gebhart/patrepeval huggingface dataset:
Design of a Robotic Gait Trainer using Spring Over Muscle Actuators for Ankle Stroke Rehabilitation (2005)

Repetitive task training is an effective form of rehabilitation for people suffering from debilitating injuries of stroke. We present the design and working concept of a robotic gait trainer (RGT), an ankle rehabilitation device for assisting stroke patients during gait. Structurally based on a tripod mechanism, the device is a parallel robot that incorporates two pneumatically powered, double-acting, compliant, spring over muscle actuators as actuation links which move the ankle in dorsiflex ion/plantarflexion and inversion/eversion. A unique feature in the tripod design is that the human anatomy is part of the robot, the first fixed link being the patient's leg. The kinematics and workspace of the tripod device have been analyzed determining its range of motion. Experimental gait data from an able-bodied person wearing the working RGT prototype are presented.
A single amino acid converts a repressor to an activator of flowering (2005)

Homologous proteins occurring through gene duplication may give rise to novel functions through mutations affecting protein sequence or expression. Comparison of such homologues allows insight into how morphological traits evolve. However, it is often unclear which changes are key to determining new functions. To address these ideas, we have studied a system where two homologues have evolved clear and opposite functions in controlling a major developmental switch. In plants, flowering is a major developmental transition that is critical to reproductive success. Arabidopsis phosphatidylethanolamine-binding protein homologues TERMINAL FLOWER 1 (TFL1) and FLOWERING LOCUS T (FT) are key controllers of flowering, determining when and where flowers are made, but as opposing functions: TFL1 is a repressor, FT is an activator. We have uncovered a striking molecular basis for how these homologous proteins have diverged. Although <60% identical, we have shown that swapping a single amino acid is sufficient to convert TFL1 to FT function and vice versa. Therefore, these key residues may have strongly contributed to the selection of these important functions over plant evolution. Further, our results suggest that TFL1 and FT are highly conserved in biochemical function and that they act as repressors or activators of flowering through discrimination of structurally related interactors by a single residue.
New Insights into Structure–Property Relationships in Thermosetting Polymers from Studies of Cocured Polycyanurate Networks (2011)

Studies of the physical properties of the cocured networks formed from three similar dicyanate ester monomers revealed a number of unexpected variations from simple linear mixing rules. These variations shed light on important synergistic effects in cocured thermosetting networks and their possible causes. The monomers utilized were the dicyanate esters of Bisphenol A (BADCy) and Bisphenol E (LECy) and the silicon-containing analogue of Bisphenol A (SiMCy). The most important of the synergistic effects was a decrease of ∼25% in moisture uptake seen only in conetworks of LECy and SiMCy. For all other systems, a clear relationship between moisture uptake and the number density of cyanurate rings was observed. This relationship generally applies to many types of cyanate esters and gives an indication of the importance of specific sites (as opposed to free volume alone) in moisture uptake. Numerous additional examples of nonlinear mixing relations were observed in the glass transition temperature, density, and thermochemical stability of fully cured networks. Interestingly, the most widespread deviations from linear behavior were observed for conetworks of SiMCy and LECy, suggesting that factors such as the mismatch in network segment size may be more important than differences in flexibility or symmetry in driving significant physical interactions among conetwork components.
Inhibition of L-Glycerol 3-Phosphate Acyltransferase from Escherichia coil by cis-9, l0-Methylenehexadecanoic Acid (1972)

Acyl-CoA: L-glycerol 3-phosphate acyltransferase [EC 2.3.1.15] from E. coli is a particulate enzyme, which was found to be inhibited by cis-9, 10-methylenehexadecanoate. The inhibition was noncompetitive with respect to L-glycerol 3-phosphate. Palmitate, elaidate, and trans-vaccenate showed no inhibition of the acyltransferase, whereas palmitoleate, oleate, and cis-vaccenate inhibited. cis-9, l0-Methylenehexadecanoate was approximately twice as inhibitory as mono-olefinic acids. The free fatty acids in the cells were also found to vary with different growth phases. There was a ten-fold increase in the amount of free cis-9, l0-methylenehexadecanoic acid in the cells from the early exponential to the stationary phase.
A portable digital DLL architecture for CMOS interface circuits (2002)

