gebhart/patrepeval huggingface dataset:
Antibiotic use in animal agriculture (1997)

Journal Article Antibiotic use in animal agriculture Get access R.H. Gustafson, R.H. Gustafson Agricultural Research Division, American Cyanamid Co., Princeton, NJ and Elanco Animal Health, Eli Lilly and Company, Greenfield, IN, USA Dr Richard Gustafson 28 Wood Hollow Road, Lawrenceville, NJ 08648, USA. Search for other works by this author on: Oxford Academic Google Scholar R.E. Bowen R.E. Bowen Agricultural Research Division, American Cyanamid Co., Princeton, NJ and Elanco Animal Health, Eli Lilly and Company, Greenfield, IN, USA Search for other works by this author on: Oxford Academic Google Scholar Journal of Applied Microbiology, Volume 83, Issue 5, 1 November 1997, Pages 531–541, https://doi.org/10.1046/j.1365-2672.1997.00280.x Published: 01 November 1997 Article history Received: 06 January 1997 Revision received: 25 March 1997 Accepted: 27 March 1997 Published: 01 November 1997
Comparative Study In Vivo and In Vitro of Uniformly 14C‐Labelled and 125I‐Labelled Recombinant Fibroblast Growth Factor 2 (1997)

Recombinant bovine fibroblast growth factor (FGF2), uniformly labelled with 14C ([14C]FGF2), was purified and showed to be highly stable and to retain full biological activity. Organ distribution of [14C]FGF2 after intravenous injection of young rats was assessed by autoradiography of whole body sections and compared with those obtained with [125I]iodinated FGF2 (125I-FGF2). Thyroid, stomach, intestine, bladder and skin were radioactively labelled only in the case of 125I-FGF2. This tissue-labelling is artefactual, probably due to free iodide binding not observed when using [14C]FGF2. High-resolution autoradiography showed a complex tissue distribution of [14C]FGF2 in kidney and adrenal organs. Incubation of frozen eye sections with [14C]FGF2 showed a specific and high-resolution labelling pattern of ocular tissues. After cellular internalization, [14C]FGF2 was processed into five distinct polypeptides of 16, 14, 8, 7, and 5.5 kDa. The 14-kDa and 7-kDa polypeptides are novel catabolic fragments not detected with radioiodinated FGF2. In terms of stability, tissue distribution specificity, and autoradiographic resolution, [14C]FGF2 proved to have more advantages than 125I-FGF2 for pharmacokinetic and catabolism studies.
Cerebral monitoring in newborn infants by magnetic resonance and near infrared spectroscopy (1987)

Phosphorus magnetic resonance spectroscopy (MRS) and near infrared spectroscopy (NIRS) have been used to study the brains of normal newborn infants and infants with cerebral disorders admitted to a neonatal intensive care unit. MRS, which involves transporting the infant to the spectrometer, allows measurement of mobile phosphorus compounds such as adenosine triphosphate and phosphocreatine in brain tissue, and has been performed on over 160 babies. NIRS gives cotside information about cerebral oxygenation and haemodynamics and has recently been introduced. These techniques, especially when used together, show promise of providing important information about the mechanisms and prognostic significance of hypoxic-ischaemic damage to the brain--the most important cause of permanent neurodevelopmental disabilities in infants who require intensive care.
Glutamate transporter gene expression in amyotrophic lateral sclerosis motor cortex (1996)

Abstract Glutamate transport is critical for synaptic inactivation of glutamate and prevention of excitotoxicity. The following four glutamate transporters have been identified in human brain: EAAT1, EAAT2, EAAT3, and EAAT4. Deficient glutamate transport has been identified in the motor cortex and the spinal cord of tissue from amyotrophic lateral sclerosis (ALS) patients. The defect appears to be due to a selective loss of the astroglial specific glutamate transporter protein EAAT2. In these studies we sought to extend our understanding of glutamate transporters in ALS by examining the mRNA for each transporter subtype in ALS motor cortex. All tissue was matched for age and postmortem delay. There was no quantitative change in mRNA for EAAT1, EAAT2, or EAAT3 in ALS motor cortex, even in patients with a large loss of EAAT2 protein (95% decrease compared with control) and decreased tissue glutamate transport (73% decrease compared with control). These studies suggest that the dramatic abnormalities in EAAT2 may be due to translational or post‐ translational processes.
Towards Energy Efficient Design of Multi-radio Platforms for Wireless Sensor Networks (2008)

