Miracle-dz/UniFAR-FTUs huggingface dataset:
Effect of protected methionine supplementation on milk production and reproduction in first calf heifers

Abstract. Sixty Holstein heifers (30 days in milk) were used to examine the effects of protected methionine on milk production, milk composition and reproduction performance up to 100 days post-partum. Heifers were randomly divided into two dietary treatment groups (30 each) receiving either 14 or 16 % crude protein. Heifers of each treatment group were assigned into three subgroups with a daily supplementation of 0, 15 or 25 g/hd/d of rumen protected methionine. Diet fed was a total mixed ration consisting of fresh alfalfa, corn silage and a concentrate mixture. In addition, alfalfa hay was offered ad libitum during the whole experimental period.
Protein kinase D mediates the synergistic effects of BMP-7 and IGF-I on osteoblastic cell differentiation

We previously showed that exogenous insulin-like growth factor-I (IGF-I) and bone morphogenetic protein-7 (BMP-7) synergistically stimulated osteoblast differentiation in fetal rat calvaria (FRC) cells. We have now shown that BMP-7 alone and the BMP-7 and IGF-I combination synergistically stimulated protein kinase D (PKD) phosphorylation at Ser744/748 and Ser916. Transfection of FRC cells with a constitutively active PKD stimulated marker expression, while transfection with a catalytically inactive PKD did not. Moreover, Gö6976, which inhibits protein kinase C (PKC) α and β1, blocked PKD phosphorylation and the synergistic action of the BMP-7 and IGF-I combination on osteoblast differentiation, whereas Gö6983, which inhibits PKCα, β, γ, δ, and ζ, did not. Our results suggest that the FRC cell differentiation induced by BMP-7 and the BMP-7 and IGF-I combination requires stimulation of PKD activity. Our results are consistent with a novel mechanism in which combined BMP-7 and IGF-I signaling activates upstream novel PKC(s), which then phosphorylates and activates PKD, leading to enhanced osteoblast differentiation.
Ambiguity in patent vocabulary: Experiments with clarity scores for claims and descriptions

The ambiguity of query terms is a major obstacle for performance in information retrieval. Clarity or ambiguity scores measure how often terms appear together with different other terms by applying the Kullback-Leibler Divergence. These scores have been used to predict the performance of queries. We calculated the clarity scores within a large patent collection and compared the ambiguity of terms selected form claims and description within the same and within the other field.
A Conserved NS3 Surface Patch Orchestrates NS2 Protease Stimulation, NS5A Hyperphosphorylation and HCV Genome Replication

Hepatitis C virus (HCV) infection is a leading cause of liver disease worldwide. The HCV RNA genome is translated into a single polyprotein. Most of the cleavage sites in the non-structural (NS) polyprotein region are processed by the NS3/NS4A serine protease. The vital NS2-NS3 cleavage is catalyzed by the NS2 autoprotease. For efficient processing at the NS2/NS3 site, the NS2 cysteine protease depends on the NS3 serine protease domain. Despite its importance for the viral life cycle, the molecular details of the NS2 autoprotease activation by NS3 are poorly understood. Here, we report the identification of a conserved hydrophobic NS3 surface patch that is essential for NS2 protease activation. One residue within this surface region is also critical for RNA replication and NS5A hyperphosphorylation, two processes known to depend on functional replicase assembly. This dual function of the NS3 surface patch prompted us to reinvestigate the impact of the NS2-NS3 cleavage on NS5A hyperphosphorylation. Interestingly, NS2-NS3 cleavage turned out to be a prerequisite for NS5A hyperphosphorylation, indicating that this cleavage has to occur prior to replicase assembly. Based on our data, we propose a sequential cascade of molecular events: in uncleaved NS2-NS3, the hydrophobic NS3 surface patch promotes NS2 protease stimulation; upon NS2-NS3 cleavage, this surface region becomes available for functional replicase assembly. This model explains why efficient NS2-3 cleavage is pivotal for HCV RNA replication. According to our model, the hydrophobic surface patch on NS3 represents a module critically involved in the temporal coordination of HCV replicase assembly.
Anti-lipolytic Action of AMP-activated Protein Kinase in Rodent Adipocytes*

