gebhart/patrepeval huggingface dataset:
Malignant Tumor Formation After Transplantation of Short-Term Cultured Bone Marrow Mesenchymal Stem Cells in Experimental Myocardial Infarction and Diabetic Neuropathy (2011)

Genetically unmodified MSCs can undergo chromosomal abnormalities even at early passages and form malignant tumors when transplanted in vivo. These results suggest that careful monitoring of chromosomal status is warranted when in vitro expanded MSCs are used for cell therapy such as for MI.
Aprotinin can inhibit the proteolytic activity of thrombin (1992)

Aprotinin has been shown to reduce blood loss and blood requirement when administered prior to surgery and this therapeutic benefit appears to be related to its specificity as a protease inhibitor. The inhibition of plasmin by aprotinin is well characterized, but little is known of its effect on thrombin. In preliminary experiments, we showed that aprotinin can prevent platelet aggregation induced by thrombin. Follow-up studies have now been performed in order to clarify the effect of aprotinin on thrombin. A fluorescence study of the direct binding of aprotinin to human alpha-thrombin was analysed according to the Michaelis-Menten model and a dissociation constant of 30 x 10(-6) mol.l-1 was determined. Aprotinin can displace p-aminobenzamidine, a fluorescent-probe molecule which binds to the active site of serine proteases, showing that the active site of thrombin was involved. Aprotinin also inhibited the ability of thrombin to induce a fibrin clot from purified fibrinogen and to induce the hydrolysis of the chromogenic substrate H-D-phenylalanylpipecolylarginine-p-nitroanalidehydrochloride++ + (S-2238). With S-2238, double-reciprocal plots show that the inhibition is competitive with a Ki of 61 microM and a Km of 1.72 microM. Aprotinin was a potent inhibitor of thrombin-induced aggregation. A Schild plot of the aggregation data yielded a slope of 0.97 +/- 0.12 and an apparent dissociation constant of 57.0 +/- 13.1 microM (mean +/- SEM). Thus, the inhibition of thrombin-induced platelet aggregation by aprotinin fits a model of competitive inhibition. Conclusions are that, in addition to a possible direct effect of aprotinin on platelets, the inhibition of thrombin-induced platelet activation by aprotinin can be also explained, in part, by a direct effect of the inhibitor on the thrombin molecule itself. This supports the concept that a proteolytic step is involved in the platelet response to thrombin. Finally, evidence is in favour of the participation of Trp245 in the fluorescence response of thrombin on binding to aprotinin.
The wired household: Teletext services pave the way for a variety of useful monitoring and control features in the home (1979)

Information retrieval is not the only capability that advanced electronics can offer to households. Other, more complex chores can be performed by specialized terminals that combine microprocessors with relatively conventional hardware. Three experimental systems now in the laboratory would do the following in homes: 1. Control the use of electricity to avert overloading at utilities that can lead to blackouts. 2. Turn the television receiver into a programmable information/entertainment center. 3. Use the telephone at idle times for meter reading, alarm reporting, and the remote monitoring and control of lighting, heating, and air-conditioning.
Regulation of Cranial Suture Morphogenesis (2004)

