Miracle-dz/UniFAR-FTUs huggingface dataset:
Efficacy of combination therapy using anorganic bovine bone graft with resorbable GTR membrane vs. open flap debridement alone in the management of grade II furcation defects in mandibular molars – A comparative study

Context: Invasion of the bifurcation and trifurcation of the multi-rooted teeth resulting in furcation involvement is one of the serious complications of periodontitis. Aim: The purpose of the study was to evaluate the efficacy of combination therapy using anorganic bovine bone graft and resorbable guided tissue regeneration (GTR) membrane versus open flap debridement alone in the management of Grade II furcation defects in mandibular molars. Materials and Methods: The study included a total number of 20 sites in 10 patients with bilateral mandibular furcation defects, out of which 10 sites were treated as test group and 10 as control group. The test group was treated with combination therapy and the control group with open flap debridement alone. The parameters were recorded on 0 day (baseline), 90th day, and 180th day, which included vertical probing depth and horizontal probing depth of the furcation defect, clinical attachment level, and defect fill. Statistical Analysis Used: Mean and standard deviation were calculated for different variables in each study group at different time points. Mean values were compared by using Wilcoxon signed ranks test, after adjusting the P values for multiple comparison by using Bonferroni correction method. Results: Both the test and control groups showed a definitive improvement in clinical parameters, which was statistically significant. On comparison, the vertical probing depth showed significant reduction in the test group with a mean reduction of 3.1 ± 0.7 mm, when compared to the control group which showed a mean reduction of 1.5 ± 0.5 mm. The horizontal probing depth of furcation defects was also significantly reduced in the test group with a mean reduction of 2.2 ± 0.6 mm, when compared to the control group in which the mean reduction was 0.9 ± 0.3 mm. There was also significant gain in attachment level in the test group which showed a mean gain of 3.2 ± 0.6 mm, when compared to the control group which showed a gain of 1.2 ± 0.6 mm. Radiographic defect fill was found to be more in the test group with a mean gain of 2.0 ± 0.1 mm, when compared to the control group which showed a defect fill of 0.2 ± 0.1 mm. Conclusions: The results of this study demonstrated that the combined use of anorganic bovine bone graft and resorbable GTR membrane is effective than open flap debridement alone in the treatment of mandibular grade II furcation defects.
Ebola Virus Does Not Block Apoptotic Signaling Pathways

ABSTRACT Since viruses rely on functional cellular machinery for efficient propagation, apoptosis is an important mechanism to fight viral infections. In this study, we sought to determine the mechanism of cell death caused by Ebola virus (EBOV) infection by assaying for multiple stages of apoptosis and hallmarks of necrosis. Our data indicate that EBOV does not induce apoptosis in infected cells but rather leads to a nonapoptotic form of cell death. Ultrastructural analysis confirmed necrotic cell death of EBOV-infected cells. To investigate if EBOV blocks the induction of apoptosis, infected cells were treated with different apoptosis-inducing agents. Surprisingly, EBOV-infected cells remained sensitive to apoptosis induced by external stimuli. Neither receptor- nor mitochondrion-mediated apoptosis signaling was inhibited in EBOV infection. Although double-stranded RNA (dsRNA)-induced activation of protein kinase R (PKR) was blocked in EBOV-infected cells, induction of apoptosis mediated by dsRNA was not suppressed. When EBOV-infected cells were treated with dsRNA-dependent caspase recruiter (dsCARE), an antiviral protein that selectively induces apoptosis in cells containing dsRNA, virus titers were strongly reduced. These data show that the inability of EBOV to block apoptotic pathways may open up new strategies toward the development of antiviral therapeutics.
Determinants of Public Indebtedness in European Union Countries

