Miracle-dz/UniFAR-FTUs huggingface dataset:
Comparison of Microscopic Modalities for the 3D Model Reconstruction of Nanodevices

As manufacturing capabilities push nanotechnology to smaller and smaller scales, novel inspection schemes must be developed to ensure product quality. The objective of our research was to implement, refine, and compare 3D reconstruction algorithms that could aid manufacturers in their ability to visualize and inspect nanodevices. Data was collected from three different microscopes: the atomic force microscope (AFM), the scanning electron microscope (SEM), and the laser scanning confocal microscope (LSCM). For each of these microscopes, a specific algorithm was implemented to generate 3D models from the raw microscope data. Scans from the AFM microscope give range information similar to laser range finders, and the conversion to 3D information was also done in a similar manner. For the SEM inspection, stereo methods were used to build dense elevation maps of the specimen. The LCSM focuses on a very thin section of the specimen so that it can optically slice the specimen into a stack of images along the z-axis. From these stacks, multifocus methods can be used to generate a 3D model. These algorithms were implemented and 3D models generated for micro-electro­ mechanical systems (MEMS), donated by MEMSCAP©, as well as calibration gratings that provide step heights of 18 nm, 100 nm, and 500 nm. Contributions are made in the refinement and comparison of each microscope's results and capabilities, as well as a novel registration method to stitch together 3D models of neighboring regions.
Biological properties of the angiotensin peptides other than angiotensin II: implications for hypertension and cardiovascular diseases

Several peptides of the RAS other than angiotensin (1–8) have been identified. They are generally referred as ‘angiotensin fragments': Ang (2–8), Ang (3–8) and Ang (1–7) and have been detected in human tissues. There is evidence that they may play a functional role in humans by acting in concert with angiotensin (1-8) and aldosterone. Available knowledge on the pathways leading to synthesis and degradation of angiotensin fragments, as well as on their interactions with receptors and on their possible role in cardiovascular homeostasis and disease are reviewed.
Induction of CD8+ T Cells to an HIV-1 Antigen through a Prime Boost Regimen with Heterologous E1-Deleted Adenoviral Vaccine Carriers 1

E1-deleted adenoviral recombinants most commonly based on the human serotype 5 (AdHu5) have been shown thus far to induce unsurpassed transgene product-specific CD8+ T cell responses. A large percentage of the adult human population carries neutralizing Abs due to natural exposures to AdHu5 virus. To circumvent reduction of the efficacy of adenovirus (Ad) vector-based vaccines by neutralizing Abs to the vaccine carrier, we developed E1-deleted adenoviral vaccine carriers based on simian serotypes. One of these carriers, termed AdC68, expressing a codon-optimized truncated form of gag of HIV-1 was shown previously to induce a potent transgene product-specific CD8+ T cell response in mice. We constructed a second chimpanzee adenovirus vaccine vector, termed AdC6, also expressing the truncated gag of HIV-1. This vector, which belongs to a different serotype than the AdC68 virus, induces high frequencies of gag-specific CD8+ T cells in mice including those pre-exposed to AdHu5 virus. Generation of an additional E1-deleted adenoviral vector of chimpanzee origin allows for sequential booster immunizations with heterologous vaccine carriers. In this study, we show that such heterologous prime boost regimens based on E1-deleted adenoviral vectors of different serotypes expressing the same transgene product are highly efficient in increasing the transgene product-specific CD8+ T cell response. They are equivalent to sequential vaccinations with an E1-deleted Ad vector followed by booster immunization with a poxvirus vector and they surpass regimens based on DNA vaccine prime followed by a recombinant adenoviral vector boost.
How to prove security of communication protocols? A discussion on the soundness of formal models w.r.t. computational ones

