Miracle-dz/UniFAR-FTUs huggingface dataset:
Millimeter-wave ink-jet printed RF energy harvester for next generation flexible electronics

In this effort, the authors present the first demonstration of a flexible, inkjet-printed mm-wave rectenna. The design considerations and processes of the individual antenna array and rectifier are described, demonstrating a realized gain of 5 dBi, and a single-lumped-component via-less rectifier with up to a 2.5V dc voltage for an input power of 18 dBm, at the operation frequency of 24 GHz. The printed system is finally demonstrated in a wireless operation test, in a bent condition, thereby setting the foundation for the emergence of mm-wave-powered smart skins and wearables for the Internet of Things (IoT).
Pharmacological interventions for improved colonic anastomotic healing: a meta-analysis.

AIM To identify pharmaceuticals for the prophylaxis of anastomotic leakage (AL), we systematically reviewed studies on anastomosis repair after colorectal surgery. METHODS We searched PubMed and EMBASE for articles published between January 1975 and December 2012. We included studies in English with the primary purpose of promoting healing of anastomoses made in the colon or rectum under uncomplicated conditions. We excluded studies on adverse events from interventions, nutritional interventions or in situ physical supporting biomaterials. The primary outcome was biomechanical strength or AL. We performed meta-analyses on therapeutic agents investigated by three or more independent research groups using the same outcome. The DerSimonian-Laird method for random effects was applied with P < 0.05. RESULTS Of the 56 different therapeutic agents assessed, 7 met our inclusion criteria for the meta-analysis. The prostacyclin analog iloprost increased the weighted mean of the early bursting pressure of colonic anastomoses in male rats by 60 mmHg (95%CI: 30-89) vs the controls, and the immunosuppressant tacrolimus increased this value by 29 mmHg (95%CI: 4-53) vs the controls. Erythropoietin showed an enhancement of bursting pressure by 45 mmHg (95%CI: 14-76). The anabolic compound growth hormone augmented the anastomotic strength by 21 mmHg (95%CI: 7-35), possibly via the up-regulation of insulin-like growth factor-1, as this growth factor increased the bursting pressure by 61 mmHg (95%CI: 43-79) via increased collagen deposition. Hyperbaric oxygen therapy increased the bursting pressure by 24 mmHg (95%CI: 13-34). Broad-spectrum matrix metalloproteinase inhibitors increased the bursting pressure by 48 mmHg (95%CI: 31-66) on postoperative days 3-4. In the only human study, the AL incidence was not significantly reduced in the 103 colorectal patients treated with aprotinin (11.7%) compared with the 113 placebo-treated patients (9.7%). CONCLUSION This systematic review identified only one randomized clinical trial and seven therapeutic agents from pre-clinical models that could be explored further for the prophylaxis of AL after colorectal surgery.
Knockdown of DEPTOR inhibits cell proliferation and increases chemosensitivity to melphalan in human multiple myeloma RPMI-8226 cells via inhibiting PI3K/AKT activity

Objective The present study determined the role of DEP domain containing mTOR-interacting protein (DEPTOR) in the proliferation, apoptosis and chemosensitivity of RPMI-8226 multiple myeloma cells, using small hairpin RNA (shRNA) to knock down DEPTOR gene expression in vitro. Methods DEPTOR mRNA and protein levels in RPMI-8226 cells treated with DEPTOR-specific shRNA were evaluated by reverse transcription–polymerase chain reaction and Western blotting. Expression of apoptosis-associated proteins (including cleaved caspase-3 and cleaved poly-ADP ribose polymerase [PARP]) and activation of the phosphatidylinositol 3-kinase (PI3K)/v-akt murine thymoma viral oncogene homologue 1 (AKT) signalling pathway were detected by Western blotting. Results Transfection of DEPTOR-specific shRNA successfully knocked down DEPTOR gene expression in transfected RPMI-8226 cells. These transfected cells, together with control RPMI-8226 cells, were treated with 20 µmol/l melphalan for 24 h. Knockdown of DEPTOR exacerbated melphalan-induced growth inhibition and apoptosis, increased levels of cleaved caspase-3 and cleaved PARP, and reduced levels of phosphor-AKT. Conclusion Downregulation of DEPTOR inhibited proliferation and increased chemosensitivity to melphalan in human multiple myeloma RPMI-8226 cells via inhibiting the PI3K/AKT pathway.
A conserved energetic footprint underpins recognition of human leukocyte antigen-E by two distinct αβ T cell receptors