Despite its importance in terms of energy homeostasis, the role of AMP-activated protein kinase in adipose tissue remains controversial. Initial studies have described an anti-lipolytic role for AMP-activated protein kinase, whereas more recent studies have suggested the converse. Thus we have addressed the role of AMP-activated protein kinase in adipose tissue by modulating AMP-activated protein kinase activity in primary rodent adipocytes using pharmacological activators or by adenoviral expression of dominant negative or constitutively active forms of the kinase. We then studied the effects of AMP-activated protein kinase activity modulation on lipolytic mechanisms. Finally, we analyzed the consequences of a genetic deletion of AMP-activated protein kinase in mouse adipocytes. AMP-activated protein kinase activity in adipocytes is represented mainly by the α1 isoform and is induced by all of the stimuli that increase cAMP in adipocytes, including fasting. When AMP-activated protein kinase activity is increased by 5-aminoimidazole-4-carboxamide-riboside, phenformin, or by the expression of a constitutively active form, isoproterenol-induced lipolysis is strongly reduced. Conversely, when AMP-activated protein kinase activity is decreased either by a dominant negative form or in AMP-activated protein kinase α1 knock-out mice, lipolysis is increased. We present data suggesting that AMP-activated protein kinase acts on hormone-sensitive lipase by blocking its translocation to the lipid droplet. We conclude that, in mature adipocytes, AMP-activated protein kinase activation has a clear anti-lipolytic effect.
Identifying and Analyzing Broadband Internet Reverse DNS Names

Reverse DNS (rDNS) names often contain information not only about core routers in some networks but about hosts on edge networks. Although the rDNS names of routers have been decoded and their naming patterns verified by researchers, the information extracted from edge host rDNS names has been limited to intuitive keywords. In this paper, we develop a methodology for identifying and analyzing rDNS names for broadband Internet end hosts without using any pre-defined keyword. With this methodology, we study whether ISPs use intuitive keywords in their rDNS names and whether rDNS names embed correct information (e.g., whether keyword "cable" indicates cable clients but not fiber or DSL clients).
CD73 is expressed by inflammatory Th17 cells in experimental autoimmune encephalomyelitis but does not limit differentiation or pathogenesis

CD73 works together with CD39 to convert extracellular ATP to immunoregulatory adenosine, thus inhibiting inflammation. TGFβ-mediated CD73 expression on ‘regulatory’ Th17 cells limits their ability to eradicate tumors, similar to the immunosuppressive mechanism described for CD73 on Tregs. However, CD73 is also expressed on Th17 cells thought to be inflammatory in Crohn’s disease. CD73 has previously been reported to contribute to inflammation in the central nervous system (CNS). In experimental autoimmune encephalomyelitis (EAE), we found that inflammatory cytokine-producing Th17 cells showed increased CD73 expression as disease progressed. We therefore hypothesized that CD73 could be important for limiting the expansion or pathogenic function of Th17 cells in autoimmune inflammation of the CNS. Surprisingly, EAE development was not enhanced or inhibited by CD73 deficiency; there was correspondingly no difference in induction of Th17-associated cytokines IL-17, IFNγ or GM-CSF or recruitment of either inflammatory or regulatory cells to the central nervous system. We confirmed that CD73 was similarly not required for differentiation of Th17 cells in vitro. These data show that while CD73 expression is regulated during EAE, this enzyme is not absolutely required to either promote or limit Th17 cell expansion or EAE severity.
Application of an allele‐specific PCR to clinical HIV genotyping samples detects additional K103N mutations in both therapy naïve and experienced patients

