Miracle-dz/UniFAR-FTUs huggingface dataset:
MicroRNAs as effectors of brain function.

MicroRNAs (miRNAs) are a recently discovered family of small, genome-encoded endogenous RNAs that are transcribed but are not translated into proteins. Early studies in Ceanorhabditis elegans revealed that an endogenous small RNA (lin-4) regulated translation of lin-14, a protein required for postembryonic development, through an RNA–RNA interaction.1 Small RNAs were then shown to mediate gene-silencing via a mechanism known as RNA interference (RNAi). 2 Fire and Mello2 were awarded the Nobel Prize in Physiology or Medicine in 2006 for the discovery of RNAi. The term miRNA was introduced in a series of back-to-back Science articles in 2001.3–5 MiRNA genes produce primary miRNA transcripts which contain at least one, but possibly more, ≈70 nucleotide hairpin loops. These transcripts are transported into the cytoplasm where they are cleaved by the endonuclease Dicer into an imperfect duplex of 20 to 25 nucleotides. One strand of the duplex is degraded and the other mature miRNA binds to Dicer and forms a complex with argonaute proteins to form RNA-induced silencing complexes.6,7 Studies from several laboratories have revealed that the predominant role of miRNAs in RNA-induced silencing complexes is to regulate post-transcriptional gene expression by translational repression, mRNA cleavage, and mRNA decay initiated by miRNA-guided rapid deadenylation. However, emerging studies support that possible involvement of miRNAs in transcriptional and translational activation. Tremendous progress has been made in unraveling the complexities of miRNAs as meta-controllers of gene expression and their impact on cell development, survival, and function, yet miRNA research is still in its infancy. Given the enormous potential for miRNA studies to translate into novel therapeutic strategies for the diagnosis and treatment of many diseases, the quest to examine all aspects …
Effects of High Intensity Resistance and Low Intensity Endurance Training on Myosin Heavy Chain Isoform Expression in Highly Trained Rowers

An important mechanism of muscle adaptation to exercise is the alteration of myosin heavy chain (MHC) isoform expression. This study investigated the effect of a high intensity resistance training (HIRT) and a low intensity endurance rowing (LIER) on MHC isoform expression in highly trained human muscle. Six well-trained male rowers underwent a training program consisting of a 3-week HIRT and a 3-week LIER, each followed by one-week of recovery. Muscle samples were taken from vastus lateralis before and at the end of each training and recovery phase. MHC isoform was analyzed by SDS-PAGE using silver stain and MHC isoform mRNA by RT-PCR. The maximum oxygen uptake and power output did not change after the training. MHC isoform composition did not change over HIRT or LIER, and there was a decrease in MHC I with concomitant increase in MHC IIa after recovery following HIRT. HIRT led to mRNA upregulation of MHC Ialpha, Ibeta and IIx (127 %, 148 % and 117 %, respectively, p < 0.05), but not MHC I protein (60 % vs 62 %, NS), and LIER led merely to MHC Ibeta mRNA upregulation (131 %, p < 0.05). Thus, different responses of MHC isoform expression to HIRT and LIER occurred in the highly trained muscle, and a "ceiling effect" in terms of MHC I expression could be observed. The upregulation of MHC Ialpha mRNA in human skeletal muscle documented in this study may encourage further observations in this field.
Alveolar brush cells in an infant with desquamative interstitial pneumonitis

A full‐term infant developed bilateral pneumothoraces and respiratory distress shortly after birth, despite initially good Apgar scores. Persistent tachypnea, hypoxemia, and a chest X‐ray remarkable for diffuse alveolar and interstitial infiltrates prompted a lung biopsy at 4 months of age. The biopsy revealed desquamative interstitial pneumonitis with the unique demonstration by electron microscopy of numerous alveolar brush cells. Respiratory brush cells occur normally in the trachea and bronchi of humans and mammals. Although identical cells have been noted in the alveoli of rats, they have never been reported in the alveoli of humans. We present the first electron microscopical demonstration of the alveolar brush cell in humans.
Oxidative stress oppositely modulates protein tyrosine phosphorylation stimulated by muscarinic G protein–coupled and epidermal growth factor receptors