αβ T cell receptors (TCRs) interact with peptides bound to the polymorphic major histocompatibility complex class Ia (MHC-Ia) and class II (MHC-II) molecules as well as the essentially monomorphic MHC class Ib (MHC-Ib) molecules. Although there is a large amount of information on how TCRs engage with MHC-Ia and MHC-II, our understanding of TCR/MHC-Ib interactions is very limited. Infection with cytomegalovirus (CMV) can elicit a CD8+ T cell response restricted by the human MHC-Ib molecule human leukocyte antigen (HLA)-E and specific for an epitope from UL40 (VMAPRTLIL), which is characterized by biased TRBV14 gene usage. Here we describe an HLA-E–restricted CD8+ T cell able to recognize an allotypic variant of the UL40 peptide with a modification at position 8 (P8) of the peptide (VMAPRTLVL) that uses the TRBV9 gene segment. We report the structures of a TRBV9+ TCR in complex with the HLA-E molecule presenting the two peptides. Our data revealed that the TRBV9+ TCR adopts a different docking mode and molecular footprint atop HLA-E when compared with the TRBV14+ TCR–HLA-E ternary complex. Additionally, despite their differing V gene segment usage and different docking mechanisms, mutational analyses showed that the TCRs shared a conserved energetic footprint on the HLA-E molecule, focused around the peptide-binding groove. Hence, we provide new insights into how monomorphic MHC molecules interact with T cells.
Open source software implementation of an integrated testing strategy for skin sensitization potency based on a Bayesian network.

An open-source implementation of a previously published integrated testing strategy (ITS) for skin sensitization using a Bayesian network has been developed using R, a free and open-source statistical computing language. The ITS model provides probabilistic predictions of skin sensitization potency based on in silico and in vitro information as well as skin penetration characteristics from a published bioavailability model (Kasting et al., 2008). The structure of the Bayesian network was designed to be consistent with the adverse outcome pathway published by the OECD (Jaworska et al., 2011, 2013). In this paper, the previously published data set (Jaworska et al., 2013) is improved by two data corrections and a modified application of the Kasting model. The new data set implemented in the original commercial software package and the new R version produced consistent results. The data and a fully documented version of the code are publicly available (http://ntp.niehs.nih.gov/go/its).
A 0.18-/spl mu/m 256-Mb DDR-SDRAM with low-cost post-mold tuning method for DLL replica

A 200-MHz double-data-rate synchronous-DRAM (DDR-SDRAM) was developed. The chip contains a delay-locked loop (DLL) which performs over a wide range of operating conditions. Post-mold-tuning allows precise replica programming. A 200-MHz intra-chip data bus is suitable for DDR operation.
Mechanisms of the Natural Reactivity of Lymphocytes from Noninfected Individuals to Membrane-Associated Leishmania infantum Antigens1

Membrane-associated Leishmania Ags (MLA) or soluble Leishmania Ags were used in vitro to stimulate cord blood or PBMC from healthy donors noninfected by Leishmania parasites. MLA, but not soluble Leishmania Ags, constantly induce strong proliferation of cord blood mononuclear cells and PBMC from noninfected individuals. Responding cells are CD3+, CD4+, TCRαβ+, CD45RO+, and CD45RA+ and secrete IFN-γ and IL-10, but not IL-4. MLA do not activate NK cells nor NKT cells. Membrane Ags also induce purified macrophages from noninfected individuals to secrete IL-10 and TNF-α, but have no effect on IL-1α or IL-12 secretion. The effects of MLA are proteinase K-sensitive and resistant to lipid extraction. The lymphoproliferative responses are inhibited by anti-HLA-DR Abs and require Ag processing by APCs, excluding that the biological effect of MLA could be attributed to a superantigen. Finally, TCR repertoire analysis shows that the T cell expansion induced by MLA uses TCR with various variable β segment rearrangements and CDR3 lengths, features much more characteristic to those observed with a polyclonal activator than with a conventional Ag. These results suggest a particular mechanism developed during the host’s natural response to Leishmania parasites that allows direct activation of naive CD4 lymphocytes by parasite membrane-associated Ags.
Estetrol review: profile and potential clinical applications

