Miracle-dz/UniFAR-FTUs huggingface dataset:
The SUFBC2D complex is required for the biogenesis of all major classes of plastid Fe‐S proteins

Iron-sulfur (Fe-S) proteins play crucial roles in plastids, participating in photosynthesis and other metabolic pathways. Fe-S clusters are thought to be assembled on a scaffold complex composed of SUFB, SUFC and SUFD proteins. However, several additional proteins provide putative scaffold functions in plastids, and, therefore, the contribution of SUFB, C and D proteins to overall Fe-S assembly still remains unclear. In order to gain insights regarding Fe-S cluster biosynthesis in plastids, we analyzed the complex composed of SUFB, C and D in Arabidopsis by blue native-polyacrylamide gel electrophoresis. Using this approach, a major complex of 170 kDa containing all subunits was detected, indicating that these proteins constitute a SUFBC2 D complex similar to their well characterized bacterial counterparts. The functional effects of SUFB, SUFC or SUFD depletion were analyzed using an inducible RNAi silencing system to specifically target the aforementioned components; resulting in a decrease of various plastidic Fe-S proteins including the PsaA/B and PsaC subunits of photosystem I, ferredoxin and glutamine oxoglutarate aminotransferase. In contrast, the knockout of potential Fe-S scaffold proteins, NFU2 and HCF101, resulted in a specific decrease in the PsaA/B and PsaC levels. These results indicate that the functions of SUFB, SUFC and SUFD for Fe-S cluster biosynthesis cannot be replaced by other scaffold proteins and that SUFBC2 D, NFU2 and HCF101 are involved in the same pathway for the biogenesis of PSI. Taken together, our results provide in vivo evidence supporting the hypothesis that SUFBC2 D is the major, and possibly sole scaffold in plastids.
Effect of Sintering Temperature on the Properties and Leaching of Incinerator Bottom Ash

The fine particle size fraction of municipal solid waste incinerator bottom ash is often problematic because reuse applications for this material are limited. In these experiments incinerator bottom ash with a particle size of less than 8 mm was processed using conventional ceramic production techniques involving wet milling, drying, compacting and sintering. The effect of sintering temperature on the sintered density, microstructure, acid neutralization capacity (ANC) and the release of metal ions as a function of leachate pH are reported. Sintering at 1080 °C produced samples with maximum density. This material contained diopside (CaMgSi2O6), clinoenstatite (Mg2Si2O6) and wollastonite (CaSiO3) as the major crystalline phases. The acid neutralization capacity of sintered samples is significantly lower than milled bottom ash, and further reduces as the sintering temperature increases. This is associated with reduced leaching of Ca from sintered ash samples under all leachate pH conditions. Heavy metals present in the incinerator bottom ash included Cr, Cu, Ni, Zn, Cd and Pb. Sintering under optimum conditions reduced the leachable fraction of these metals under aggressive acid conditions (leachate pH 3) by factors ranging from 90% for Ni to greater than 99% for Cr, Cd, Zn and Pb.
Prenatal Programming of Pulmonary Hypertension Induced by Chronic Hypoxia or Ductal Ligation in Sheep

Pulmonary hypertension of the newborn is caused by a spectrum of functional and structural abnormalities of the cardiopulmonary circuit. The existence of multiple etiologies and an incomplete understanding of the mechanisms of disease progression have hindered the development of effective therapies. Animal models offer a means of gaining a better understanding of the fundamental basis of the disease. To that effect, a number of experimental animal models are being used to generate pulmonary hypertension in the fetus and newborn. In this review, we compare the mechanisms associated with pulmonary hypertension caused by two such models: in utero ligation of the ductus arteriosus and chronic perinatal hypoxia in sheep fetuses and newborns. In this manner, we make direct comparisons between ductal ligation and chronic hypoxia with respect to the associated mechanisms of disease, since multiple studies have been performed with both models in a single species. We present evidence that the mechanisms associated with pulmonary hypertension are dependent on the type of stress to which the fetus is subjected. Such an analysis allows for a more thorough evaluation of the disease etiology, which can help focus clinical treatments. The final part of the review provides a clinical appraisal of current treatment strategies and lays the foundation for developing individualized therapies that depend on the causative factors.
Two-dimensional measurement of proton T1rho relaxation in unlabeled proteins: mobility changes in alpha-bungarotoxin upon binding of an acetylcholine receptor peptide.