Low‐level drug resistance is not detected by routine consensus sequence genotype analysis (CSA) but low levels of specific mutations, such as the non‐nucleoside reverse transcriptase inhibitor (NNRTI)‐resistant mutation K103N, can be quantitated by allele‐specific PCR (ASP). This study has applied an ASP to quantitate low‐level K103N in patients presenting for clinical HIV genotyping and assess the correlation with antiretroviral treatment history and outcomes. HIV RNA was extracted from patient plasma and subjected to PCR amplification of the reverse transcriptase (RT) region followed by genotyping by CSA and real‐time ASP for K103N. When applied to samples from patients presenting for genotyping, the ASP detects K103N, not K103 nor K103R, but cross‐reacts with K103S. ASP identified all samples that were K103N by CSA (10.5%) and an additional 14% by ASP only, representing patients who were therapy naïve and with NNRTI treatment history. ASP detected therapy‐acquired K103N at low levels up to 6 years after cessation of NNRTI therapy. In three patients with new HIV diagnosis and K103N detected by ASP only, K103N virus declined rapidly from the circulation but persisted in PBMC DNA at >12 months post‐diagnosis. Efavirenz (EFV) combination therapy in three patients with low‐level K103N suppressed successfully viral load, although one patient developed failure and CSA‐detectable K103N after 15 months of therapy. Thus, analysis of K103N by ASP in conjunction with CSA genotyping provides additional information that reflects K103N transmission and persistence but detection of low‐level K103N does not preclude successful EFV‐containing combination therapy. J. Med. Virol. 81:1983–1990, 2009. © 2009 Wiley‐Liss, Inc.
Early Seafarers of the Comoro Islands: the Dembeni Phase of the IXth-Xth Centuries AD

Although previous volumes of Azania have carried articles and notes on Madagascar and Mozambique as well as allusions to the Comoro Islands (as in Derek Nurse's study of Swahili linguistic history in XVIII), this is the first article specifically on the Archipelago. Being concerned with the earliest recognised human settlements on the Comores, which show similarities to the earliest levels at Kilwa, Manda and Shanga on the African coast with their maritime connections with the Persian Gulf, the article is especially appropriate in Azania, even more so this year to coincide with the publication of the late Neville Chittick's Manda (BIEA Memoir 9). Those scholars who have recently been questioning received wisdom that Qanbalu was on Pemba and suggesting instead its location on the Comores may search for support in this article, but the author advises caution at this stage. Especially valuable is the food-crop evidence recovered. The indication of Setaria (‘foxtail millet’) is perhaps unexpected. Although it.
HYPERSENSITIVE TO RED AND BLUE 1, a ZZ-Type Zinc Finger Protein, Regulates Phytochrome B–Mediated Red and Cryptochrome-Mediated Blue Light Responses

Plant photoreceptors that regulate photomorphogenic development include red/far-red-light–absorbing phytochromes and blue/UV-A-light–absorbing cryptochromes. We have undertaken a genetic screen to identify additional components downstream of the photoreceptors in Arabidopsis thaliana. We identified a short hypocotyl mutant under red and blue light, hypersensitive to red and blue 1 (hrb1). Mutation in HRB1 also enhances the end-of-day far-red light response, inhibits leaf expansion and petiole elongation, and attenuates the expression of CAB3 and CHS. Double mutant analysis indicates that phyB is epistatic to hrb1 under red light, and cry1 cry2 is epistatic to hrb1 under blue light for both hypocotyl growth and light-regulated gene expression responses. HRB1 localizes to the nucleus and belongs to a protein family of Drought induced 19 (Di19). HRB1 and all other family members contain a ZZ-type zinc finger domain, which in other organisms is implicated in protein–protein interactions between dystrophin and calmodulin and between transcriptional adaptors and activators. HRB1 activity is also required for red and blue light–induced expression of PHYTOCHROME INTERACTING FACTOR 4 (PIF4). pif4 shows a very similar hypersensitive response as hrb1 to both red light and blue light and is epistatic to hrb1 in control of light-regulated gene expression responses. Thus, the roles of HRB1 and PIF4 together in regulating both red and blue light responses may represent points where red light signaling and blue light signaling intersect.
Protective Effect of N-Acetyl Cysteine Against Formaldehyde-Induced Neuronal Damage in Cerebellum of Mice