Security protocols are short programs that aim at securing communication over a public network. Their design is known to be error-prone with flaws found years later. That is why they deserve a careful security analysis, with rigorous proofs. Two main lines of research have been (independently) developed to analyse the security of protocols. On the one hand, formal methods provide with symbolic models and often automatic proofs. On the other hand, cryptographic models propose a tighter modeling but proofs are more difficult to write and to check. An approach developed during the last decade consists in bridging the two approaches, showing that symbolic models are \emph{sound} w.r. t. symbolic ones, yielding strong security guarantees using automatic tools. These results have been developed for several cryptographic primitives (e.g. symmetric and asymmetric encryption, signatures, hash) and security properties. While proving soundness of symbolic models is a very promising approach, several technical details are often not satisfactory. Focusing on symmetric encryption, we describe the difficulties and limitations of the available results.
GeneChip analysis of hippocampal gene expression profiles of short‐ and long‐attack‐latency mice: Technical and biological implications

To gain insight into the molecular mechanisms underlying the behavioral differences between two mouse lines genetically selected for long and short attack latency (LAL and SAL mice, respectively), we have recently applied the large‐scale gene expression profiling method known as serial analysis of gene expression (SAGE) to generate hippocampal gene expression profiles of these mice. The aim of the present study is to extend and validate the SAGE expression profile of hippocampi of LAL and SAL mice using GeneChips (Affymetrix, Santa Clara, CA; one array per mouse, n = 5 per mouse line). As was the case with SAGE, GeneChips detect only medium‐ to high‐abundance genes in the hippocampus. Extensive analysis of GeneChip data using very stringent parameters shows differential expression of 122 genes, all except one of which were expressed at higher levels in LAL mice (P < 0.01). As predicted by SAGE, our data indicate higher expression of several cytoskeleton genes in LAL mice, suggesting longer axonal and dendritic projections in the hippocampus of these mice. This is consistent with our tentative model, in which the behavioral differences between LAL and SAL mice may be related to structural differences in the hippocampus. In addition, a group of 76 genes with diverse biological function and 46 expressed sequence tags (ESTs) were all expressed at higher levels in LAL mice. A novel finding in this study was the significantly lower expression of only a single gene, growth arrest‐specific gene (gas5), in LAL mice. As gas5 does not encode a protein but several small nuclear RNAs, our data suggest that small RNAs may contribute to the molecular mechanisms underlying the extreme behavioral differences between LAL and SAL mice. © 2003 Wiley‐Liss, Inc.
Downlink beamforming avoiding DOA estimation for cellular mobile communications

A new technique to overcome the induced difficulties of FDD (frequency division duplex) for the design of a forward link beamformer in cellular mobile communications systems is presented. It takes advantage of the array topology at the basestation, used to transpose second order statistics of the propagation channel from the uplink frequency to the downlink frequency, thus enabling one to optimize directly any beamforming criterion based on these statistics at the downlink frequency, without feedback nor DOA (direction of arrival) estimation. It can be applied whatever the criterion used to design the beamformer. The effectiveness is verified by the mean of simulation results.
odeling soil parameters using hyperspectral image reflectance in ubtropical coastal wetlands aveen

Developing spectral models of soil properties is an important frontier in remote sensing and soil science. Several studies have focused on modeling soil properties such as total pools of soil organic matter and carbon in bare soils. We extended this effort to model soil parameters in areas densely covered with coastal vegetation. Moreover, we investigated soil properties indicative of soil functions such as nutrient and organic matter turnover and storage. These properties include the partitioning of mineral and organic soil between particulate (>53 m) and fine size classes, and the partitioning of soil carbon and nitrogen pools between stable and labile fractions. Soil samples were obtained from Avicennia germinans mangrove forest and Juncus roemerianus salt marsh plots on the west coast of central Florida. Spectra corresponding to field plot locations from Hyperion hyperspectral image were extracted and analyzed. The spectral information was regressed against the soil variables to determine the best single bands and optimal band combinations for the simple ratio (SR) and normalized difference index (NDI) indices. The regression analysis yielded levels of correlation for soil variables with R2 values ranging from 0.21 to 0.47 for best individual bands, 0.28 to 0.81 for two-band indices, and 0.53 to 0.96 for partial leastsquares (PLS) regressions for the Hyperion image data. Spectral models using Hyperion data adequately (RPD > 1.4) predicted particulate organic matter (POM), silt + clay, labile carbon (C), and labile nitrogen (N) (where RPD = ratio of standard deviation to root mean square error of cross-validation [RMSECV]). The SR (0.53 m, 2.11 m) model of labile N with R2 = 0.81, RMSECV= 0.28, and RPD = 1.94 produced the best results in this study. Our results provide optimism that remote-sensing spectral models can successfully predict soil properties indicative of ecosystem nutrient and organic matter turnover and storage, and do so in areas with dense canopy cover.
Regular expression matching with multi-strings and intervals