A method for the measurement of proton T(1)(rho) relaxation times in unlabeled proteins is described using a variable spin-lock pulse after the initial nonselective 90 degrees excitation in a HOHAHA pulse sequence. The experiment is applied to alpha-bungarotoxin (alpha-BTX) and its complex with a 25-residue peptide derived from the acetylcholine receptor (AChR) alpha-subunit. A good correlation between high T(1)(rho) values and increased local motion is revealed. In the free form, toxin residues associated with receptor binding according to the NMR structure of the alpha-BTX complex with an AChR peptide and the model for alpha-BTX with the AChR [Samson, A. O. , et al. (2002) Neuron 35, 319-332] display high mobility. When the AChR peptide binds, a decrease in the relaxation times and the level of motion of residues involved in binding of the receptor alpha-subunit is exhibited, while residues implicated in binding gamma- and delta-subunits retain their mobility. In addition, the quantitative T(1)(rho) measurements enable us to corroborate the mapping of boundaries of the AChR determinant strongly interacting with the toxin [Samson, A. O. , et al. (2001) Biochemistry 40, 5464-5473] and can similarly be applied to other protein complexes in which peptides represent one of the two interacting proteins. The presented method is advantageous because of its simplicity, generality, and time efficiency and paves the way for future investigation of proton relaxation rates in small unlabeled proteins.
Separating the effects of predation risk and interrupted foraging upon mass changes in the blue tit Parus caeruleus

The optimal amount of reserves that a small bird should carry depends upon a number of factors, including the availability of food and environmental predation risk levels. Theory predicts that, if predation risk increases, then a bird should maintain a lower level of reserves. Previous experiments have given mixed results: some have shown reduced reserves and some, increased reserves. However, the birds in these studies may have been interpreting a staged predation event as a period when they were unable to feed rather than a change in predation risk: theory predicts that, if the food supply within the environment is variable, then reserves should be increased. In the present study, we presented blue tits (Parus caeruleus) with a potential predator and compared this response (which could have been potentially confounded by perceived interruption effects) with a response to an actual interruption in the environment during both long and short daytime lengths. During long (but not short) days, the birds responded in line with theoretical predictions by increasing their reserves in response to interruption and reducing them in response to predation. These results are examined in the light of other experimental manipulations and we discuss how well experimental tests have tested the predictions made by theoretical models.
The FBI1/Akirin2 Target Gene, BCAM, Acts as a Suppressive Oncogene

Basal cell adhesion molecule (BCAM), known to be a splicing variant of Lutheran glycoprotein (LU), is an immunoglobulin superfamily membrane protein that acts as a laminin α5 receptor. The high affinity of BCAM/LU for laminin α5 is thought to contribute to the pathogenesis of sickle red blood cells and to various developmental processes. However, the function of BCAM in carcinogenesis is poorly understood. Based on microarray expression analysis, we found that BCAM was one of the target genes of the oncogenic 14-3-3β-FBI1/Akirin2 complex, which acts as a transcriptional repressor and suppresses MAPK phosphatase-1 gene expression. To elucidate the detailed function of BCAM in malignant tumors, we established BCAM-expressing hepatoma K2 cells. These cells lost the malignant characteristics of parental cells, such as anchorage-independent growth, migration, invasion, and tumorigenicity. Moreover, luciferase reporter assays and chromatin immunoprecipitation analysis revealed that the 14-3-3β-FBI1/Akirin2 complex bound to the BCAM promoter and repressed transcription. Thus, these data indicate that BCAM is a suppressive oncoprotein, and that FBI1/Akirin2 is involved in tumorigenicity and metastasis of hepatoma through the downregulation of suppressive oncogenes.
Jean-Martin Charcot at the Birth of Russian Neurology