Abstract The paper strives to determine the impact of fiscal variables on factors determining the dynamics of public debt in European Union countries. Based on the literature, the dynamics of public debt are determined by changes of three elements: the primary balance, interest-rate-growth-differential and the change of government assets. Therefore, it seems reasonable to estimate the dynamics of these three values to find the variables crucial for limiting the growth of public debt. Three groups of dynamic panel regressions were estimated based on the one-step Generalized Method of Moments. The data was collected for the 1995-2015 period for 27 EU countries. Dependent variables included: primary balance, interest-rate-growth-differential and change of government assets. Independent variables consisted of: interest payable to GDP ratio, unemployment rate, squared unemployment rate, FDI stock to GDP, net FDI inflow to GDP, general government expenditures to GDP, share of social security expenditures and openness of the economy measured by the ratio of export and import to GDP. On the basis of statistical data, three components of debt changes were distinguished, and estimations of the dynamic panel regressions were applied to find the impact of independent variables. According to the basic models, the primary balance is lower for: countries with higher unemployment, greater FDI stock and higher general government expenditures. The interest-rate-growth-differential is lower in the case of: high subsidies and for a more open economy. However, unemployment and FDI remain the most important determinants of this variable. The change of government’s assets ratio decreases as FDI net inflows or the share of expenditures to GDP increase as well as in the case of very high unemployment.
Epstein-Barr Virus Nuclear Protein EBNA3A Is Critical for Maintaining Lymphoblastoid Cell Line Growth

ABSTRACT To evaluate the role of Epstein-Barr Virus (EBV) nuclear antigen 3A (EBNA3A) in the continuous proliferation of EBV-infected primary B lymphocytes as lymphoblastoid cell lines (LCLs), we derived LCLs that are infected with a recombinant EBV genome that expresses EBNA3A fused to a 4-hydroxy-tamoxifen (4HT)-dependent mutant estrogen receptor hormone binding domain (EBNA3AHT). The LCLs grew similarly to wild-type LCLs in medium with 4HT despite a reduced level of EBNA3AHT fusion protein expression. In the absence of 4HT, EBNA3AHT moved from the nucleus to the cytoplasm and was degraded. EBNA3AHT-infected LCLs were unable to grow in medium without 4HT. The precise time to growth arrest varied inversely with cell density. Continued maintenance in medium without 4HT resulted in cell death, whereas readdition of 4HT restored cell growth. Expression of other EBNAs and LMP1, of CD23, and of c-myc was unaffected by EBNA3A inactivation. Wild-type EBNA3A expression from an oriP plasmid transfected into the LCLs protected the EBNA3AHT-infected LCLs from growth arrest and death in medium without 4HT, whereas EBNA3B or EBNA3C expression was unable to protect the LCLs from growth arrest and death. These experiments indicate that EBNA3A has a unique and critical role for the maintenance of LCL growth and ultimately survival. The EBNA3AHT-infected LCLs are also useful for genetic and biochemical analyses of the role of EBNA3A domains in LCL growth.
Efficacy of Edaravone, a Free Radical Scavenger, on Left Ventricular Function and Structure in Diabetes Mellitus

This study was designed to assess the efficacy of edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger that possesses anti-oxidant effects, on cardiac function and fine structure of the left ventricular myocardium in diabetes mellitus. Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of spontaneous development of type II diabetes (30 weeks; n = 15) were divided into two groups and treated with edaravone 30 mg/kg/d or vehicle for 2 weeks. OLETF rats showed hyperglycemia (352 ± 71 mg/dl vs normal control; 128 ± 52 mg/dl), increased thiobarbituric acid-reactive substances (TBARS; 6.9 ± 2.5 n M/ml vs 2.8 ± 0.6 n M/ml), and decreased superoxide dismutase activity (21.5 ± 0.9 U/ml vs 25.8 ± 0.7 U/ml). Increased left ventricular end-diastolic pressure (12 ± 3 mm Hg vs 6 ± 2 mm Hg) and hypertrophied cardiocytes (23.1 ± 1.4 vs 17.6 ± 1.0 &mgr;m) were also observed (P < 0.05, respectively). Edaravone could not improve plasma glucose level and hemodynamic parameters but significantly decreased TBARS values (3.8 ± 0.5) and increased superoxide dismutase activity (24.5 ± 0.8) (vs OLETF, P < 0.05, respectively). Moreover, edaravone effectively preserved cardiocyte diameter (18.2 ± 0.9 &mgr;m) and the fine structure of mitochondria. Thus, edaravone exhibits modest cardiac protection in diabetes mellitus independent of blood sugar level.
Energy compensation after an aerobic exercise session in high-fat/low-fit and low-fat/high-fit young male subjects