We study the problem of concurrently supporting multiple radios with different capabilities and interfaces on a single sensor node platform. Through a detailed experimental study on hardware multi-radio platforms, using the two representative radio technologies 802.15.4 and 802.11, we identify bottlenecks and design tradeoffs that are usually overlooked and that, as we show, have a significant impact on the sensor network's performance and energy efficiency. Our findings are threefold. We show that a proper pairing of processor and radio is crucial for taking the full advantage of the energy efficiency of higher bandwidth radios. The processor/radio pairing affects the energy balance of a sensor node, thus making the design of dynamic switching among multiple radios more challenging. Second, we demonstrate and quantify the impact of network traffic on energy consumption of a sensor node while varying network parameters, and illustrate the deficiency of existing energy-optimizing protocols. Our results indicate that by properly adjusting network parameters, such as packet size and transmission period, energy savings of up to 50% can be achieved under heavy network traffic conditions when a CSMA-based MAC is used. We conclude by presenting a set of guidelines for designing and implementing energy efficient multi-radio platforms.
The last tree: reclaiming the environment in tropical Asia (1991)

The human habitat the transformation of the land the politics of resource use citizen action.
Temperature-sensitive copy number mutants of CoIE1 are located in an untranslated region of the plasmid genome. (1982)

We have isolated two mutant plasmid derivatives of ColE1 that exhibit temperature-sensitive replication properties. Both mutants have a normal copy number at 30 degrees C but increase their copy number 30- to 40-fold after a shift in temperature to 42 degrees C. A plasmid-encoded enzyme, beta-lactamase (penicillinase, EC 3.5.2.6), undergoes a 30- to 40-fold increase in specific activity concomitant with the increase in plasmid copy number. The copts phenotype of these mutants is not due to the synthesis of a temperature-sensitive polypeptide. Both mutations are located in an untranslated region of the plasmid genome encoding two overlapping transcripts involved in plasmid replication: a small transcript known as RNA I that acts as a negative control element in replication and a large transcript that has been characterized as the replication primer in vitro. The mutations alter the sequence encoding the primer but lie immediately 5' to the initiating nucleotide of RNA I, in the RNA I promoter region. The possibility that the temperature-dependent plasmid DNA amplification is a consequence of a temperature-sensitive RNA I promoter was tested by inserting the RNA I promoters from the wild-type and mutant plasmids into a plasmid in which galactokinase expression is dependent upon an exogenous promoter. These experiments demonstrate that the mutant promoters are not temperature-sensitive. Rather, the mutations may affect the secondary structure of the replication primer in a region important for RNA I interaction.
Per-packet load-balanced, low-latency routing for clos-based data center networks (2013)

Clos-based networks including Fat-tree and VL2 are being built in data centers, but existing per-flow based routing causes low network utilization and long latency tail. In this paper, by studying the structural properties of Fat-tree and VL2, we propose a per-packet round-robin based routing algorithm called Digit-Reversal Bouncing (DRB). DRB achieves perfect packet interleaving. Our analysis and simulations show that, compared with random-based load-balancing algorithms, DRB results in smaller and bounded queues even when traffic load approaches 100%, and it uses smaller re-sequencing buffer for absorbing out-of-order packet arrivals. Our implementation demonstrates that our design can be readily implemented with commodity switches. Experiments on our testbed, a Fat-tree with 54 servers, confirm our analysis and simulations, and further show that our design handles network failures in 1-2 seconds and has the desirable graceful performance degradation property.
Crystal Structure of the Catalytic Domain of Matrix Metalloproteinase-1 in Complex with the Inhibitory Domain of Tissue Inhibitor of Metalloproteinase-1 (2006)