In this review paper, the existing information on the human fetal steroid estetrol (E4) has been summarized. In the past, E4 was considered as a weak estrogen and interest disappeared. However, recent new research has demonstrated that E4 is a potent, orally bioavailable, natural human fetal selective estrogen receptor modulator, since it acts in the rat as an estrogen on all tissues investigated except breast tumor tissue, where it has estrogen antagonistic properties in the presence of estradiol. Based on its safety data, its pharmacokinetic properties, its pharmacological profile and the results of first human studies, E4 may be suitable as a potential drug for human use in applications such as hormone replacement therapy (vaginal atrophy, hot flushes), contraception and osteoporosis. Additional areas worth exploring are the treatment of breast and prostate cancer, hypoactive sexual desire disorder and topical use (wrinkles) in women, auto-immune diseases, migraine, cardiovascular applications and the treatment of selected obstetric disorders.
A model of four hierarchical levels to train Chinese residents’ teaching skills for “practice-based learning and improvement” competency

Abstract Objectives: The current study focused on validating a protocol for training and auditing the resident’s practice-based learning and improvement (PBLI) and quality improvement (QI) competencies for primary care. Methods: Twelve second-year (R2), 12 first-year (R1) and 12 postgraduate year-1 residents were enrolled into group A, B and C, respectively, as trainees. After three training protocols had been completed, a writing test, self-assessed questionnaire and mini-OSTE and end-of-rotation assessment were used in auditing the PBLI competency, performance and teaching ability of trainees. Results: Baseline expert-assessed PBLI and QI knowledge application tool writing scores were low for the R1 and R2 residents. After three training protocols, PBLI and QI proficiencies, performance and teaching abilities were improved to similar levels cross the three training levels of residents based on the expert-assessed writing test-audited assessments and on the faculty and standardized clerk-assessed end-of-rotation-/mini-OSTE-audited assessments. Conclusion: The different four-level hierarchical protocols used to teach group A, B and C were equally beneficial and fitted their needs; namely the different levels of the trainees. Specifically, each level was able to augment their PBLI and QI proficiency. This educational intervention helps medical institutions to train residents as PBLI instructors.
PHAGOCYTES , GRANULOCYTES , AND MYELOPOIESIS Two independent killing mechanisms of Candida albicans by human neutrophils : evidence from innate immunity defects

The occurrence of fungal infections such as those with Candida and Aspergillus spp has progressively increased over the last decades as a consequence of the extensive use of immunosuppressive therapies. Invasive fungal infections, in particular, are associated with mortality rates of 40% to 50%. Neutrophils are the most important effector immune cells in fungal killing. It appears that adaptive immunity is primarily responsible for controllingCandida infection at the mucosal level by interleukin-17 (IL-17)–producing lymphocytes,whereas cells of the innate immune system are critical for preventing systemic candidiasis. The latter is illustrated by the increased prevalence of invasive fungal infections in patients with chemotherapy-induced neutropenia or with neutrophil functional defects, such as genetic deficiencies of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase as seen in chronic granulomatous disease (CGD) patients. The neutrophil mechanism of fungal killing is poorly understood. First, it is not known which pathogen recognition receptors and their downstream signaling pathways are involved in the killing of Candida albicans. Both C-type lectin receptors (CLRs; including dectin-1, dectin-2, and mincle, and also integrins, especially complement receptor 3 [CR3; CD11b/CD18, aMb2]) have been demonstrated to recognize the b-glucans and mannans exposed on the C albicans cell wall. However, 2 studies performed with dectin-1 knockoutmice contradict each other: 1 showed that dectin-1 was required for the control of systemic candidiasis, whereas the other claimed that this receptor was not relevant. The differential requirement of dectin-1 appeared to be Candida strain-specific. In humans, only 1 family with 3 dectin-1–deficient patients has been reported so far, showing clinically mucocutaneous fungal infections, but no invasive fungal infections.Moreover, aswe have previously shown for human neutrophils, CR3 and not dectin-1 seems to be the major receptor for b-glucan recognition. Patients with a leukocyte adhesion defect (either LAD-I in which CD11/CD18 integrins are lacking or LAD-III [also known as LAD1/variant] syndrome with a deficiency of kindlin-3 required for leukocyte integrin activation) are genetically predisposed to invasive bacterial and fungal infections. In mouse models, both dectin-1 and CR3 have been described to trigger spleen-tyrosine kinase (Syk) and phosphatidylinositol3-kinase (PI3K) to elicit a cytotoxic response and to activate the signaling adaptor protein CARD9 [caspase recruitment domaincontaining protein 9]. Recently, human patients with CARD9 deficiency have been characterized to suffer, typically, fromCandida meningitis, and this was found to be associated with an impaired killing capacity of CARD9-deficient neutrophils toward Candida.
IsdC from Staphylococcus lugdunensis Induces Biofilm Formation under Low-Iron Growth Conditions