This study's goals were to more fully define the activation of protein tyrosine phosphorylation stimulated by muscarinic receptors, to test if this signaling process is affected by oxidative stress induced by H2O2, and to compare the effects of H2O2 on protein tyrosine phosphorylation activated by epidermal growth factor (EGF) receptors. Experiments used human neuroblastoma SH‐SY5Y cells which express endogenous M3 muscarinic and EGF receptors. Carbachol induced time‐dependent increases in phosphotyrosine immunoreactivity of several protein bands, which were quantitated, and immunoprecipitation was used to identify the adhesion‐related proteins focal adhesion kinase, p130Cas/HEF1, and paxillin, and three shc adapter proteins. Carbachol‐induced tyrosine phosphorylation of the adhesion‐related proteins was mediated by muscarinic receptors, and was inhibited by a src family kinase inhibitor, PP1. That carbachol can activate src family kinases was indicated further by the finding that carbachol induced an increase in tyrosine phosphorylation of p120‐src substrate, which was inhibited by PP1. Oxidative stress induced by H2O2 concentration dependently inhibited carbachol‐induced tyrosine phosphorylation of each of the adhesion‐related proteins. EGF increased the phosphotyrosine immunoreactivity of 180‐ and 116‐kDa proteins, identified as the EGF receptor and Cbl, respectively. In contrast to the results with carbachol, H2O2 potentiated EGF‐induced tyrosine phosphorylation. These results demonstrate that muscarinic receptor activation induces previously unrecognized increases in tyrosine phosphorylation, and that this signaling process is impaired by H2O2, whereas protein tyrosine phosphorylation stimulated by EGF is increased by H2O2. Thus, oxidative stress can oppositely modulate protein tyrosine phosphorylation induced by activation of G protein–coupled and growth factor receptors in the same cells. J. Neurosci. Res. 55:329–340, 1999. © 1999 Wiley‐Liss, Inc.
Nonlinear feedback stabilization of incompressible flows via updated Riccati-based gains

The stabilization or set point control of incompressible laminar flows has been under vivid investigation since long. All linearization based approaches suffer from the conceptual shortcoming of a possibly small domain of attraction. In order to get the system into the regime where, e.g., Riccati-based feedback stabilization works, nonlinear control laws are necessary. Therefore, we propose a scheme that continuously updates an initial feedback, that guarantees decay of solutions under locally checkable conditions, and that can be realized through solving large-scale linear equations.
Semantic Compression and Pattern Extraction with Fascicles

Often many records in a database share similar values for several attributes. If one is able to identify and group these records together that share similar values for some — even if not all — attributes, not only does one have the possibility of a more parsimonious representation of the data, but one may also gain useful insight into the data from an analysis and mining perspective. In this thesis, we introduce the notion of fascicles. A fascicle F(k,t) is a subset of records that have k compact attributes. An attribute A of a collection F of records is compact if the width of the range of A-values (for numeric attributes) or the number of distinct A-values (for categorical attributes) of all the records in F does not exceed t. We introduce and study two problems related to fascicles. First, we consider how to find fascicles such that the total storage of the relation is minimized. Second, we study how best to extract fascicles whose sizes exceed a given minimum threshold and that represent patterns of maximal quality, where quality is measured by the pair (k,t). We develop algorithms to attack both of the above problems. We show that these two problems are very hard to solve optimally. But we demonstrate empirically that good solutions can be obtained using our algorithms.
Role of eicosanoids, inositol phosphates and extracellular Ca2+ in cell-volume regulation of rat liver.

