizophrenia habituate less than healthy subjects. From previous studies, it is clear that typical antipsychotics have little or no effect on either sensorimotor gating or habituation, while only limited data is available on the effects of atypical antipsychotics on these processes. Forty-four schizophrenic patients (27 stable on typical and 17 stable on atypical antipsychotics) and 35 healthy control subjects were tested in a PPI paradigm. The prepulse and startle stimuli were pure tones of 1500 Hz (duration 40ms, intensity 80 dB and 110 dB respectively), with a fixed interstimulus interval of 120 milliseconds. Block effects in PPI and startle amplitude to the pulse alone trials (habituation) were analyzed over the three groups, using comedication (i.e., benzodiazepines) as a covariate. Main effect for block was found for startle amplitude (habituation), while main effects for group and block were found for percentage PPI. Further analysis displayed significant differences in PPI between the patients treated with typical antipsychotics and the healthy control group, while patients treated with atypical antipsychotics did not differ from either the healthy control group, or the patients treated with typical antipsychotics. Furthermore, post-hoc division of the patients treated with atypical antipsychotics in patients treated with clozapine and risperidone revealed that this superiority from atypical antipsychotics over typical antipsychotics appeared to be mainly based on the effects of clozapine. Patients with schizophrenia who are treated with atypical antipsychotics appear to have levels of sensorimotor gating that are more consistent with healthy controls than patients who are treated with typical antipsychotics. Furthermore, within the class of atypical antipsychotics, clozapine appears most potent in restoring this process.
Input‐output relationships of central neural circuits involved in respiration in cats

1. Inspiratory output responses, measured as integrated phrenic activity, to hypercapnia, to unilateral and bilateral carotid sinus nerve stimulation and to combinations of these stimuli were determined in paralysed, vagotomized and glomectomized cats whose end‐tidal PCO2 was kept constant by means of a servo‐controlled ventilator. In addition, the effect on these responses of the mechanism that causes the respiratory after‐discharge was determined.
Characterization of Diabetogenic CD8+ T Cells

Type 1 diabetes mellitus is caused by the killing of insulin-producing β cells by CD8+T cells. The disease progression, which is chronic, does not follow a course like responses to conventional antigens such as viruses, but accelerates as glucose tolerance deteriorates. To identify the unique features of the autoimmune effectors that may explain this behavior, we analyzed diabetogenic CD8+ T cells that recognize a peptide from the diabetes antigen IGRP (NRP-V7-reactive) in prediabetic NOD mice and compared them to others that shared their phenotype (CD44+CD62LloPD-1+CXCR3+) but negative for diabetes antigen tetramers and to LCMV (lymphocytic choriomeningitis)-reactive CD8+ T cells. There was an increase in the frequency of the NRP-V7-reactive cells coinciding with the time of glucose intolerance. The T cells persisted in hyperglycemic NOD mice maintained with an insulin pellet despite destruction of β cells. We compared gene expression in the three groups of cells compared with the other two subsets of cells, and the NRP-V7-reactive cells exhibited gene expression of memory precursor effector cells. They had reduced cellular proliferation and were less dependent on oxidative phosphorylation. When prediabetic NOD mice were treated with 2-deoxyglucose to block aerobic glycolysis, there was a reduction in the diabetes antigen versus other cells of similar phenotype and loss of lymphoid cells infiltrating the islets. In addition, treatment of NOD mice with 2-deoxyglucose resulted in improved β cell granularity. These findings identify a link between metabolic disturbances and autoreactive T cells that promotes development of autoimmune diabetes.