ABSTRACT Staphylococcus lugdunensis is a coagulase-negative staphylococcus that is a commensal of humans and an opportunistic pathogen. It can cause a spectrum of infections, including those that are associated with the ability to form biofilm, such as occurs with endocarditis or indwelling medical devices. The genome sequences of two strains revealed the presence of orthologues of the ica genes that are responsible for synthesis of poly-N-acetylglucosamine (PNAG) that is commonly associated with biofilm in other staphylococci. However, we discovered that biofilm formed by a panel of S. lugdunensis isolates growing in iron-restricted medium was susceptible to degradation by proteases and not by metaperiodate, suggesting that the biofilm matrix comprised proteins and not PNAG. When the iron concentration was raised to 1 mM biofilm formation by all strains tested was greatly reduced. A mutant of strain N920143 lacking the entire locus that encodes iron-regulated surface determinant (Isd) proteins was defective in biofilm formation under iron-limited conditions. An IsdC-null mutant was defective, whereas IsdK, IsdJ, and IsdB mutants formed biofilm to the same level as the parental strain. Expression of IsdC was required both for the primary attachment to unconditioned polystyrene and for the accumulation phase of biofilm involving cell-cell interactions. Purified recombinant IsdC protein formed dimers in solution and Lactococcus lactis cells expressing only IsdC adhered to immobilized recombinant IsdC but not to IsdJ, IsdK, or IsdB. This is consistent with a specific homophilic interaction between IsdC molecules on neighboring cells contributing to accumulation of S. lugdunensis biofilm in vivo.
Drought avoidance and vulnerability in the Australian Araucariaceae.

The Araucariaceae is an iconic tree family. Once globally important, the Araucariaceae declined dramatically over the Cenozoic period. Increasing aridity is thought to be responsible for extinction and range contraction of Araucariaceae in Australia, yet little is known about how these trees respond to water stress. We examined the response to water stress of the recently discovered tree Wollemia nobilis Jones, W.G. , Hill, K.D. & Allen, J.M. (Araucariaceae) and two closely related and widespread tree species, Araucaria bidwillii Hook. and Araucaria cunninghamii Mudie, and the island-endemic species, Araucaria heterophylla (Salisb.) Franco. Leaf water potential in all Araucaria spp. remained remarkably unchanged during both dehydration and rehydration, indicating strong isohydry. The xylem tensions at which shoot and stem hydraulic conductances were reduced to 50% (P50shoot and P50stem) were closely correlated in all species. Among the four species, W. nobilis exhibited greater resistance to xylem hydraulic dysfunction during water stress (as indicated by P50shoot and P50stem). Unexpectedly, W. nobilis also experienced the highest levels of crown mortality in response to dehydration, suggesting that this was the most drought-sensitive species in this study. Our results highlight that single traits (e.g., P50) should not be used in isolation to predict drought survival. Further, we found no clear correlation between species' P50 and rainfall across their distributional range. Diversity in drought response among these closely related Araucariaceae species was surprisingly high, considering their reputation as a functionally conservative family.
Immune Responses and Therapeutic Antitumor Effects of an Experimental DNA Vaccine Encoding Human Papillomavirus Type 16 Oncoproteins Genetically Fused to Herpesvirus Glycoprotein D