Russian neurology was virtually nonexistent in the middle of the 19th century which made a traineeship abroad an absolute necessity. Charcot and his school did not just offer professional training, but created the best minds, which would determine the direction of neurology and psychiatry in Russia for many decades. After returning home, young Russian doctors not only implemented everything they had learned in Western Europe, but proceeded to make their own original contributions. The most talented pupils of Charcot, including such prominent names as Kozhevnikov, Korsakov, Minor, Bekhterev and Darkshevich, became the founders of neurological schools in Russia. They laid the basis for the further development of neurology and psychiatry. Remarkably, though trained by the same teachers, each of these future ‘founding fathers’ of these neurological and psychiatric schools followed his own individual path which resulted in an undeniable diversity in Russian neurology and psychiatry during the period of their formation.
Multiple Bit Error Tolerant Galois Field Architectures Over GF (2m)

Radiation induced transient faults like single event upsets (SEU) and multiple event upsets (MEU) in memories are well researched. As a result of the technology scaling, it is observed that the logic blocks are also vulnerable to malfunctioning when they are deployed in radiation prone environment. However, the current literature is lacking efforts to mitigate such issues in the digital logic circuits when exposed to natural radiation prone environment or when they are subjected to malicious attacks by an eavesdropper using highly energized particles. This may lead to catastrophe in critical applications such as widely used cryptographic hardware. In this paper, novel dynamic error correction architectures, based on the BCH codes, is proposed for correcting multiple errors which makes the circuits robust against radiation induced faults irrespective of the location of the errors. As a benchmark test case, the finite field multiplier circuit is considered as the functional block which can be the target for major attacks. The proposed scheme has the capability to handle stuck-at faults that are also a major cause of failure affecting the overall yield of a nano-CMOS integrated chip. The experimental results show that the proposed dynamic error detection and correction architecture results in 50% reduction in critical path delay by dynamically bypassing the error correction logic when no error is present. The area overhead for the larger multiplier is within 150% which is 33% lower than the TMR and comparable to 130% overhead of single error correcting Hamming and LDPC based techniques.
Relationship between chicken cellular immunity and endotoxin levels in dust from chicken housing environments

Hazardous biochemical agents in animal husbandry indoor environments are known to promote the occurrence of various illnesses among workers and animals. The relationship between endotoxin levels in dust collected from chicken farms and various immunological markers was investigated. Peripheral blood was obtained from 20 broiler chickens and 20 laying hens from four different chicken farms in Korea. Concentrations of total or respirable dust in the inside the chicken farm buildings were measured using a polyvinyl chloride membrane filter and mini volume sampler. Endotoxin levels in the dust were determined by the Limulus Amebocyte Lysate Kinetic method. Interferon-γ production by peripheral blood mononuclear cells stimulated with concanavalin A was significantly lower in broilers or layers from the farms with higher endotoxin concentrations than the chickens from the farms with lower endotoxin levels. An opposite pattern was observed for plasma cortisol concentrations with higher cortisol levels found in chickens from the farms with higher endotoxin levels. When peripheral lymphocytes were examined, the percentage of CD3-Ia+ B cells was lower in layers from farms with higher endotoxin levels than those from locations with lower endotoxin levels. Overall, these results suggest a probable negative association between dust endotoxin levels and cell-mediated immunity in chickens.
Role of chloride channels in bradykinin‐induced guinea pig airway vagal C‐fibre activation