Regular expression matching is a key task (and often computational bottleneck) in a variety of software tools and applications. For instance, the standard grep and sed utilities, scripting languages such as perl, internet traffic analysis, XML querying, and protein searching. The basic definition of a regular expression is that we combine characters with union, concatenation, and kleene star operators. The length <i>m</i> is proportional to the number of characters. However, often the initial operation is to concatenate characters in fairly long strings, e.g., if we search for certain combinations of words in a firewall. As a result, the number <i>k</i> of strings in the regular expression is significantly smaller than <i>m</i>. Our main result is a new algorithm that essentially replaces <i>m</i> with <i>k</i> in the complexity bounds for regular expression matching. More precisely, after an <i>O</i>(<i>m</i> log <i>k</i>) time and <i>O</i>(<i>m</i>) space preprocessing of the expression, we can match it in a string presented as a stream of characters in <i>O</i>(<i>k</i> log <i>w</i>/<i>w</i> + log <i>k</i>) time per character, where <i>w</i> is the number <i>w</i> of bits in a memory word. For large <i>w</i>, this corresponds to the previous best bound of <i>O</i>(<i>m</i> log <i>w</i>/<i>w</i> + log<i>m</i>). Prior to this work no <i>O</i>(<i>k</i>) bound per character was known. We further extend our solution to efficiently handle character class interval operators <i>C</i>{<i>x, y</i>}. Here, <i>C</i> is a set of characters and <i>C</i>{<i>x, y</i>}, where <i>x</i> and <i>y</i> are integers such that 0 ≤ <i>x</i> ≤ <i>y</i>, represents a string of length between <i>x</i> and <i>y</i> from <i>C</i>. These character class intervals generalize variable length gaps which are frequently used for pattern matching in computational biology applications.
Restoration of Hydrogen Sulfide Production in Diabetic Mice Improves Reparative Function of Bone Marrow Cells

Background: Bone marrow cell (BMC)–based treatment for critical limb ischemia in diabetic patients yielded a modest therapeutic effect resulting from cell dysfunction. Therefore, approaches that improve diabetic stem/progenitor cell functions may provide therapeutic benefits. Here, we tested the hypothesis that restoration of hydrogen sulfide (H2S) production in diabetic BMCs improves their reparative capacities. Methods: Mouse BMCs were isolated by density-gradient centrifugation. Unilateral hind limb ischemia was conducted in 12- to 14-week-old db/+ and db/db mice by ligation of the left femoral artery. The H2S level was measured by either gas chromatography or staining with florescent dye sulfidefluor 7 AM. Results: Both H2S production and cystathionine &ggr;-lyase (CSE), an H2S enzyme, levels were significantly decreased in BMCs from diabetic db/db mice. Administration of H2S donor diallyl trisulfide (DATS) or overexpression of CSE restored H2S production and enhanced cell survival and migratory capacity in high glucose (HG)–treated BMCs. Immediately after hind limb ischemia surgery, the db/+ and db/db mice were administered DATS orally and/or given a local intramuscular injection of green fluorescent protein–labeled BMCs or red fluorescent protein–CSE–overexpressing BMCs (CSE-BMCs). Mice with hind limb ischemia were divided into 6 groups: db/+, db/db, db/db+BMCs, db/db+DATS, db/db+DATS+BMCs, and db/db+CSE-BMCs. DATS and CSE overexpression greatly enhanced diabetic BMC retention in ischemic hind limbs followed by improved blood perfusion, capillary/arteriole density, skeletal muscle architecture, and cell survival and decreased perivascular CD68+ cell infiltration in the ischemic hind limbs of diabetic mice. It is interesting to note that DATS or CSE overexpression rescued high glucose–impaired migration, tube formation, and survival of BMCs or mature human cardiac microvascular endothelial cells. Moreover, DATS restored nitric oxide production and decreased endothelial nitric oxide synthase phosphorylation at threonine 495 levels in human cardiac microvascular endothelial cells and improved BMC angiogenic activity under high glucose condition. Last, silencing CSE by siRNA significantly increased endothelial nitric oxide synthase phosphorylation at threonine 495 levels in human cardiac microvascular endothelial cells. Conclusions: Decreased CSE-mediated H2S bioavailability is an underlying source of BMC dysfunction in diabetes mellitus. Our data indicate that H2S and overexpression of CSE in diabetic BMCs may rescue their dysfunction and open novel avenues for cell-based therapeutics of critical limb ischemia in diabetic patients.
Evaluation of serum transferrin receptor concentration in diagnosing and differentiating iron deficiency anaemia from anaemia of chronic disorders.