There is general agreement that exercise-induced energy expenditure is not entirely compensated for at the next meal or over the following 24 h, but inter-individual variability is high. The role of ‘fatness and fitness’ in this variability has never been assessed. Therefore, eighteen non-obese male subjects aged 22·2 (sd 2·0) years were selected and separated into a ‘high-fatness and low-fitness’ (Hfat/Lfit, n 9) and a ‘low-fatness and high-fitness’ (Lfat/Hfit, n 9) group, according to three criteria: maximal oxygen uptake; weekly hours of physical activity; fat mass index. At 1 h before lunch, they were subjected to 60 min of exercise on a cycle ergometer (70 % VO2max), or stayed at rest. Then, they self-reported food intake in diaries until the next breakfast. Intake at lunch was not different between conditions, but was higher after exercise than after rest over the 24 h, leading to a significant but partial mean level of compensation of 49·8 (sem 16·5) and 37·8 (sem 24·6) % for the Hfat/Lfit and Lfat/Hfit groups, respectively. Energy compensation at lunch and over the 24 h were strongly correlated (r 0·76, P< 0·001). Both groups consumed more fat and protein after exercise than after rest over the 24 h, but the percentage of energy derived from fat increased only in the Hfat/Lfit group (2·1 (sem 0·6) %, P= 0·026). Thus, the energy cost of an aerobic exercise session was partially compensated over the next 24 h independently of the ‘fatness and fitness’ status, but ‘high-fat and low-fit’ individuals compensated more specifically on fats.
Vancomycin Bonded to Bone Grafts Prevents Bacterial Colonization

ABSTRACT Infection is an important medical problem associated with the use of bone allografts. To retard bacterial colonization, we have recently reported on the modification of bone allografts with the antibiotic vancomycin (VAN). In this report, we examine the ability of this antibiotic-modified allograft to resist bacterial colonization and biofilm formation. When antibiotic was coupled to the allograft, a uniform distribution of the antibiotic was apparent. Following challenges with Staphylococcus aureus for 6 h, the covalently bonded VAN decreased colonization as a function of inoculum, ranging from 0.8 to 2.0 log10 CFU. Furthermore, the VAN-modified surface resisted biofilm formation, even in topographical niches that provide a protected environment for bacterial adhesion. Attachment of the antibiotic to the allograft surface was robust, and the bonded VAN was stable whether incubated in aqueous media or in air, maintaining levels of 75 to 100% of initial levels over 60 days. While the VAN-modified allograft inhibited the Gram-positive S. aureus colonization, in keeping with VAN′s spectrum of activity, the VAN-modified allograft was readily colonized by the Gram-negative Escherichia coli. Finally, initial toxicity measures indicated that the VAN-modified allograft did not influence osteoblast colonization or viability. Since the covalently tethered antibiotic is stable, is active, retains its specificity, and does not exhibit toxicity, it is concluded that this modified allograft holds great promise for decreasing bone graft-associated infections.
Sector-Specific Investment in a MRIO CGE Model

Concerns with the measurement of systemic risk are heightened in today’s interconnected, post-GFC world. However, as it is recognised by the academic community, empirical analyses quantifying the impact of shocks to the world economy on agent risk are scarce if not inexistent. A widely used framework for performing such analysis is computable general equilibrium (CGE) modelling. This paper documents work in progress on developing a global CGE model. A key challenge in the development of the global model lies in the combining of the strengths of the GTAP and WIOD databases. Contrary to the GTAP database, the World Input-Output Database (WIOD) does not rely on the common sourcing assumption but recognises that demand in a region for a given commodity from another region may differ across users. On the other hand, limited data are available in WIOD on taxes, tariffs and international transport margins, while the GTAP database has all the necessary data to incorporate a realistic structure of these variables into the model. The main purpose of the simulations in this paper is to illustrate the usefulness of applying a multi-region input-output database to a CGE model. The analysis shows that, at the macroeconomic level, the advantage of a real sourcing-differentiated database is relatively insignificant. However, at the industry level, it can result in significant differences in prices that are relevant in analysing policy reforms in the global supply chain.
Cultivation of a highly enriched ammonia-oxidizing archaeon of thaumarchaeotal group I.1b from an agricultural soil.