We tested the hypothesis that an ionic current carried by chloride ions contributes to bradykinin (BK)‐induced membrane depolarization and activation of vagal afferent C‐fibres. In an ex vivo innervated trachea/bronchus preparation, BK (1 μm) consistently produced action potential discharge in vagal afferent C‐fibres with receptive fields in the trachea or main stem bronchus. The Ca2+‐activated Cl− channel (CLCA) inhibitor, niflumic acid (NFA, 100 μm), significantly reduced BK‐induced action potential discharge to 21 ± 7% of the control BK response. NFA did not inhibit capsaicin‐induced or citric‐acid‐induced action potential discharge in tracheal C‐fibres. The inhibitory effect of NFA was mimicked by another CLCA inhibitor, 5‐nitro‐2‐(3‐phenylpropylamino)‐benzoic acid (NPPB, 100 μm). NFA also inhibited the BK‐induced inward current in gramicidin‐perforated whole‐cell patch‐clamp recordings of capsaicin‐sensitive jugular ganglion neurones retrogradely labelled from the airways. NFA did not inhibit the BK‐induced increase in intracellular free Ca2+. The TRPV1 inhibitor, iodo‐resiniferatoxin (1 μm), also partially inhibited BK‐induced action potential discharge, and the combination of iodo‐resiniferatoxin and NFA virtually abolished the BK‐induced action potential discharge. We concluded that in vagal afferent C‐fibres, BK evokes membrane depolarization and action potential discharge through the additive effects of TRPV1 and Cl− channel activation.
Physical unclonable functions-based linear encryption against code reuse attacks

Recently, code reuse attacks (CRAs) have emerged as a new class of ingenious security threatens. Attackers can utilize CRAs to hijack the control flow of programs to perform malicious actions without injecting any codes. Existing defenses against CRAs often incur high memory and performance overheads or require extending the existing processors' instruction set architectures (ISAs). To tackle these issues, we propose a hardware-based control flow integrity (CFI) that employs physical unclonable functions (PUF)-based linear encryption architecture (LEA) to protect against CRAs with negligible hardware extending and run time overheads. The proposed method can protect ret and indirect jmp instructions from return oriented programming (ROP) and jump oriented programming (JOP) without any additional software manipulations and extending ISAs. The pre-process will be conducted on codes once the executable binary is loaded into memory, and the real-time control flow verification based on LEA can be done while ret and jmp instructions are executed. Performance evaluations on benchmarks show that the proposed method only introduces 0.61% run-time overhead and 0.63% memory overhead on average.
Ribonucleoprotein Assembly Defects Correlate with Spinal Muscular Atrophy Severity and Preferentially Affect a Subset of Spliceosomal snRNPs

Spinal muscular atrophy (SMA) is a motor neuron disease caused by reduced levels of the survival motor neuron (SMN) protein. SMN together with Gemins2-8 and unrip proteins form a macromolecular complex that functions in the assembly of small nuclear ribonucleoproteins (snRNPs) of both the major and the minor splicing pathways. It is not known whether the levels of spliceosomal snRNPs are decreased in SMA. Here we analyzed the consequence of SMN deficiency on snRNP metabolism in the spinal cord of mouse models of SMA with differing phenotypic severities. We demonstrate that the expression of a subset of Gemin proteins and snRNP assembly activity are dramatically reduced in the spinal cord of severe SMA mice. Comparative analysis of different tissues highlights a similar decrease in SMN levels and a strong impairment of snRNP assembly in tissues of severe SMA mice, although the defect appears smaller in kidney than in neural tissue. We further show that the extent of reduction in both Gemin proteins expression and snRNP assembly activity in the spinal cord of SMA mice correlates with disease severity. Remarkably, defective SMN complex function in snRNP assembly causes a significant decrease in the levels of a subset of snRNPs and preferentially affects the accumulation of U11 snRNP—a component of the minor spliceosome—in tissues of severe SMA mice. Thus, impairment of a ubiquitous function of SMN changes the snRNP profile of SMA tissues by unevenly altering the normal proportion of endogenous snRNPs. These findings are consistent with the hypothesis that SMN deficiency affects the splicing machinery and in particular the minor splicing pathway of a rare class of introns in SMA.
Cardiac Involvement in Patients With Hematologic Malignancies

Authors have reviewed literature about the management of patients with cardiologic disease occurring secondary to hematologic pathology itself or its therapy, with a focus on infiltration of myocardium in acute and chronic leukemia, lymphoma, multiple myeloma, and hypereosinophilic syndrome. Moreover, they evaluated chemotherapy-associated toxicity, particularly for new drugs such as monoclonal antibody therapy, tyrosine kinase inhibitors, arsenic trioxide, bortezomib, and epigenetic therapy. In fact, cardiac toxicity may range from asymptomatic subclinical abnormalities, such as electrocardiographic changes and left ventricular ejection decline, to life-threatening events and lead to chemotherapy dose reduction and delay and, in some cases, for patients with severe side effects, discontinuation of treatment. Finally, they discussed on the identification of early markers of cardiac injury and on cardiac stem cell therapy as a promising approach to facilitate myocardial regeneration.
Video Game Training Enhances Visuospatial Working Memory and Episodic Memory in Older Adults