Background: Formaldehyde, a colorless aldehyde with pungent odor, has negative effects on central nervous system. But, there are a little data about protective substances against neuronal damage induced by formaldehyde. Therefore, the present study was to examine histological changes in the cerebellum of formaldehyde exposed mice and possible effects of N-acetyl cysteine on these changes at histopatological level. Methods: Forty eight adult male NMRI mice were randomly divided into six groups: (I) control, (II) treated with 10 mg/kg formaldehyde, (III) treated with formaldehyde and 50 mg/kg N-acetyl cysteine, (IV) treated with formaldehyde and 100 mg/kg N-acetyl cysteine, (V) treated with formaldehyde and 200 mg/kg N-acetyl cysteine, (VI) treated with formaldehyde and 400 mg/kg N-acetyl cysteine. At the end of 14 days, the cerebellums were processed histologically and morphometric study was carried out using Image J software. Data were analyzed using SPSS software version 20.0 and ANOVA test. Results: The present study demonstrated a remarkable decrease in both the thickness and the number of the neurons of granular layer as well as the mean size and the mean number of Purkinje cells in formaldehyde-treated mice. Treatment with 50 mg/kg NAC increased the number of the neurons in molecular layer of the cerebellum as well as the thickness of the gray and white matter. Moreover, it increased the numbers of Purkinje cells (8.47±3.01 vs. 5.82±1.41). Conclusions: Our results suggest that administration with 50 mg/kg N-acetyl cysteine prevents formaldehyde-induced neuronal damage in cerebellum of mice.
The Style of Processing Scale: Normative and Reliability Data

Three student samples (n s = 624, 653, and 566) yielded normative data for the Style of Processing scale. Analysis of subsamples found acceptable internal reliability (overall r = .78) and good test-retest reliability (overall r = .81, 6-mo. interval). The scale appears to have satisfactory reliability for assessing verbal-visual cognitive style, but further work is needed to test the scale's validity.
Downstaging hepatocellular carcinoma: A systematic review and pooled analysis

Downstaging can facilitate liver transplantation (LT) for patients outside of Milan criteria with hepatocellular carcinoma (HCC); however, the optimal protocol and downstaging outcomes are poorly defined. We aimed to characterize rates of successful downstaging to within Milan criteria and post‐LT recurrence and survival among patients who underwent downstaging. We performed a systematic literature review using the MEDLINE and Embase databases from January 1996 through March 2015 and a search of national meeting abstracts from 2010 to 2014. Rates of downstaging success (defined as a decrease of tumor burden to within Milan) and post‐LT recurrence with 95% confidence intervals (CIs) were calculated. Prespecified subgroup analyses were conducted by treatment modality, study design, and patient characteristics. Thirteen studies (n = 950 patients) evaluating downstaging success had a pooled success rate of 0.48 (95% CI, 0.39‐0.58%). In subgroup analyses, there was no significant difference comparing transarterial chemoembolization (TACE) versus transarterial radioembolization (TARE; P = 0.51), but there were higher success rates in prospective versus retrospective studies (0.68 versus 0.44; P < 0.001). The 12 studies (n = 320 patients) evaluating post‐LT HCC recurrence had a pooled recurrence rate of 0.16 (95% CI, 0.11‐0.23). There was no significant difference in recurrence rates between TACE and TARE (P = 0.33). Post‐LT survival could not be aggregated because of heterogeneity in survival data reporting. Current data have heterogeneity in baseline tumor burden, waiting time, downstaging protocols, and treatment response assessments. There are also notable limitations including inconsistent reporting of inclusion criteria, downstaging protocols, and outcome assessment criteria. In conclusion, the success rate of downstaging HCC to within Milan criteria exceeds 40%; however, posttransplant HCC recurrence rates are high at 16%. Downstaging protocols for HCC should be systematically studied and optimized to minimize the risk of post‐LT HCC recurrence. Liver Transpl 21:1142‐1152, 2015. © 2015 AASLD.
Recognizing Digitization as a Preservation Reformatting Method

Recognizing Digitization as a Preservation Reformatting Method Cultural institutions serve the international community by building, protecting, preserving and ensuring continued access to diverse collections and resources. The challenges of preserving collections have been addressed in different ways over time. Libraries have used conservation to preserve the original artifact and reformatting strategies, such as microfilming and the creation of print facsimiles, to retain content, enhance access, and protect the original from excessive wear. Over the past several years, libraries have moved towards using digitization as an additional method for reformatting endangered and fragile paper-based materials to both preserve and provide access to library collections.
PAD4 Deficiency Decreases Inflammation and Susceptibility to Pregnancy Loss in a Mouse Model