OBJECTIVE To diagnose and differentiate iron deficiency anaemia (IDA) from anaemia of chronic disorders (ACD) using serum concentration of soluble transferrin receptors (sTfR). METHODS One hundred and seventy six adult anaemic patients were diagnosed on bone marrow examination as IDA and ACD in the Department of Haematology, Armed Forces Institute of Pathology, Rawalpindi from November 2001 to May 2003. They were further evaluated with sTfR, serum iron, total iron binding capacity (TIBC) and serum ferritin. These biochemical investigations were compared with results of bone marrow iron status, which served as gold standard. Absence of stainable iron in the bone marrow was diagnostic of iron deficiency, whereas abundance of iron along with decreased siderocytes and sideroblasts was considered diagnostic of ACD. Data was collected on a proforma and analysed using software SPSS (version 11.0) and t-test was used to test the statistical significance. Specificity, sensitivity positive and negative predictive value of the sTfR test was calculated. RESULTS Out of 176 patients studied, 90 (51.1%) were diagnosed as ACD whereas 86 (48.8%) as IDA. The mean +/- SD sTfR levels in IDA patients was 9.68 +/- 2.48 mg/I, whereas mean +/- SD sTfR levels in ACD patients was 2.96 +/- 1.28 mg/I, thus clearly separating the two categories of anaemic patients. Both the sensitivity and specificity of sTfR in IDA was found to be 100%, whereas in ACD, these were 66.6% and 100% respectively. The positive and negative predictive value, in case of IDA was 100%, whereas in ACD it was 100% and 74.1% respectively. The results of serum iron, TIBC and serum ferritin correlated well in IDA, with a fall in serum iron, raised TIBC and decreased serum ferritin, except in few cases in which concomitant inflammatory conditions resulted in falsely high serum ferritin level. Serum iron and TIBC were not useful in cases of ACD. However, the serum ferritin cutoff level of 90 ng/ml was evaluated which virtually excludes IDA, and found this highly effective in cases of IDA alongwith chronic inflammatory conditions. CONCLUSION The results show that in case of simple IDA, sTfR concentration is significantly raised and it has a very high test efficiency in this condition. However in case of ACD the positive predictive value is high (100%) but the negative predictive value is compromised (74.1%). It is therefore a reliable laboratory index of IDA and in distinguishing IDA from ACD).
Genetic Risk Factors of Systemic Lupus Erythematosus in the Malaysian Population: A Minireview

SLE is an autoimmune disease that is not uncommon in Malaysia. In contrast to Malays and Indians, the Chinese seem to be most affected. SLE is characterized by deficiency of body's immune response that leads to production of autoantibodies and failure of immune complex clearance. This minireview attempts to summarize the association of several candidate genes with risk for SLE in the Malaysian population and discuss the genetic heterogeneity that exists locally in Asians and in comparison with SLE in Caucasians. Several groups of researchers have been actively investigating genes that are associated with SLE susceptibility in the Malaysian population by screening possible reported candidate genes across the SLE patients and healthy controls. These candidate genes include MHC genes and genes encoding complement components, TNF, FcγR, T-cell receptors, and interleukins. However, most of the polymorphisms investigated in these genes did not show significant associations with susceptibility to SLE in the Malaysian scenario, except for those occurring in MHC genes and genes coding for TNF-α, IL-1β, IL-1RN, and IL-6.
Brain Superoxide Anion Generation in Asphyxiated Piglets and the Effect of Indomethacin at Therapeutic Dose