The mammalian collagenases are a subgroup of the matrix metalloproteinases (MMPs) that are uniquely able to cleave triple helical fibrillar collagens. Collagen breakdown is an essential part of extracellular matrix turnover in key physiological processes including morphogenesis and wound healing; however, unregulated collagenolysis is linked to important diseases such as arthritis and cancer. The tissue inhibitors of metalloproteinases (TIMPs) function in controlling the activity of MMPs, including collagenases. We report here the structure of a complex of the catalytic domain of fibroblast collagenase (MMP-1) with the N-terminal inhibitory domain of human TIMP-1 (N-TIMP-1) at 2.54 A resolution. Comparison with the previously reported structure of the TIMP-1/stromelysin-1 (MMP-3) complex shows that the mechanisms of inhibition of both MMPs are generally similar, yet there are significant differences in the protein-protein interfaces in the two complexes. Specifically, the loop between beta-strands A and B of TIMP-1 makes contact with MMP-3 but not with MMP-1, and there are marked differences in the roles of individual residues in the C-D connector of TIMP-1 in binding to the two MMPs. Structural rearrangements in the bound MMPs are also strikingly different. This is the first crystallographic structure that contains the truncated N-terminal domain of a TIMP, which shows only minor differences from the corresponding region of the full-length protein. Differences in the interactions in the two TIMP-1 complexes provide a structural explanation for the results of previous mutational studies and a basis for designing new N-TIMP-1 variants with restricted specificity.
Effect of ultrasound parameters for unilamellar liposome preparation (2009)

In this study, it was investigated the effects of ultrasound, namely power input, distance from ultrasound tip to base of reactor and treatment time, in the formation of liposomes. Results indicate a dependence on cavitation events that are a function of power input, and consequently dependent on the position of the probe within the reaction vessel and the wave behaviour. Short treatment times are required to achieve nanosized vesicles in anti-nodal (lambda/4; 19mm) reactor geometries. In this wave point the cavitation phenomenon is more pronounced when compared with the nodal point (lambda/2; 38mm). Therefore, the consideration of the above parameters is vital if dependable and repeatable results are to be achieved.
Effect of Cultured Autologous Chondrocytes on Repair of Chondral Defects in a Canine Model* (1997)

Articular cartilage has a limited capacity for repair. In recent clinical and animal experiments, investigators have attempted to elicit the repair of defects of articular cartilage by injecting cultured autologous chondrocytes under a periosteal flap (a layer of periosteum). The objective of the present study was to determine the effect of cultured autologous chondrocytes on healing in an adult canine model with use of histomorphometric methods to assess the degree of repair. A total of forty-four four-millimeter-diameter circular defects were created down to the zone of calcified cartilage in the articular cartilage of the trochlear groove of the distal part of the femur in fourteen dogs. The morphology and characteristics of the original defects were defined in an additional six freshly created defects in three other dogs. Some residual noncalcified articular cartilage, occupying approximately 2 per cent of the total cross-sectional area of the defect, was sometimes left in the defect. The procedure sometimes damaged the calcified cartilage, resulting in occasional microfractures or larger fractures, thinning of the zone of calcified cartilage, or, rarely, small localized penetrations into subchondral bone. The forty-four defects were divided into three treatment groups. In one group, cultured autologous chondrocytes were implanted under a periosteal flap. In the second group, the defect was covered with a periosteal flap but no autologous chondrocytes were implanted. In the third group (the control group), the defects were left empty. The defects were analyzed after twelve or eighteen months of healing. Histomorphometric measurements were made of the percentage of the total area of the defect that became filled with repair tissue, the types of tissue that filled the defect, and the integration of the repair tissue with the adjacent cartilage at the sides of the defects and with the calcified cartilage at the base of the defect. In histological sections made through the center of the defects in the three groups, the area of the defect that filled with new repair tissue ranged from a mean total value of 36 to 76 per cent, with 10 to 23 per cent of the total area consisting of hyaline cartilage. Integration of the repair tissue with the adjacent cartilage at the edges of the defect ranged from 16 to 32 per cent in the three groups. Bonding between the repair tissue and the calcified cartilage at the base of the defect ranged from 41 to 89 per cent. With the numbers available, we could detect no significant difference among the three groups with regard to any of the parameters used to assess the quality of the repair. In the two groups in which a periosteal flap was sutured to the articular cartilage surrounding the defect, the articular cartilage showed degenerative changes that appeared to be related to that suturing.
Fatty acid chlorohydrins and bromohydrins are cytotoxic to human endothelial cells (2001)