Nitrification of excess ammonia in soil causes eutrophication of water resources and emission of atmospheric N(2) O gas. The first step of nitrification, ammonia oxidation, is mediated by Archaea as well as Bacteria. The physiological reactions mediated by ammonia-oxidizing archaea (AOA) and their contribution to soil nitrification are still unclear. Results of non-culture-based studies have shown the thaumarchaeotal group I.1b lineage of AOA to be dominant over both AOA of group I.1a and ammonia-oxidizing bacteria in various soils. We obtained from an agricultural soil a highly enriched ammonia-oxidizing culture dominated by a single archaeal population [c. 90% of total cells, as determined microscopically (by fluorescence in situ hybridization) and by quantitative PCR of its 16S rRNA gene]. The archaeon (termed 'strain JG1') fell within thaumarchaeotal group I.1b and was related to the moderately thermophilic archaeon, Candidatus Nitrososphaera gargensis, and the mesophilic archaeon, Ca. Nitrososphaera viennensis with 97.0% and 99.1% 16S rRNA gene sequence similarity respectively. Strain JG1 was neutrophilic (growth range pH 6.0-8.0) and mesophilic (growth range temperature 25-40°C). The optimum temperature of strain JG1 (35-40°C) is > 10°C higher than that of ammonia-oxidizing bacteria (AOB). Membrane analysis showed that strain JG1 contained a glycerol dialkyl glycerol tetraether, GDGT-4, and its regioisomer as major core lipids; this crenarchaeol regioisomer was previously detected in similar abundance in the thermophile, Ca. N. gargensis and has been frequently observed in tropical soils. Substrate uptake assays showed that the affinity of strain JG1 for ammonia and oxygen was much higher than those of AOB. These traits may give a competitive advantage to AOA related to strain JG1 in oligotrophic environments. (13) C-bicarbonate incorporation into archaeal lipids of strain JG1 established its ability to grow autotrophically. Strain JG1 produced a significant amount of N(2) O gas - implicating AOA as a possible source of N(2) O emission from soils. Sequences of archaeal amoA and 16S rRNA genes closely related to those of strain JG1 have been retrieved from various terrestrial environments in which lineage of strain JG1 is likely engaged in autotrophic nitrification.
Use of Histone Deacetylase 8 (HDAC8), a New Marker of Smooth Muscle Differentiation, in the Classification of Mesenchymal Tumors of the Uterus

Uterine smooth muscle tumors (SMTs) are usually recognized on the basis of their routine morphologic features; however, their distinction from endometrial stromal tumors (ESTs), the second most common mesenchymal tumor of the uterus, is sometimes problematic. Histone deacetylases (HDACs) were originally identified as nuclear enzymes regulating histone acetylation. We have recently shown that in normal human tissues, HDAC8 is exclusively expressed in the cytoplasm of cells showing smooth muscle differentiation. In this study, we examined HDAC8 expression in SMTs and ESTs of the uterus to determine whether HDAC8 may be a useful diagnostic tool in the classification of problematic uterine mesenchymal tumors. HDAC8 immunohistochemical staining was performed in 15 leiomyomas (LMs), 9 highly cellular leiomyomas (HCLs), 8 epithelioid SMTs, 13 leiomyosarcomas (LMSs), and 17 ESTs, including 3 with sex-cord differentiation and 5 with smooth muscle differentiation. All tumors were also stained for other smooth muscle markers (desmin, h-caldesmon, smooth muscle actin [SMA], smooth muscle myosin heavy chain) and for CD10. All LMs had moderate to strong expression of all smooth muscle markers. HDAC8 was detected in 8 of 9 HCLs and in all epithelioid SMTs (8 of 8); however, it was weak in 4 epithelioid SMTs. In contrast, desmin, h-caldesmon and smooth muscle myosin were positive in only 2 of 8, 1 of 8 and 4 of 8 epithelioid SMTs, respectively. All smooth muscle markers had similar frequency of staining in LMSs; however, HDAC8 showed overall moderate intensity compared with other smooth muscle markers, which showed stronger staining. HDAC8, h-caldesmon, and smooth muscle myosin did not stain conventional areas of ESTs or ESTs with sex-cord differentiation, whereas SMA and desmin were positive in those areas in 4 of 12 and 3 of 12 ESTs, respectively. Areas of smooth muscle differentiation in ESTs were positive for HDAC8 in all cases, but they were less constantly positive for the other smooth muscle markers. CD10 was expressed in most ESTs (14 of 17), but it was also positive in 15 of 45 SMTs. In conclusion: 1) HDAC8 seems to be a specific marker of SM differentiation because conventional ESTs and ESTs with sex-cord differentiation are negative for HDAC8, whereas areas of smooth muscle differentiation in these tumors are consistently positive; 2) HDAC8 gives similar results to those obtained with desmin, h-caldesmon, and smooth muscle myosin in both LMs and LMSs, although the staining for HDAC8 in LMSs tends to be less intense; 3) HDAC8 may be a more sensitive marker than desmin and h-caldesmon in epithelioid SMTs. Thus, HDAC8 detection may be useful in helping the differential diagnosis of uterine mesenchymal tumors.
New final finish stack including a custom nano-crystalline silver alloy for mobile connector systems with high cycling wear and powered environmental exposure requirements