A digital DLL was developed which achieves infinite phase range and 40 ps worst-case phase resolution at 400 MHz. The architecture uses dual delay lines with an end-of-cycle detector, phase blenders, and duty cycle correctors. This more easily process-portable DLL achieves jitter performance comparable to a more complex analog DLL, when placed into identical high-speed interface circuits fabricated on the same die in a 0.4 /spl mu/m CMOS process.
Effect of probiotics on pro-inflammatory cytokines and NF-κB activation in ulcerative colitis (2010)

Oral supplementation with probiotics could be helpful in maintaining remission and preventing relapse of UC.
A study of rituximab and ifosfamide, carboplatin, and etoposide chemotherapy in children with recurrent/refractory B‐cell (CD20+) non‐Hodgkin lymphoma and mature B‐cell acute lymphoblastic leukemia: A report from the Children's Oncology Group (2008)

The combination of rituximab and ICE chemotherapy was associated with an encouraging objective response (OR) rate and an acceptable toxicity profile.
Enteral nutrition with eicosapentaenoic acid, γ-linolenic acid and antioxidants in the early treatment of sepsis: results from a multicenter, prospective, randomized, double-blinded, controlled study: the INTERSEPT Study (2011)

ClinicalTrials.gov: NCT00981877.
Human endoplasmic reticulum oxidoreductin 1‐α is a novel predictor for poor prognosis of breast cancer (2013)

Human endoplasmic reticulum oxidoreductin 1-α (hERO1-α) is an oxidizing enzyme that exists in the endoplasmic reticulum and its expression is augmented under hypoxia. It regulates a redox state of various kinds of protein through reoxidation of "client" protein disulfide isomerase. Interestingly, although the expression of hERO1-α in normal tissues was comparatively limited, various types of cancer cells expressed it in large amounts. Therefore, we examined the role of ERO1-α in tumor growth using murine breast cancer line 4T1 and found that knockdown of murine ERO1-α inhibited in vivo tumor growth and decreased lung metastasis compared with wild-type 4T1. Moreover, we investigated the relationship between expression of hERO1-α and prognosis in breast cancer patients. Seventy-one patients with breast cancer who underwent surgery between 2005 and 2006 in Sapporo Medical University Hospital (Sapporo, Japan) were analyzed in this study. Significant differences were found between the hERO1-α-positive group (n = 33) and hERO1-α-negative group (n = 38) in nuclear grade (P < 0.001) and intrinsic subtype (P = 0.021) in univariate analysis. More importantly, in multivariate analysis of disease-free survival by Cox regression, expression of hERO1-α was the only independent prognosis factor (P = 0.035). Finally, in univariate survival analysis, patients positive for hERO1-α had significantly shorter disease-free survival and overall survival than those patients negative for hERO1-α. These findings indicate that the expression of hERO1-α in cancer cells is associated with poorer prognosis and thus can be a prognostic factor for patients with breast cancer.
Multiple NSAID-Induced Hits Injure the Small Intestine: Underlying Mechanisms and Novel Strategies (2012)

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) injury including jejunal/ileal mucosal ulceration, bleeding, and even perforation in susceptible patients. The underlying mechanisms are largely unknown, but they are distinct from those related to gastric injury. Based on recent insights from experimental models, including genetics and pharmacology in rodents typically exposed to diclofenac, indomethacin, or naproxen, we propose a multiple-hit pathogenesis of NSAID enteropathy. The multiple hits start with an initial pharmacokinetic determinant caused by vectorial hepatobiliary excretion and delivery of glucuronidated NSAID or oxidative metabolite conjugates to the distal small intestinal lumen, where bacterial β-glucuronidase produces critical aglycones. The released aglycones are then taken up by enterocytes and further metabolized by intestinal cytochrome P450s to potentially reactive intermediates. The "first hit" is caused by the NSAID and/or oxidative metabolites that induce severe endoplasmic reticulum stress or mitochondrial stress and lead to cell death. The "second hit" is created by the significant subsequent inflammatory response that would follow such a first-hit injury. Based on these putative mechanisms, strategies have been developed to protect the enterocytes from being exposed to the parent NSAID and/or oxidative metabolites. Among these, a novel strategy already demonstrated in a murine model is the selective disruption of bacteria-specific β-glucuronidases with a novel small molecule inhibitor that does not harm the bacteria and that alleviates NSAID-induced enteropathy. Such mechanism-based strategies require further investigation but provide potential avenues for the alleviation of the GI toxicity caused by multiple NSAID hits.
Molecular Recognition and Colorimetric Detection of Cholera Toxin by Poly(diacetylene) Liposomes Incorporating Gm1 Ganglioside (1997)