The cranial sutures are the primary sites of bone formation during skull growth. Morphogenesis and phenotypic maintenance of the cranial sutures are regulated by tissue interactions, especially those with the underlying dura mater. Removal of the dura mater in fetuses causes abnormal suture development and premature suture obliteration. The dura mater interacts with overlying tissues of the cranial vault by providing: (1) intercellular signals, (2) mechanical signals and (3) cells, which undergo transformation and migrate to the suture. The intercellular signaling governing suture development employs the fibroblast growth factors (FGFs). In rats during formation of the sutures in the fetus, FGF-1 is localized mainly in the dura mater, while other FGFs are expressed in the overlying tissues. By birth, FGF-2 largely replaces FGF-1 in the dura mater. FGFs present in the calvaria bind either the IIIb or IIIc mRNA splice variants of the FGF receptors (FGFRs) 1, 2, or 3. Monoclonal antibodies to the b variant of FGFR2 were used to determine the distribution of FGFR2IIIb during suture development and its extracellular localization. FGFR2IIIb is present in association with mature osteoblasts and osteogenic precursor cells of the suture in the fetus. Ectodomains of FGFR2IIIb, the products of proteolytic cleavage of the receptors, were present throughout the extracellular matrix of sutures resisting obliteration (coronal and sagittal), but absent from the core of sutures undergoing normal fusion (posterior intrafrontal). This observation is consistent with a possible mechanism, in which truncated receptors bind FGFs, thus regulating free FGF available to nearby cells. Mechanical signaling in the calvaria results from tensional forces in the dura mater generated during rapid expansion of the neurocranium. Posterior intrafrontal sutures of rats, which fuse between days 16 and 24, were subjected to cyclical tensional forces in vitro. Significant delay in the timing of suture fusion and increases in the expression domains of FGFR1 and 2 were observed, demonstrating the sensitivity of suture patency to mechanical signals and a possible role of the FGF system in mediating such stimuli. Finally, cells of the dura mater beneath the intrafrontal and sagittal sutures were observed to undergo a morphological transformation to a dendritic morphology and migrate into the suture mesenchyme between days 10 and 16 of development. This process may participate in suture and bone morphogenesis and influence the patency of the sutures along the anterior-posterior axis.
A loop network within the anthrax toxin pore positions the phenylalanine clamp in an active conformation (2006)

Heptameric pores formed in the endosomal membrane by the protective antigen moiety of anthrax toxin serve as portals for entry of the enzymatic moieties of the toxin into the cytosol. In the aqueous lumen of each pore is a "Phe clamp," a heptad of narrowly apposed Phe residues (Phe-427), that catalyzes the unfolding and translocation of the enzymatic moieties across the membrane. Here, we provide evidence for a "loop swap" between neighboring protective antigen subunits, which is required for efficient translocation and is mediated by a salt bridge formed between the side chains of Lys-397 and Asp-426. We propose that the interaction between residues 397 and 426 creates a structural framework that positions Phe-427 within the pore lumen, forming a functional Phe clamp and, hence, a translocation-competent pore.
Forced expression of NESH suppresses motility and metastatic dissemination of malignant cells. (2002)

To characterize the function of a novel Src homology 3 (SH3) adapter protein termed NESH, we have established transfectants stably expressing NESH. We observed that every clone of NESH transfectants caused a marked reduction in motility, although the clones exhibited no significant differences in intrinsic cell growth compared with the control cells in vitro. The NESH transfectants also exhibited significant reduction in tumor metastatic potential in vivo. We found that NESH expression is frequently lost in invasive cancer cell lines despite its ubiquitous expression in normal tissues. The SH3 domain of NESH seems to interact with p21-activated kinase (PAK), which is involved in regulation of cell motility. Furthermore, a significant decrease in PAK phosphorylation at (402)Thr was found in NESH transfectants. Taken together, these results suggest that NESH inhibits ectopic metastasis of tumor cells as well as cell migration through interaction with intracellular molecules such as PAK that are essential for cell motility.
A survey of corneal graft practice in the United Kingdom. (1995)

A questionnaire designed to survey current corneal graft practice was sent to 498 consultant ophthalmologists in the United Kingdom. Three hundred and twenty-nine completed questionnaires (66%) were returned. Seventy per cent of these were from consultants who perform corneal grafts, of whom 36% had a specialist interest in corneal surgery. The survey found that most consultants preferred to perform corneal grafts on an inpatient basis with the patient under general anaesthesia. Agreement (> 80%) was also found in the following areas: use of a hand-held trephine, concurrent cataract surgery (if indicated), post-operative immunosuppression, and refraction to assess post-operative astigmatism. There was less agreement on the choice of donor material, use of tissue matching, donor-trephine size disparity, suture technique, relative timing of trabeculectomy surgery (if required), the management of intraocular lenses during surgery for pseudophakic bullous keratopathy, timing of discharge after surgery, use of prophylactic acyclovir, management of astigmatism, routine removal of all corneal sutures, and discharge of uncomplicated cases from routine follow-up.
Human acid sphingomyelinase (2003)