In this longitudinal intervention study with experimental and control groups, we investigated the effects of video game training on the visuospatial working memory (WM) and episodic memory of healthy older adults. Participants were 19 volunteer older adults, who received 15 1-h video game training sessions with a series of video games selected from a commercial package (Lumosity), and a control group of 20 healthy older adults. The results showed that the performance of the trainees improved significantly in all the practiced video games. Most importantly, we found significant enhancements after training in the trained group and no change in the control group in two computerized tasks designed to assess visuospatial WM, namely the Corsi blocks task and the Jigsaw puzzle task. The episodic memory and short-term memory of the trainees also improved. Gains in some WM and episodic memory tasks were maintained during a 3-month follow-up period. These results suggest that the aging brain still retains some degree of plasticity, and that video game training might be an effective intervention tool to improve WM and other cognitive functions in older adults.
Unstable power threatens the powerful and challenges the powerless: evidence from cardiovascular markers of motivation

Possessing social power has psychological and biological benefits. For example, during task interactions, people high in power are more likely to display a benign cardiovascular (CV) response pattern indicative of “challenge” whereas people low in power are more likely to display a maladaptive CV pattern indicative of “threat” (Scheepers et al., 2012). Challenge is marked by high cardiac output (CO) and low total peripheral resistance (TPR), while threat is marked by low CO and high TPR (Blascovich and Mendes, 2010). In the current work we addressed a possible moderator of the power-threat/challenge relationship, namely the stability of power. We examined the influence of the stability of power (roles could or could not change) on CV responses during a dyadic task where one person was the “chief designer” (high power) and one person was the “assistant” (low power). During the task, different CV-measures were taken [CO, TPR, heart rate, pre-ejection period). Whereas participants in the unstable low power condition showed a stronger tendency toward challenge, participants in the unstable high power condition showed a stronger tendency toward threat. Moreover, participants in the stable low power condition showed CV signs of task disengagement. Results are discussed in terms of the importance of contextual variables in shaping the relationship between power and benign/maladaptive physiological responses.
Molecular epidemiology of tuberculosis in the Czech Republic, 2004: analysis of M. tuberculosis complex isolates originating from the city of prague, south Moravia and the Moravian-Silesian region.

OBJECTIVES To compare M. tuberculosis complex genotypes from representative regions of the Czech Republic in order to estimate changes in strain prevalence and in the extent of imported drug-resistant tuberculosis. METHODS Primary M. tuberculosis complex isolates (n=155) and follow-up isolates (n=15) from 155 patients from the first half of 2004 (98 from Prague, 37 from South Moravia and 35 from the Moravian-Silesian region) were genotyped by IS6110-RFLP, spoligotyping, and partly by VNTR-genotyping. RESULTS Based on IS6110-RFLP, 110 of 155 (71%) primary isolates were unique. Forty-five isolates (29%) were found in 15 clusters comprising two to six patients and all but one cluster were also discriminated by MIRU-VNTR-genotyping. Four clusters comprised patients from different regions, and six were ongoing for several years. An indication of MDR-strain transmission was found in one instance. All four Beijing-type isolates with any resistance were associated with immigration from Eastern Europe. CONCLUSIONS The molecular epidemiological data of this period-prevalence, population based study and its comparison to earlier investigations point to a low extent of clustering between M. tuberculosis complex isolates in representative regions of the Czech Republic. Few clusters extending geographically and/or over several years were identified, providing a means for an in-depth analysis of risk factors of transmission. Beijing genotype isolates were shown to increase in prevalence to reach 6.5%. Drug resistant isolates of this genotype were associated with immigration of from Eastern Europe, although direct transmission of a resistant isolate was probable only in one of eleven cases.