1. In isolated perfused rat liver, the time-course of volume-regulatory K+ efflux following exposure to hypoosmolar perfusate resembled the leukotriene-C4-induced K+ efflux in normotonic perfusion. Omission of Ca2+ from the perfusion fluid had no effect on volume-regulatory K+ efflux, but abolished completely the leukotriene-C4-induced K+ efflux. 2. Volume-regulatory K+ fluxes following hypoosmolar exposure (225 mOsmol l-1) and subsequent reexposure to normotonic media (305 mOsmol l-1) were not significantly affected by the cyclooxygenase inhibitors indomethacin (5 mumol l-1) or ibuprofen (50 mumol l-1), the leukotriene D4/C4-receptor antagonist 1-[2-hydroxy-3-propyl-4-[4-(1H-tetrazol-5-yl)butoxy]phenyl]etha none (YL 171883, 50 microM), the lipoxygenase inhibitor nordihydroguaiaretic acid (20 microM), the phospholipase-A2 inhibitor bromophenacyl bromide (50 microM) or the thromboxane-receptor antagonist 4-[2-(benzenesulfonamido)ethyl]-phenoxyacetic acid (BM 13.177, 20 microM). Also the effects of hypoosmotic cell swelling on lactate, pyruvate and glucose balance across the liver remained largely unaffected in presence of these inhibitors. Neither exposure of perfused rat liver to hypoosmolar (225 mOsmol l-1) nor to hyperosmolar (385 mOsmol l-1) perfusion media affected hepatic prostaglandin-D2 release. 3. When livers were 3H-labeled in vivo by an intraperitoneal injection of myo-[2-3H]inositol about 16 h prior to the perfusion experiment, cell swelling due to lowering the perfusate osmolarity from 305 mOsmol l-1 to 225 mOsmol l-1 led to about a threefold stimulation of [3H]inositol release. The maximum of hypotonicity-induced [3H]inositol release preceded maximal volume-regulatory K+ efflux by about 30 s, but came after the maximum of water shift into the cells. Hypotonicity-induced [3H]inositol release was largely prevented in presence of Li+ (10 mM), but simultaneously inositol monophosphate accumulated inside the liver within 10 min and a small, but significant increase of inositol trisphosphate 1 min after onset of hypoosmolar exposure was detectable. No stimulation of [3H]inositol release was observed during cell shrinkage by switching the perfusate osmolarity from 225 mOsmol l-1 to 305 mOsmol l-1 or from 305 mOsmol l-1 to 385 mOsmol l-1. No stimulation of [3H]inositol release was observed upon swelling of preshrunken livers by lowering the osmolarity from 385 mOsmol l-1 to 305 mOsmol l-1, although the volume-regulatory K+ efflux under these conditions was almost identical to that observed after lowering the osmolarity from 305 mOsmol l-1 to 225 mOsmol l-1. 4. (ABSTRACT TRUNCATED AT 400 WORDS)
[Establishment of rat models with altered anterior guidance and observation of histological changes in temporomandibular joint synovium].

OBJECTIVE This study aims to establish a stable animal model with altered anterior guidance and investigate histological changes on temporomandibular joint (TMJ) synovium in rats. METHODS Thirty-two rats were divided into four groups, namely, control group, anterior-guidance-deficient group (T1), and anterior guidance inclined up to 15 degree (T2) and 30 degree (T3) groups. Metal crowns that add 15 and 30 degrees to the palatal side were cemented to the incisors of maxilla to increase the inclination of anterior guidance. The low-speed diamond wheel shorts for both upper and lower incisors of rats were applied to avoid contact between anterior teeth in all direction, thus establishing an anterior guidance deletion model. TMJ joints on one side of two animals in each group were harvested after 3, 7, 14, and 28 days. Pathological changes were investigated in the TMJ synovium using hematoxylin-eosin (HE) staining. RESULTS The weight of T1 decreased briefly at first, and then increased slightly (P<0.05). The weight of T3 obviously reduced and then slowly increased, but remained below the initial weight (P<0.05). T3 manifested obvious synovial lining proliferation and vascular dilation (P<0.05). CONCLUSIONS The rat model of anterior guidance inclined up to 30 degree could imitate the pathological features of TMJ synovium with excessive increase in anterior guidance. A higher inclination of anterior guidance might cause more damage of TMJ synovium. The effect of anterior guidance deletion on TMJ synovium is yet to be determined.
CCR2 expression correlates with prostate cancer progression

Although the primary role of chemokines and their receptors is controlling the trafficking of leukocytes during inflammatory responses, they also play pleoitropic roles in cancer development. There is emerging evidence that cancer cells produce chemokines that induce tumor cell proliferation or chemotaxis in various cancer types. We have previously reported that MCP‐1 acts as a paracrine and autocrine factor for prostate cancer (PCa) growth and invasion. As the cellular effects of MCP‐1 are mediated by CC chemokine receptor 2 (CCR2), we hypothesized that CCR2 may contribute PCa progression. Accordingly, we first determined CCR2 mRNA and protein expression in various cancer cell lines, including PCa and other cancer types. All cells expressed CCR2 mRNA and protein, but in PCa, more aggressive cancer cells such as C4‐2B, DU145, and PC3 expressed a higher amount of CCR2 compared with the less aggressive cancer cells such as LNCaP or non‐neoplastic PrEC and RWPE‐1 cells. Further, we found a positive correlation between CCR2 expression and PCa progression by analyzing an ONCOMINE gene array database. We confirmed that CCR2 mRNA was highly expressed in PCa metastatic tissues compared with the localized PCa or benign prostate tissues by real‐time RT‐PCR. Finally, CCR2 protein expression was examined by immunohistochemical staining on tissue microarray specimens from 96 PCa patients and 31 benign tissue controls. We found that CCR2 expression correlated with Gleason score and clinical pathologic stages, whereas lower levels of CCR2 were expressed in normal prostate tissues. These results suggest that CCR2 may contribute to PCa development. J. Cell. Biochem. 101: 676–685, 2007. © 2007 Wiley‐Liss, Inc.
Properties of motor units in the transversus abdominis muscle of the garter snake.