Human acid sphingomyelinase (haSMase, EC 3.1.4.12) catalyzes the lysosomal degradation of sphingomyelin to ceramide and phosphorylcholine. An inherited haSMase deficiency leads to Niemann-Pick disease, a severe sphingolipid storage disorder. The enzyme was purified and cloned over 10 years ago. Since then, only a few structural properties of haSMase have been elucidated. For understanding of its complex functions including its role in certain signaling and apoptosis events, complete structural information about the enzyme is necessary. Here, the identification of the disulfide bond pattern of haSMase is reported for the first time. Functional recombinant enzyme expressed in SF21 cells using the baculovirus expression system was purified and digested by trypsin. MALDI-MS analysis of the resulting peptides revealed the four disulfide bonds Cys120-Cys131, Cys385-Cys431, Cys584-Cys588 and Cys594-Cys607. Two additional disulfide bonds (Cys221-Cys226 and Cys227-Cys250) which were not directly accessible by tryptic cleavage, were identified by a combination of a method of partial reduction and MALDI-PSD analysis. In the sphingolipid activator protein (SAP)-homologous N-terminal domain of haSMase, one disulfide bond was assigned as Cys120-Cys131. The existence of two additional disulfide bridges in this region was proved, as was expected for the known disulfide bond pattern of SAP-type domains. These results support the hypothesis that haSMase possesses an intramolecular SAP-type activator domain as predicted by sequence comparison [Ponting, C.P. (1994) Protein Sci., 3, 359-361]. An additional analysis of haSMase isolated from human placenta shows that the recombinant and the native human protein possess an identical disulfide structure.
Tetrahydrobiopterin and Parkinson's disease (1989)

Two patients with Parkinson's disease were treated with 1 g tetrahydrobiopterin (BH4) for 5 days. Clinical improvement was not observed. In the cerebrospinal fluid (CSF) a 4-8 fold increase in the concentration of homovanillic acid (HVA), and a 3-fold increase in the concentration of 5-hydroxyindole acetic acid (5-HIAA) was measured. However, the concentration of HVA reached, was only approximately half as high, as that of patients treated with madopar (DOPA + benserazid). In urine, the excretion of HVA increased 13-37 fold, when the patients were treated with madopar, whereas no increase in the HVA excretion was measured after the BH4 administration. Additionally, 2 patients with Parkinson's disease were treated with 1 g BH4 in combination with 15 g tyrosine for 3 days, and 1 parkinsonian patient was treated with 15 g tyrosine daily for 7 weeks. No increase in the CSF concentrations of HVA or 5-HIAA was observed. The results suggest, the BH4 in the dosage used, is not effective in the treatment of Parkinson's disease.
STRIDER: A Black-box, State-based Approach to Change and Configuration Management and Support (2003)

Permission is granted for noncommercial reproduction of the work for educational or research purposes.
ChemInform Abstract: Carbohydrate‐Based Combinatorial Libraries (1998)

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
Escherichia coli cytotoxins and enterotoxins (1992)

Vero cell cytotoxins and cytotonic enterotoxins produced by E. coli are toxic proteins, which have been implicated in a number of specific diseases in humans and animals. Nomenclature for these toxins is complicated by the existence of different names for the same toxin. The Vero cell cytotoxins are called verotoxins because they are lethal for Vero cells in culture; they are also known as Shiga-like toxins (SLTs) because they are clearly related to Shiga toxin in structure, amino acid sequence, mechanism of action, and biological activity. SLTs belong to two classes. SLT-I is identical with Shiga toxin and is in a class by itself (class I). The other SLTs are closely related to each other and form a second class (class II). Class II SLTs include SLT-II, SLT-IIv, SLT-IIvha, SLT-IIvhb, and SLT-IIva. All SLTs that have been investigated are A-B subunit protein toxins, whose A subunits possess N-glycosidase activity against 28S rRNA and cause inhibition of protein synthesis in eukaryotic cells. These toxins are enterotoxic as well as cytotoxic. SLTs produced in the intestine are absorbed into the blood stream and affect vascular endothelial cells in target organs. They may also have a direct toxic effect on enterocytes. Diseases in which E. coli SLTs have been implicated include diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome in humans and edema disease in pigs. Variation in receptor specificities among SLTs may be the reason for different disease syndromes in different host species. The E. coli enterotoxins belong to three distinct classes: heat-labile enterotoxin (LT), heat-stable enterotoxin type I or type a (STI, STa), and heat-stable enterotoxin type II or type b (STII, STb). There is clear evidence that these cytotonic enterotoxins play an essential role in diarrheal disease. LT is an A-B subunit protein toxin, closely related to cholera toxin. Following binding of LT to receptors in enterocytes the A subunit is internalized. The enzymatically active A subunit transfers ADP-ribose from NAD to a GTP-dependent adenylate cyclase regulatory protein, thereby elevating intracellular levels of adenylate cyclase. The increased levels of cyclic AMP cause stimulation of A kinase and lead to hypersecretion of electrolytes and fluid. STI is a small peptide of 18 or 19 amino acids. It binds to receptors in enterocytes and stimulates particulate guanyl cyclase. Elevated intracellular cyclic GMP stimulates G kinase, resulting in increased Cl- secretion and impaired absorption of Na+Cl-. STII is a peptide toxin whose mechanism of action is unknown.(ABSTRACT TRUNCATED AT 400 WORDS)
Retroviral Gene Transfer Is Inhibited by Chondroitin Sulfate Proteoglycans/Glycosaminoglycans in Malignant Pleural Effusions (1997)