ABSTRACT Inflammation is thought to play a critical role in the pathogenesis of placentation disorders such as recurrent miscarriages, growth restriction, and preeclampsia. Recently, neutrophil extracellular traps (NETs) have emerged as a potential mechanism for promoting inflammation in both infectious and noninfectious disorders. To investigate a pathogenic role for NETs in placentation disorders, we studied a model of antiangiogenic factor-mediated pregnancy loss in wild-type (WT) mice and in mice deficient in peptidylarginine deiminase 4 (Padi4−/−) that are unable to form NETs. Overexpression of soluble fms-like tyrosine kinase 1 (sFlt-1), an antiangiogenic protein that is pathogenically linked with abnormal placentation disorders during early gestation, resulted in pregnancy loss and large accumulation of neutrophils and NETs in WT placentas. Interestingly, sFlt-1 overexpression in Padi4−/− mice resulted in dramatically lower inflammatory and thrombotic response, which was accompanied by significant reduction in pregnancy losses. Inhibition of NETosis may serve as a novel target in disorders of impaired placentation.
Critical machine cluster identification using the equal area criterion

The paper introduces a new method to early identify the critical machine cluster (CMC) after a transient disturbance. For transient stability assessment with methods based on the equal area criterion it is necessary to split the generators into a group of critical and non-critical machines. The generators in the CMC are those likely to lose synchronism. The early and reliable identification of the CMC is crucial and one of the major challenges. The proposed new approach is based on the assessment of the rotor dynamics between two machines and the evaluation of their coupling strength. A novel coupling coefficient is derived and a cluster identification algorithm is developed. The algorithm determines the CMC based on the impact of the fault on the derived coupling coefficient of individual generator pairs. The results from two cases are presented and discussed, where the CMC is successfully determined just after fault clearance.
Post-translational Formylglycine Modification of Bacterial Sulfatases by the Radical S-Adenosylmethionine Protein AtsB*

Cα-Formylglycine (FGly) is the catalytic residue of sulfatases. FGly is generated by post-translational modification of a cysteine (prokaryotes and eukaryotes) or serine (prokaryotes) located in a conserved (C/S)XPXR motif. AtsB of Klebsiella pneumoniae is directly involved in FGly generation from serine. AtsB is predicted to belong to the newly discovered radical S-adenosylmethionine (SAM) superfamily. By in vivo and in vitro studies we show that SAM is the critical co-factor for formation of a functional AtsB·SAM·sulfatase complex and for FGly formation by AtsB. The SAM-binding site of AtsB involves 83GGE85 and possibly also a juxtaposed FeS center coordinated by Cys39 and Cys42, as indicated by alanine scanning mutagenesis. Mutation of these and other conserved cysteines as well as treatment with metal chelators fully impaired FGly formation, indicating that all three predicted FeS centers are crucial for AtsB function. It is concluded that AtsB oxidizes serine to FGly by a radical mechanism that is initiated through reductive cleavage of SAM, thereby generating the highly oxidizing deoxyadenosyl radical, which abstracts a hydrogen from the serine-CβH2-OH side chain.
A Comparison of Multivariate SARIMA and SVM Models for Emergency Department Admission Prediction

A comparison of multivariate SARIMA model with a multivariate regression-based time series based on a Support Vector Machine model was performed for emergency department admissions prediction. The same input variables were used in both models. Both models were trained with consecutive daily samples of data corresponding to the January 2009 – August 2012 period (n=1339). Performance was evaluated on the September 2012 test dataset (n=30). The results obtained with the Support Vector Machine were found to be more accurate with a 46,53% RMSE improvement and a 48,89% MAE improvement on the train set. The experiment was repeated six times with varying time periods. The SVM approach produced better results in all cases. Error measurements on the test set were compared with a paired T test. The differences between all comparisons were found to be statistically significant in all cases with a 95% CI.
Reliable robust flight tracking control: an LMI approach

This paper studies the reliable robust tracking controller design problem against actuator faults and control surface impairment for aircraft. First, models of actuator faults and control surface impairment are presented. Then a reliable robust tracking controller design method is developed. This method is based on the mixed linear quadratic (LQ)//H/sub /spl infin// tracking performance index and multiobjective optimization in terms of linear matrix inequalities. Flight control examples are given, and both linear and nonlinear simulations are given.