1. The organization of motor units in the single‐fibre‐thick transversus abdominis muscle of the garter snake has been studied. This small segmental muscle (60‐100 fibres) contains three distinct fibre types (faster twitch, F; slower twitch, S; and tonic, T) which are predominantly arranged in the repeating pattern F, T, S, T, F, T, etc. 2. Motor‐unit maps were obtained by activating an individual motor axon and identifying all of the muscle fibres innervated by that axon, using either the activity‐induced uptake of extracellular marker molecules to label presynaptic terminals of the stimulated axon, or systematic intracellular recording to identify muscle fibres activated by the axon. 3. Each muscle contained three types of motor units (F, T and S) that corresponded to the three types of fibres. All of the muscle fibres in a motor unit were of the same type. Each segmental muscle contained approximately the same number of motor units: one to two faster twitch, three to four slower twitch, and three tonic. 4. Each motor unit was dispersed widely throughout the muscle. Fibres within a motor unit were neither clustered nor anticlustered. This suggests that despite the fact that axons are constrained to innervate fibres of the appropriate type, the distribution of each motor unit does not generate the alternating pattern of fibre types. 5. In several experiments, all of the twitch motor units in one segmental component of the muscle were mapped. The projection of any one axon appeared random not only with respect to the muscle's fibre type pattern, but also with respect to the innervation supplied by other axons. 6. Twitch motor units were arranged according to a hierarchy of sizes. In each muscle examined, the largest motor unit was faster twitch; a single faster twitch motor axon usually innervated all of the faster twitch fibres in the muscle (fourteen to twenty‐four fibres). This was followed by three to four slower twitch motor units which varied in size from eight to ten fibres to very small motor units containing only four to five fibres. 7. Each tonic motor axon innervated an average of ninety‐three end‐plates per segmental muscle. The relatively large size of tonic motor units compared to twitch motor units is related to the ability of tonic muscle fibres to retain polyneuronal innervation into adulthood, both by providing five to seven end‐plate sites per fibre, and by allowing terminal boutons from different tonic motor axons to co‐innervate the same end‐plate. (ABSTRACT TRUNCATED AT 400 WORDS)
Long-term calcium addition increases growth release, wound closure, and health of sugar maple (Acer saccharum) trees at the Hubbard Brook Experimental Forest

We surveyed and wounded forest-grown sugar maple (Acer saccharum Marsh.) trees in a long-term, replicated Ca manipulation study at the Hubbard Brook Experimental Forest in New Hampshire, USA. Plots received applications of Ca (to boost Ca availability above depleted ambient levels) or Al (to compete with Ca uptake and further reduce Ca availability). We found significantly greater total foliar and membrane-associated Ca in foliage of trees in plots fertilized with Ca when compared with trees from Al-addition and control plots (P = 0.005). Coinciding with foliar Ca differences, trees exhibited a significant difference in crown vigor and in percent branch dieback among treatments (P < 0.05), with a trend towards improved canopy health as Ca levels increased. Annual basal area increment growth for the years following treatment initiation (1998–2004) was significantly greater in trees subjected to Ca addition compared with trees in control and Al treatments. Treatment-related improvements in growth were parti.
Is the input to a GABAergic or cholinergic synapse the sole asymmetry in rabbit's retinal directional selectivity?