Gene therapy may be an important adjuvant for treating cancer in the pleural space. The initial results of retroviral gene transfer to cancer cells in malignant pleural effusions revealed that transduction was markedly inhibited, and studies to characterize the inhibitory factor(s) were performed. The inhibition was contained within the soluble, rather than cellular, components of the effusions and was demonstrated with amphotropic, gibbon ape leukemia virus, and vesicular stomatitis virus-glycoprotein pseudotyped retroviral vectors. After excluding complement proteins, a series of studies identified chondroitin sulfates (CSs) as the inhibitory substances. First, treatment of the effusions with mammalian hyaluronidase or chondroitinases, but not Streptomyces hyaluronidase, abolished the inhibitory activity. Second, addition of exogenous CS glycosaminoglycans mimicked the inhibition observed with pleural effusions. Third, immunoassays and biochemical analyses of malignant pleural effusion specimens revealed CS in relevant concentrations within pleural fluid. Fourth, proteoglycans/glycosaminoglycans isolated from the effusions inhibited retroviral gene transfer. Analyses of the mechanism of inhibition indicate that the chondroitin sulfates interact with vector in solution rather than at the target cell surface. These results suggest that drainage of the malignant pleural effusion, and perhaps enzymatic pretreatment of the pleural cavity, will be necessary for efficient retroviral vector mediated gene delivery to pleural metastases.
High-Performance Liquid Chromatography for Hormone Assay (2006)

High-performance liquid chromatography (HPLC) is a refinement of traditional column chromatographic techniques. The speed of analysis and the resolution are increased with new column-packing materials and eluant pumped through the column at high pressure. The potential for achieving measurements of hormones in small volumes of plasma or urine is limited, both in normal and pathological situations. Using HPLC with ultraviolet absorption, the detection limit is only nanogram amounts of hormones per milliliter of blood serum. The applications of the technique to specific hormones from recent and older literature will be used throughout this chapter to illustrate aspects of the technology.
Successful Treatment of Tardive Dystonia with Clozapine and Clonazepam (1996)

This report adds to two other cases suggesting that the combination of clozapine and clonazepam may be an effective treatment for tardive dystonia.
A Novel Recessive Mutation in Fibroblast Growth Factor-23 Causes Familial Tumoral Calcinosis (2005)

Gain-of-function mutations in fibroblast growth factor-23 (FGF23) are responsible for autosomal dominant hypophosphatemic rickets, a disorder of isolated renal phosphate wasting. Patients with the disorder display hypophosphatemia with normocalcemia as well as inappropriately normal 1,25-dihydroxyvitamin D [1,25(OH)2D3] concentrations. Reciprocally tumoral calcinosis (TC) patients are often hyperphosphatemic with inappropriately normal or elevated serum 1,25(OH)2D3 levels and have ectopic and vascular calcifications, a phenotype similar to that of Fgf23 null mice. Therefore, the goal of the present studies was to test whether FGF23 was a candidate gene for TC. Two sisters in a consanguineous TC family had hyperphosphatemia and normal 1,25(OH)2D3 levels with characteristic ectopic and vascular calcifications. Interestingly, these patients had low-normal intact serum FGF23 levels but demonstrated FGF23 concentrations approximately 40 times normal when assessed with a C-terminal FGF23 serum assay. Mutational analyses identified a homozygous S71G mutation in FGF23 in the TC patients, which was not found in control alleles. Finally, modeling demonstrated that the S71G mutation most likely destabilizes full-length FGF23. In summary, recessive FGF23 mutations can lead to TC. Additionally, our findings indicate that FGF23 may adopt an unstable conformation in some TC patients, possibly leading to nonfunctional FGF23 protein.
Diastolic heart function—pathophysiology, characterization, and therapeutic approaches (1993)