Reaction of unsaturated lipids with the hypohalous acids (hypochlorous acid and hypobromous acid) results in the addition of the halide (X) across double bonds to form halohydrins (-CH2CH(OH)CH(X)CH2-). These modified lipids could be potentially destabilising to cell membranes due to their increased polarity. We have investigated the effect of pre-formed halohydrins on human umbilical vein endothelial cells (HUVEC) by incubating cultured cells with oleic acid micelles containing chlorohydrins or bromohydrins. Cell detachment and necrotic death were observed with increasing doses of halohydrins, whereas the cells were unaffected by equivalent doses of oleic acid. Bromohydrins caused more lysis than did chlorohydrins at equivalent doses. Complete lysis was seen with 200 microM fatty acid/chlorohydrin micelles and with 50 microM fatty acid/bromohydrin micelles. Chlorohydrin uptake was much less than the oleic acid control whereas bromohydrins were incorporated into the endothelial cells similarly to oleic acid. This difference or the bulkier nature of the bromohydrins could account for their increased toxicity. This study has demonstrated the potential toxicity of the halohydrins, and implications for their formation in inflammation are discussed.
Notch ligand Delta-like 4 blockade attenuates atherosclerosis and metabolic disorders (2012)

Atherosclerosis and insulin resistance are major components of the cardiometabolic syndrome, a global health threat associated with a systemic inflammatory state. Notch signaling regulates tissue development and participates in innate and adaptive immunity in adults. The role of Notch signaling in cardiometabolic inflammation, however, remains obscure. We noted that a high-fat, high-cholesterol diet increased expression of the Notch ligand Delta-like 4 (Dll4) in atheromata and fat tissue in LDL-receptor–deficient mice. Blockade of Dll4-Notch signaling using neutralizing anti-Dll4 antibody attenuated the development of atherosclerosis, diminished plaque calcification, improved insulin resistance, and decreased fat accumulation. These changes were accompanied by decreased macrophage accumulation, diminished expression of monocyte chemoattractant protein-1 (MCP-1), and lower levels of nuclear factor-κB (NF-κB) activation. In vitro cell culture experiments revealed that Dll4-mediated Notch signaling increases MCP-1 expression via NF-κB, providing a possible mechanism for in vivo effects. Furthermore, Dll4 skewed macrophages toward a proinflammatory phenotype (“M1”). These results suggest that Dll4-Notch signaling plays a central role in the shared mechanism for the pathogenesis of cardiometabolic disorders.
p19Arf Represses Platelet-Derived Growth Factor Receptor β by Transcriptional and Posttranscriptional Mechanisms (2012)