Abstract We examined contrast, direction of motion, and concentration dependencies of the effects of GABAergic and cholinergic antagonists, and anticholinesterases on responses to movement of On—Off directionally selective (DS) ganglion cells of the rabbit's retina. The drugs tested were curare and hexamethonium bromide (cholinergic antagonists), physostigmine (anticholinesterase), and picrotoxin (GABAergic antagonist). They all reduced the cells' directional selectivity, while maintaining their preferred-null axis. However, cholinergic antagonists did not block directional selectivity completely even at saturating concentrations. The failure to eliminate directional selectivity was probably not due to an incomplete blockade of cholinergic receptors. In a extension of a Masland and Ames (1976) experiment, saturating concentrations of antagonists blocked the effects of exogenous acetylcholine or nicotine applied during synaptic blockade. Consequently, a noncholinergic pathway may be sufficient to account for at least some directional selectivity. This putative pathway interacts with the cholinergic pathway before spike generation, since physostigmine eliminated directional selectivity at contrasts lower than those saturating responses. This elimination apparently resulted from cholinergic-induced saturation, since reduction of contrast restored directional selectivity. Under picrotoxin, directional selectivity was lost in 33% of the cells regardless of contrast. However, 47% maintained their preferred direction despite saturating concentrations of picrotoxin, and 20% reversed the preferred and null directions. Therefore, models based solely on a GABAergic implementation of Barlow and Levick's asymmetric-inhibition model or solely on a cholinergic implementation of asymmetric-excitation models are not complete models of directional selectivity in the rabbit. We propose an alternate model for this retinal property.
Correction: All ß Cells Contribute Equally to Islet Growth and Maintenance

Correction for: Brennand K, Huangfu D, Melton D (2007) All β cells contribute equally to islet growth and maintenance. PLoS Biol 5(7): e163. doi:10.1371/journal.pbio. 0050163 The labels in Figure 2B indicating the “Pulse” and “No Pulse” FACS conditions for the Rosa26-rtTA;tetO-H2BGFP cells were switched. Labeled properly, the middle left panel should be titled “No Pulse,” and the bottom left panel should be titled “Pulse. ”
Self-Stabilizing Routing Protocol for General Networks

Given an asynchronous network with at most nodes we present a self-stabilizing distributed algorithm for routing (nodes can be added or can crash at any time, so their number can vary up to the upper bound n). It starts in some arbitrary state, with no knowledge of the network architecture and eventually builds in each node a correct routing table regarding the t closest neighbors (t depends on the network needs: it can be n when each node needs to know shortest paths to all other nodes, or less when we need only partial knowledge). The size of the table in any node v is O((t + ∆v) log(n)) bits (∆v is the degree of node v), and a total of O(n t log(n)) bits per network. The stabilization time of the algorithm is O(d+c) time units (d is the maximum diameter of the network, and c is a large constant depending on the local computation time of a node).
A new non competitive unsupervised neural network for clustering

In this paper a new unsupervised neural network, characterized by the absence of competition between its elements, is introduced. The kernel of this network is a new neural unit able to perform clustering even acting alone. It is shown how this network overcomes some of the major drawbacks of classical unsupervised competitive architectures. <<ETX>>
Toxoplasma gondii Asexual Development: Identification of Developmentally Regulated Genes and Distinct Patterns of Gene Expression

ABSTRACT Asexual development in Toxoplasma gondii is a vital aspect of the parasite's life cycle, allowing transmission and avoidance of the host immune response. Differentiation of rapidly dividing tachyzoites into slowly growing, encysted bradyzoites involves significant changes in both physiology and morphology. We generated microarrays of ∼4,400 Toxoplasma cDNAs, representing a minimum of ∼600 genes (based on partial sequencing), and used these microarrays to study changes in transcript levels during tachyzoite-to-bradyzoite differentiation. This approach has allowed us to (i) determine expression profiles of previously described developmentally regulated genes, (ii) identify novel developmentally regulated genes, and (iii) identify distinct classes of genes based on the timing and magnitude of changes in transcript levels. Whereas microarray analysis typically involves comparisons of mRNA levels at different time points, we have developed a method to measure relative transcript abundance between genes at a given time point. This method was used to determine transcript levels in parasites prior to differentiation and to further classify bradyzoite-induced genes, thus allowing a more comprehensive view of changes in gene expression than is provided by standard expression profiles. Newly identified developmentally regulated genes include putative surface proteins (a SAG1-related protein, SRS9, and a mucin-domain containing protein), regulatory and metabolic enzymes (methionine aminopeptidase, oligopeptidase, aminotransferase, and glucose-6-phosphate dehydrogenase homologues), and a subset of genes encoding secretory organelle proteins (MIC1, ROP1, ROP2, ROP4, GRA1, GRA5, and GRA8). This analysis permits the first in-depth look at changes in gene expression during development of this complex protozoan parasite.