ABSTRACT: We have previously shown that generation of superoxide anion occurs in cerebral cortex during asphyxia/reventilation in newborn pigs and that a high dose of indornethacin (5 mg/kg i.v.) abolishes superoxide anion production. The purposes of this study were 1) to determine whether the generation of superoxide anion occurs primarily during asphyxia or whether reventilation must take place, 2) to investigate the effects of indornethacin pretreatment at a therapeutic dose of 0.2 mg/kg i.v. on superoxide anion generation, and 3) to investigate the effects of oxypurinol, an oxygen free radical scavenger, on superoxide anion production during asphyxia/reventilation. Superoxide anion production on cerebral cortex was determined by superoxide dismutase-inhibitable nitroblue tetrazolium (NBT) reduction using closed cranial windows. Superoxideanion generation during asphyxia without reventilation was 4 ± 2 pmol NBT/mm2 per 20 min, which was significantly lower than during asphyxia/reventilation (16 ± 4 pmol NBT/mm2 per 20 min) but comparable to the control group (3 ± 1 pmol NBT/mm2 per 20 min). Indomethacin given at therapeutic dosage before asphyxia/reventilation decreased superoxide anion production to 3 ± 1 pmol NBT/mm2 per 20 min, values not significantly different from the control group and from piglets pretreated with oxypurinol at a dose of 50 mg/kg i.v. (4 ± 2 pmol NBT/mm2 per 20 min). We conclude that in newborn pigs 1) superoxide anions are generated largely during reventilation rather than during asphyxia; 2) the therapeutic dose of indomethacin (0.2 mg/kg) is effective in inhibiting the superoxide anion generation during asphyxia/reventilation; and 3) oxypurinol reduces the superoxide anion accumulation on cerebral cortex during asphyxia/reventilation.
Frontiers in Aging Neuroscience Aging Neuroscience Review Article Temporal Profile of Microglial Activation Nsaids: How They Work and Their Prospects as Therapeutics in Alzheimer's Disease

A potential target of NSAIDs is thought to be the microglia associated with the senile plaques. This is supported by a study by Mackenzie and Munoz (1998) showing in non-demented patients that those treated with NSAIDs had three times less activated microglia as non-treated controls. These data have been confi rmed by in vivo treatment with NSAIDs in mouse models of AD, which have shown decreases in microglial activation and in infl amma-tory mediators such as iNOS, COX and cytokines (Lim et al., 2000; Heneka et al., 2005). Experiments carried out in cultured microglia have revealed that incubation with NSAIDs decreased the secretion of pro-infl ammatory cytokines and may increase Aβ phagocytosis (Lleo et al., 2007). However, the reduction of activated microglia and astroglia by NSAIDs was not signifi cant in AD patients, indicating an age or stage dependent difference in the glial response i.e. in their activation rate (Alafuzoff et al., 2000). Recently, these fi ndings have been backed up by observations indicating that microglia may change from alternative to classical phenotype over time (Colton et al., although probably there is a heterogeneous population. In addition, a paper of Meyer-Luehmann et al. (2008) using two-photon microscopy showed that microglia in the aged mouse brain is less motile and posses fewer processes. Therefore, the response of NSAIDs may differ in " young " vs " old " microglia (Figure 1). It has been hypothesized that early microglial activation in AD delays disease progression by promoting clearance of Aβ before formation of senile plaques. It is conceivable that glial activation is protective through mechanisms such as phagocytosis and clearance of Aβ deposits (through release of insulin degrading enzyme, IDE), forming a protective barrier between Aβ and neurons and Many infl ammatory pathways have been implicated in Alzheimer's disease (AD), yet these pathways are not suffi ciently well delineated to defi ne those processes and targets that may be pathogenic as opposed to those that may be protective. A clearer understanding of these distinctions is critical to the design of therapeutic strategies. The fi nding that treatment with non-steroidal anti-infl ammatory drugs (NSAIDs) is associated with a reduced risk and age of onset of AD reinforces the hypothesis that modulating infl ammation could have therapeutic effi cacy. The benefi cial effects of NSAIDs have also been associated with reductions in Aβ generation, since experiments in vitro and in AD animal models indicate …