Electronic interconnections frequently employ a combination of electroplated nickel or nickel alloy as a barrier layer to the substrate and electroplated gold as a topcoat. However, under extended mating cycles (>103) and potential bias in wet environments, these gold on nickel stacks often fail due to wear through and/or corrosion of the connector base substrate. This paper reports on a new custom-engineered, electroplated, nano-crystalline silver alloy (NCSA) material stack that differentiates itself from both traditional hard gold and other silver technologies by offering improved wear durability up to and beyond 104 mating cycles, as well as improved corrosion protection for immersion environmental exposures. Voltage-biased immersion tests involving common liquids such as perspiration and saline solutions as well as high cycling wear beyond 104 mating cycles have been conducted on a gold-on-nickel stack as well as two embodiments of the new NCSA final finish stack: 1) with the NCSA plated onto a nano-crystalline nickel-tungsten alloy (NCNA) as a barrier layer and 2) with the NCSA plated directly on the substrate with no nickel-based barrier layer. Both embodiments of the NCSA stack exhibited at least equivalent performance, and in some cases outperformed a standard gold-on-nickel stack in both wear durability and biased corrosion resistance.
Development of the olfactory bulb: Evidence for glia‐neuron interactions in glomerular formation

Olfactory bulb (OB) glomeruli have long been considered functional units in the processing of odor information. Recently, it has been shown that axons from olfactory receptor neurons (ORNs) expressing the same odorant receptor gene converge onto two or a few topographically fixed glomeruli in the OB. The interactions between ORN axons, mitral/tufted cell dendrites, juxtaglomerular (JG) cells, and glial cells during the development of glomeruli is of great importance in light of this receptor gene glomerular topography in the primary olfactory projection. To explore the development of mammalian olfactory glomeruli, we investigated the relationships among radial glia (RG), astrocytes, ORNs, JG cells, mitral/tufted cell dendrites, and olfactory Schwann cells throughout embryonic and early postnatal development. Our results indicate that glomeruli are formed through an invariant sequence of cellular events: (1) pioneering ORN axons contact the rostral telencephalon at approximately E11–14, which coincides with the onset of morphologic changes in telencephalic RG; (2) at E15–16, RG branch and begin to form two plexuses, one located in the subventricular layer and the other superficial to the presumptive mitral cell layer; (3) at E17–18, ORN axons accumulate in a dense band superficial to the outer radial glia plexus; (4) at E19–20, processes from RG and astrocytes begin to ramify to form glial tufts, or glial glomeruli. Coincident with the formation of these glial glomeruli, ORN axons intermingle with the glial processes and form proto‐glomeruli; (5) at E21 to P0, JG cells begin to migrate into position surrounding glomeruli, (6) and at P4, the apical tuft of mitral cells becomes restricted to a single glomerulus. Interestingly, glomerular development also occurs in a distinct rostral to caudal gradient. That is, glomeruli in the rostral OB develop earlier than those in the caudal OB, but the sequence of cellular events at any point in the bulb is invariant. These results demonstrate that glomeruli are formed in a specific spatiotemporal sequence beginning with ORN axon‐glia contacts, then JG cell arrival, and finally mitral cell apical dendrite restriction. J. Comp. Neurol. 415:423–448, 1999. © 1999 Wiley‐Liss, Inc.