Molecular recognition sites on cell membranes serve as the main communication channels between the inside of a cell and its surroundings. Upon receptor binding, celular messages such as ion channel opening or activation of enzymes are triggered. In this report, we demonstrate that artificial cell membranes made from conjugated lipid polymers (poly(diacetylene)) can, on a simple level, mimic membrane processes of molecular recognition and signal transduction. The ganglioside GM1 was incorporated into poly(diacetylene) liposomes. Molecular recognition of cholera toxin at the interface of the liposome resulted in a change of the membrane color due to conformational changes in the conjugated (ene−yne) polymer backbone. The "colored liposomes" might be used as simple colorimetric sensors for drug screening or as new tools to study membrane−membrane or membrane−receptor interactions.
25-Hydroxycholesterol 3-Sulfate Recovers Acetaminophen Induced Acute Liver Injury via Stabilizing Mitochondria in Mouse Models (2021)

Acetaminophen (APAP) overdose is one of the most frequent causes of acute liver failure (ALF). N-acetylcysteine (NAC) is currently being used as part of the standard care in the clinic but its usage has been limited in severe cases, in which liver transplantation becomes the only treatment option. Therefore, there still is a need for a specific and effective therapy for APAP induced ALF. In the current study, we have demonstrated that treatment with 25-Hydroxycholesterol 3-Sulfate (25HC3S) not only significantly reduced mortality but also decreased the plasma levels of liver injury markers, including LDH, AST, and ALT, in APAP overdosed mouse models. 25HC3S also decreased the expression of those genes involved in cell apoptosis, stabilized mitochondrial polarization, and significantly decreased the levels of oxidants, malondialdehyde (MDA), and reactive oxygen species (ROS). Whole genome bisulfite sequencing analysis showed that 25HC3S increased demethylation of <sup>5m</sup>CpG in key promoter regions and thereby increased the expression of those genes involved in MAPK-ERK and PI3K-Akt signaling pathways. We concluded that 25HC3S may alleviate APAP induced liver injury via up-regulating the master signaling pathways and maintaining mitochondrial membrane polarization. The results suggest that 25HC3S treatment facilitates the recovery and significantly decreases the mortality of APAP induced acute liver injury and has a synergistic effect with NAC in propylene glycol (PG) for the injury.
A systematic examination of surface coatings on the optical and chemical properties of semiconductor quantum dots (2006)

A number of procedures are currently available to encapsulate and solubilize hydrophobic semiconductor Quantum Dots (QDs) for biological applications. Most of these procedures are based on the use of small-molecule coordinating ligands, amphiphilic polymers, or amphiphilic lipids. However, it is still not clear how these different surface coating molecules affect the optical, colloidal, and chemical properties of the solubilized QDs. Here we report a systematic study to examine the effects of surface coating chemistry on the hydrodynamic size, fluorescence quantum yield, photostability, chemical stability, and biocompatibility of water-soluble QDs. The results indicate that quantum dots with the smallest hydrodynamic sizes are best prepared by direct ligand exchange with hydrophilic molecules, but the resulting particles are less stable than those encapsulated in amphiphilic polymers. For stability against chemical oxidation, QDs should be protected with a hydrophobic bilayer. For high stability under acidic conditions, the best QDs are prepared by using hyperbranched polyethylenimine. For stability in high salt buffers, it is preferable to have uncharged, sterically-stabilized QDs, like those coated with polyethylene glycol (PEG). These insights are expected to benefit the development of quantum dots and related nanoparticle probes for molecular and cellular imaging applications.
Genetic Engineering of Targeted Retroviral Vectors (2002)