In recent years diastolic cardiac function has attracted increasing attention since parameters of diastolic function were found to be altered earlier or more specifically than parameters of systolic function. Diastolic cardiac function is determined by both active (muscular relaxation, redistribution of calcium, synchronization, etc.) and passive (myocardial structure, fibrosis, etc.) factors. As a consequence, a comprehensive assessment of diastolic cardiac function cannot be based on one single parameter. For a complete analysis of diastolic function it is necessary to perform invasive diagnostic procedures involving the measurement of atrial and ventricular pressures, as well as the registration of volume changes with a high time resolution. In addition, it is necessary to measure wall thickness and ventricular configuration, so that apart from filling parameters the stress-strain relationship can be obtained. Noninvasive techniques (Doppler echocardiography, radionuclear ventriculography, apexcardiography) may suggest alterations in diastolic function as well. They ought to be complemented by additional diagnostic procedures (pulmonary pressure, stress testing, etc.). Therapy must consider potentially harmful effects on diastolic function parameters, particularly if changes in myocardial oxygen consumption may result (heart rate, parietal wall stress). Calcium antagonists (verapamil, diltiazem, nifedipine), phosphodiesterase inhibitors (milrinone), beta-adrenergic agonists and antagonists with vasodilating effects (e.g., celiprolol) all have beneficial effects on diastolic myocardial function. A range of diastolic function parameters is being reviewed in the following paper. Their role in the estimation of cardiac function and their responsiveness to therapy in hypertrophy, cardiomyopathy, and coronary heart disease is being discussed.
Augmented transition networks as a representation for knowledge-based history-taking systems. (1992)

Numerous history-taking systems have been built to automate the medical history-taking process. These systems differ in their control methods, input and output modalities, and kinds of questions asked. Thus, there has emerged no standard way of representing interviewing knowledge--the expert knowledge used to govern the sequence of questions asked in an interview. This paper discusses how we use an augmented transition network (ATN) to represent the knowledge of a speech-driven automated history-taking program, Q-MED, and how, more generally, ATNs could be used as a representation for any knowledge-based history-taking system. We identify three characteristics of ATNs that facilitate the use of ATNs in interviewing systems: explicitness, hierarchical structure, and generality.
Scheme for reducing decoherence in quantum computer memory (1995)

Recently, it was realized that use of the properties of quantum mechanics might speed up certain computations dramatically. Interest has since been growing in the area of quantum computation. One of the main difficulties of quantum computation is that decoherence destroys the information in a superposition of states contained in a quantum computer, thus making long computations impossible. It is shown how to reduce the effects of decoherence for information stored in quantum memory, assuming that the decoherence process acts independently on each of the bits stored in memory. This involves the use of a quantum analog of errorcorrecting codes.Received 17 May 1995DOI:https://doi.org/10.1103/PhysRevA.52.R2493©1995 American Physical Society
An aqueous ethanol extraction process for cottonseed oil (1984)

Abstract A bench‐top process for the extraction of cottonseed flakes with aqueous ethanol has been developed. The process consists of cottonseed meat flaking, drying and extraction with boiling, aqueous ethanol (95% by volume) at atmospheric pressure. The resulting miscella is chilled, producing free oil, emulsified oil and mucilaginous gum. The heterogeneous solution is processed through a phase separator where free and emulsified oil and gum are separated from oil‐lean miscella. The oil and gum phases are treated with caustic soda and centrifuged to produce semirefined oil containing about 4% volatiles. The miscella phase, containing about 3.3% lipid‐like material and 1% petroleum ether insolubles, is reheated and recycled to the extractor. After the marc is pressed foots are added, and it is desolventized to produce a meal having a residual oil content less than 1%. Although not yet otpimized, the process shows potential for scaleup to pilot plant processing and adaptability to current oil mill solvent operations.