ABSTRACT Recombinant adenovirus or DNA vaccines encoding herpes simplex virus type 1 (HSV-1) glycoprotein D (gD) genetically fused to human papillomavirus type 16 (HPV-16) oncoproteins (E5, E6, and E7) induce antigen-specific CD8+ T-cell responses and confer preventive resistance to transplantable murine tumor cells (TC-1 cells). In the present report, we characterized some previously uncovered aspects concerning the induction of CD8+ T-cell responses and the therapeutic anticancer effects achieved in C57BL/6 mice immunized with pgD-E7E6E5 previously challenged with TC-1 cells. Concerning the characterization of the immune responses elicited in mice vaccinated with pgD-E7E6E5, we determined the effect of the CD4+ T-cell requirement, longevity, and dose-dependent activation on the E7-specific CD8+ T-cell responses. In addition, we determined the priming/boosting properties of pgD-E7E6E5 when used in combination with a recombinant serotype 68 adenovirus (AdC68) vector encoding the same chimeric antigen. Mice challenged with TC-1 cells and then immunized with three doses of pgD-E7E6E5 elicited CD8+ T-cell responses, measured by intracellular gamma interferon (IFN-γ) and CD107a accumulation, to the three HPV-16 oncoproteins and displayed in vivo antigen-specific cytolytic activity, as demonstrated with carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled target cells pulsed with oligopeptides corresponding to the H-2Db-restricted immunodominant epitopes of the E7, E6, or E5 oncoprotein. Up to 70% of the mice challenged with 5 × 105 TC-1 cells and immunized with pgD-E7E6E5 controlled tumor development even after 3 days of tumor cell challenge. In addition, coadministration of pgD-E7E6E5 with DNA vectors encoding pGM-CSF or interleukin-12 (IL-12) enhanced the therapeutic antitumor effects for all mice challenged with TC-1 cells. In conclusion, the present results expand our previous knowledge on the immune modulation properties of the pgD-E7E6E5 vector and demonstrate, for the first time, the strong antitumor effects of the DNA vaccine, raising promising perspectives regarding the development of immunotherapeutic reagents for the control of HPV-16-associated tumors.
The impact of board ethnic diversity on firm performance: evidence from public listed firms in Malaysia

This paper examines the impact of board ethnic diversity on firm performance (FP) as well as the interacting effects of board independence and board meeting attendance. Unlike prior local research which mainly studied Bumiputera and non-Bumiputera (Malays and non-Malays) directors, this paper views the board from the perspective of diversity. We hand-collected the directors' details and identified them as Malay, Chinese, Indian or other ethnics directors. Using panel data analysis of public listed firms in Malaysia, this paper reveals that diverse ethnic directors in the board increase FP only if more than half of the board consists of independent directors. The finding suggests that when the board is independent, this effectively functioning board allows the diverse ethnic directors to participate in the board activities and make decision that ensure the benefits of all stakeholders, which ultimately increase FP.
Postoperative radiotherapy of glioblastoma multiforme: analysis and critical assessment of different treatment strategies and predictive factors.

BACKGROUND AND PURPOSE Different factors influence glioblastoma patients' prognosis. The aim of this retrospective, explorative analysis was to define the role of recent treatment strategies and to examine the value of different prognostic factors. PATIENTS AND METHODS A total of 110 patients was analyzed. Complete resection, partial resection, and biopsy was accomplished in 69, 22, and 19 patients, respectively. 56 patients received conventionally fractionated radiotherapy with a median total dose of 60 Gy, 2 Gy daily. 54 patients received hyperfractionated accelerated radiotherapy with a median total dose of 54 Gy, 2 x 1.8 Gy daily. 20 patients had concomitant temozolomide (50-75 mg/m2/d), and 20 patients concomitant topotecan (0.5 mg/m2 as continuous venous infusion over 21 days). 37 patients received temozolomide as salvage therapy. RESULTS Median overall (OS) and disease-free survival (DFS) were 8.7 and 4.8 months. After complete resection, partial resection, and biopsy, OS was 9.5, 8.5, and 5.5 months, respectively. OS was 8.5, 13.8, and 8.2 months for radiotherapy alone, concomitant temozolomide, and concomitant topotecan, respectively. Hazard ratio was 0.29 (OS; p = 0.002) and 0.32 (DFS; p = 0.003) for concomitant temozolomide compared to radiotherapy alone. Topotecan led to an increased toxicity. With 9.7 months for conventionally fractionated radiotherapy and 8.1 months for hyperfractionated radiotherapy, OS differed significantly (p = 0.003, log-rank test). OS in patients with RPA (recursive partitioning analysis) score III, IV, V, and VI was 14.1, 10, 9.5, and 5.8 months (p = 0.003, log-rank test). In the univariate (p = 0.0001, log-rank test) and multivariate analysis (p = 0.002, Cox regression), salvage temozolomide led to a statistically significant survival benefit (10.6 vs. 7.7 months). CONCLUSION Concomitant topotecan or the use of hyperfractionated radiotherapy did not show to be superior in outcome in this retrospective analysis. Topotecan led to an increased toxicity. An attempt at complete resection is justified. Temozolomide should be integrated in therapy initially. As salvage therapy, temozolomide is also effective.