At the turn of the century, gene therapy remains poised at the threshold of modernizing medicine. While holding great promise for the treatment of numerous diseases, the field of gene therapy has been disappointingly slow in the development of safe and efficient gene delivery systems (Anderson, 1998). In recent years, we developed a targeting strategy that now enables gene therapy vectors to target “areas of pathology” within the body. Taking advantage of the physiologic surveillance function present in a discrete collagen-binding domain of coagulation von Willebrand factor (vWF), we incorporated these coding sequences into the primary structure of the murine leukemia virus (MuLV) 4070A amphotropic envelope protein. The resultant matrix-targeted vector exhibited a lesion-seeking feature, i.e., the ability to accumulate at sites of exposed collagen within the lesions that are created by growing tumors or vascular neointima. In this chapter, we will discuss the evolution of various retroviral vector targeting strategies in our laboratories, with particular emphasis on the clinical potential of this lesion-seeking injectable vector system in the treatment of metastatic cancer, balloon angioplasty/stent injury-induced vascular restenosis and post-Excimer laser corneal haze.
Porcine Circovirus Type 2 Infection Decreases the Efficacy of a Modified Live Porcine Reproductive and Respiratory Syndrome Virus Vaccine (2006)

Porcine reproductive and respiratory syndrome virus (PRRSV)-induced pneumonia is a major problem, and vaccination is used to reduce losses associated with PRRSV. Porcine circovirus type 2 (PCV2) causes lymphoid depletion, and there is concern that this adversely affects the immune response. The objective of this study was to investigate the effect of PCV2 infection on the efficacy of modified live virus (MLV) PRRSV vaccine. Sixty-nine 2-week-old pigs were randomly assigned to one of seven groups of 9 to 10 pigs each. At 6 weeks of age, pigs in groups 4, 5, and 6 were inoculated intranasally with PCV2 ISU-40895. At 8 weeks of age, groups 3, 4, 6, and 7 were vaccinated with a PRRSV MLV vaccine. At 12 weeks of age, groups 2, 3, and 4 were challenged with PRRSV SDSU73. All pigs were necropsied 14 days after PRRSV challenge. PCV2-infected, PRRSV-vaccinated, and PRRSV-challenged pigs had significantly (P < 0.05) more-severe macroscopic lung lesions than did the PRRSV-vaccinated and PRRSV-challenged pigs that were not exposed to PCV2 prior to PRRSV vaccination. Nonvaccinated PRRSV-infected pigs had a significantly (P < 0.001) higher incidence of PRRSV antigen in lungs than did all other groups except the group infected with PCV2 prior to PRRSV vaccination and challenge. The nonvaccinated PRRSV-challenged group and the group challenged with PCV2 prior to PRRSV vaccination and challenge had significantly (P < 0.001) lower average daily weight gain than did the control and the vaccinated groups. This work suggests that PCV2 infection has an adverse effect on the development of protective immunity induced by PRRSV vaccine.
Adenoviruses: update on structure and function (2008)

Adenoviruses have been studied intensively for over 50 years as models of virus-cell interactions and latterly as gene vectors. With the advent of more sophisticated structural analysis techniques the disposition of most of the 13 structural proteins have been defined to a reasonable level. This review seeks to describe the functional properties of these proteins and shows that they all have a part to play in deciding the outcome of an infection and act at every level of the virus's path through the host cell. They are primarily involved in the induction of the different arms of the immune system and a better understanding of their overall properties should lead to more effective ways of combating virus infections.
Alefacept treatment in psoriatic arthritis: Reduction of the effector T cell population in peripheral blood and synovial tissue is associated with improvement of clinical signs of arthritis (2002)

The changes in ST, together with the improvement in clinical joint scores, after treatment with alefacept support the hypothesis that T cell activation plays an important role in this chronic inflammatory disease. Furthermore, since alefacept, a T cell-specific agent, led to decreased macrophage infiltration, the data indicate that T cells are highly involved in synovial inflammation in PsA.
A video codec LSI for high-definition TV systems with one-transistor DRAM line memories (1989)

A video codec LSI for high-definition television (HDTV) systems has been developed. By using a time-compressed integration encoding technique, it converts a 20.0-MHz bandwidth luminance signal and two 5.0-MHz chrominance signals into a compressed image signal at 48.6-MHz sampling frequency. It is useful in many HDTV application systems, such as 400-Mb/s digital transmission system, a video disk player system, or an analog transmission system. Over 288000 elements, including a 52-kb one-transistor DRAM (dynamic random access memory) line memory specially developed for this LSI, were integrated on a 12.16*12.10-mm/sup 2/ chip. A standard cell layout method and a 1.2- mu m CMOS logic LSI process were used.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
A monomeric histidine kinase derived from EnvZ, an Escherichia coli osmosensor (2000)