In addition to cancer surveillance, p19(Arf) plays an essential role in blocking signals stemming from platelet-derived growth factor receptor β (Pdgfrβ) during eye development, but the underlying mechanisms have not been clear. We now show that without Arf, pericyte hyperplasia in the eye results from enhanced Pdgfrβ-dependent proliferation from embryonic day 13.5 (E13.5) of mouse development. Loss of Arf in the eye increases Pdgfrβ expression. In cultured fibroblasts and pericyte-like cells, ectopic p19(Arf) represses and Arf knockdown enhances the expression of Pdgfrβ mRNA and protein. Ectopic Arf also represses primary Pdgfrβ transcripts and a plasmid driven by a minimal promoter, including one missing the CCAAT element required for high-level expression. p19(Arf) uses both p53-dependent and -independent mechanisms to control Pdgfrβ. In vivo, without p53, Pdgfrβ mRNA is elevated and eye development abnormalities resemble the Arf (-/-) phenotype. However, effects of p53 on Pdgfrβ mRNA do not appear to be due to direct p53 or RNA polymerase II recruitment to the promoter. Although p19(Arf) controls Pdgfrβ mRNA in a p53-dependent manner, it also blunts Pdgfrβ protein expression by blocking new protein synthesis in the absence of p53. Thus, our findings demonstrate a novel capacity for p19(Arf) to control Pdgfrβ expression by p53-dependent and -independent mechanisms involving RNA transcription and protein synthesis, respectively, to promote the vascular remodeling needed for normal vision.
The Neurobiology of Stress and Development (2006)

Stress is a part of every life to varying degrees, but individuals differ in their stress vulnerability. Stress is usefully viewed from a biological perspective; accordingly, it involves activation of neurobiological systems that preserve viability through change or allostasis. Although they are necessary for survival, frequent neurobiological stress responses increase the risk of physical and mental health problems, perhaps particularly when experienced during periods of rapid brain development. Recently, advances in noninvasive measurement techniques have resulted in a burgeoning of human developmental stress research. Here we review the anatomy and physiology of stress responding, discuss the relevant animal literature, and briefly outline what is currently known about the psychobiology of stress in human development, the critical role of social regulation of stress neurobiology, and the importance of individual differences as a lens through which to approach questions about stress experiences during development and child outcomes.
Use of botulinum toxin in pediatric spasticity (cerebral palsy) (2004)

Local injection of botulinum toxin (BT) is a well-established treatment option for spastic movement disorders in children. BT blocks the release of acetylcholine from the axon terminal into the synaptic cleft of the motor endplate resulting in paresis of the injected musculature. Such localised, temporary chemodenervation of affected muscles can lead to functional gains and may improve the child's daily routine and rehabilitative care. We summarise state-of-the-art treatment of spasticity in children with BT type A, addressing critical issues and introducing recent advances, such as sonography-guided injection of BT and the distal injection of the psoas muscle without the need for general anaesthesia. First-hand experience with BT type B in children is presented.
Transforming growth factor beta is essential for spindle cell conversion of mouse skin carcinoma in vivo: implications for tumor invasion. (1998)

Transforming growth factor beta1 (TGF-beta1) regulates both cell growth and cellular plasticity and is therefore important in the molecular control of both the developmental and neoplastic processes. It has been suggested that TGF-beta1 may be a positive or negative regulator of tumorigenesis. Stimulation of tumorigenesis could be due to its action as an immunosuppressor or as an inducer of angiogenesis, or by its direct action on the cell in promoting cellular plasticity. In the current study, we provide evidence that TGF-beta1 can act directly on keratinocytes in vivo to induce the reversible epithelial-mesenchymal conversion of a malignant metastatic keratinocyte cell line. Two squamous clones from the cell line were shown to undergo a reversible conversion to a fibroblastoid phenotype after culture in 1 ng/ml TGF-beta1. The morphological conversion became apparent at 24 h post-TGF-beta treatment and was complete after another 24 h. The conversion was characterized by a rapid delocalization of E-cadherin within 6-12 h posttreatment, followed by down-regulation of E-cadherin levels by 72 h. These squamous clones spontaneously converted to a fibroblastoid phenotype after s.c. injection in nude mice. Importantly, four of four clones that had been stably transfected with a dominant negative TGF-beta type II receptor were unable to undergo this mesenchymal switch in vivo, despite the fact that all clones stably transfected with neomyocin resistance alone retained their spindle characteristics in vivo. This demonstrates that the epithelial-mesenchymal conversion event is mediated directly via the TGF-beta signaling pathway of the tumor cell per se, and that it is sufficient to significantly enhance tumorigenicity and the malignant and invasive characteristics of the tumor in vivo.