Histidine kinases function as dimers. The kinase domain of the osmosensing histidine kinase EnvZ of Escherichia coli consists of two domains: domain A (67 residues) responsible for histidine phosphotransfer and dimerization, and domain B (161 residues) responsible for the catalytic and ATP-binding function. The individual structures of these two domains have been recently solved by NMR spectroscopy. Here, we demonstrate that an enzymatically functional monomeric histidine kinase can be constructed by fusing in tandem two domains A and one domain B to produce a single polypeptide (A-A-B). We show that this protein, EnvZc[AAB], is soluble and exists as a stable monomer. The autophosphorylation and OmpR kinase activities of the monomeric EnvZc[AAB] are similar to that of the wild-type EnvZ, while OmpR-binding and phosphatase functions are reduced. V8 protease digestion and mutational analyses indicate that His-243 of only the amino proximal domain A is phosphorylated. Based on these results, molecular models are proposed for the structures of EnvZc[AAB] and the kinase domain of EnvZ. The present results demonstrate for the first time the construction of a functional, monomeric histidine kinase, further structural studies of which may provide important insights into the structure-function relationships of histidine kinases.
Function of the sarcoplasmic reticulum and expression of its Ca2(+)-ATPase gene in pressure overload-induced cardiac hypertrophy in the rat. (1990)

The reduction in Ca2+ concentration during diastole and relaxation occurs differently in normal hearts and in hypertrophied hearts secondary to pressure overload. We have studied some possible molecular mechanisms underlying these differences by examining the function of the sarcoplasmic reticulum and the expression of the gene encoding its Ca2(+)-ATPase in rat hearts with mild and severe compensatory hypertrophy induced by abdominal aortic constriction. Twelve sham-operated rats and 31 operated rats were studied 1 month after surgery. Eighteen animals exhibited mild hypertrophy (left ventricular wt/body wt less than 2.6) and 13 animals severe hypertrophy (left ventricular wt/body wt greater than 2.6). During hypertrophy we observed a decline in the function of the sarcoplasmic reticulum as assessed by the oxalate-stimulated Ca2+ uptake of homogenates of the left ventricle. Values decreased from 12.1 +/- 1.2 nmol Ca2+/mg protein/min in sham-operated rats to 9.1 +/- 1.5 and 6.7 +/- 1.1 in rats with mild and severe hypertrophy, respectively (p less than 0.001 and p less than 0.001, respectively, vs. shams). This decrease was accompanied by a parallel reduction in the number of functionally active CA2(+)-ATPase molecules, as determined by the level of Ca2(+)-dependent phosphorylated intermediate: 58.8 +/- 7.4 and 48.1 +/- 13.5 pmol P/mg protein in mild and severe hypertrophy, respectively, compared with 69.7 +/- 8.2 in shams (p less than 0.05 and p less than 0.01, respectively, vs. shams). Using S1 nuclease mapping, we observed that the Ca2(+)-ATPase messenger RNA (mRNA) from sham-operated and hypertrophied hearts was identical. Finally, the relative level of expression of the Ca2(+)-ATPase gene was studied by dot blot analysis at both the mRNA and protein levels using complementary DNA clones and a monoclonal antibody specific to the sarcoplasmic reticulum Ca2(+)-ATPase. In mild hypertrophy, the concentrations of Ca2(+)-ATPase mRNA and protein in the left ventricle were unchanged when compared with shams (mRNA, 93.8 +/- 10.6% vs. sham, NS; protein, 105.5 +/- 14% vs. sham, NS). in severe hypertrophy, the concentration of Ca2(+)-ATPase mRNA decreased to 68.7 +/- 12.9% and that of protein to 80.1 +/- 15.5% (p less than 0.001 and p less than 0.05, respectively), whereas the total amount of mRNA and enzyme per left ventricle was either unchanged or slightly increased. The slow velocity of relaxation of severely hypertrophied heart can be at least partially explained by the absence of an increase in the expression of the Ca2(+)-ATPase gene and by the relative diminution in the density of the Ca2+ pumps.(ABSTRACT TRUNCATED AT 400 WORDS)