gebhart/patrepeval huggingface dataset:
Domain‐boundary structure of styrene‐isoprene block copolymer films cast from solutions. III. Preliminary results on spherical microdomains (1977)

Abstract The microdomain structure of styrene‐isoprene A‐B type block copolymers having a nearly constant fraction of polyisoprene block segments (13 ∼ 22 wt percent) was investigated by small‐angle X‐ray scattering (SAXS) as a function of the molecular weights of the copolymers. The styrene‐rich block copolymers all have spherical microdomains of polyisoprene block segments dispersed in a matrix of polystyrene block segments. The size of the spherical domains increases with increasing molecular weight of the polyisoprene segment with a power of ca. 0.6. The thickness of the domain‐boundary interphase arising from a partial mixing of the incompatible segments at the domain‐boundary interface is also estimated by analyzing a systematic deviation of the SAXS intensity distribution from Porod's law at large scattering angles on the basis of the infinite slit‐height approximation. The results indicate the interfacial thickness to be about 20Å and to be almost independent of the molecular weight of the block copolymers studied. The applicability of the infinite‐slit height approximation in the analysis of SAXS intensity distributions at large scattering angles is also discussed in an approximate fashion.
Beta dose point kernels for radionuclides of potential use in radioimmunotherapy. (1989)

Beta dose point kernels for 32P, 67Cu, 90Y, 131I, 186Re, and 188Re nuclides appropriate for radioimmunotherapy are calculated based upon Monte Carlo results. The calculations are shown to differ significantly from values based upon solutions to the electron transport equation. Agreement with experiment for 32P is found to be improved for the former as compared with the latter. Values of the scaled dose point kernels are tabulated at 4% intervals of the continuous slowing down approximation range for each of the six radionuclides. Beta dose distributions are also tabulated at corresponding distances from the source. This data may be used to calculate the spatial dose distribution expected following administration of radiolabeled monoclonal antibodies, aiding in optimum selection of the appropriate radionuclide. Parameters for functions providing analytic representation of the calculated scaled dose point kernels of individual beta groups are presented.
Electroluminescence from triplet excited states of benzophenone (1996)

We report the electroluminescent characteristics of organic multilayer light-emitting diodes (LEDs) with a benzophenone (BP) dispersed poly(methylmethacrylate) (PMMA) film as an emitting layer. The electroluminescence (EL) intensity of these LEDs increases with decreasing temperature from 273 to 100 K when they are operated at the same voltages or the same current densities. The EL spectrum of the LEDs, which peaks at around 450 nm, is identical to the phosphorescence spectrum of BP in PMMA. In addition, the EL decay time was determined as 46.8 μs at 100 K by applying a rectangular voltage pulse. These results indicate that the EL of the LED originates from the triplet excited states of BP.
A peptide mimetic of human interferon (IFN)-beta (2003)

Type I interferons (IFNs) are cytokines that are used clinically as antiviral and antitumour agents. The interaction of IFNs with their heterodimeric type I IFN receptor comprised of IFNAR1 and IFNAR2 is a first step to inducing biological actions. Here, we describe the successful mimicry of IFN-beta by a peptide isolated by phage-display screening using a neutralizing anti-IFN-beta monoclonal antibody. The 15-mer peptide, designated SYR6, was shown to compete with IFN-beta for binding to type I IFN receptor in a concentration-dependent manner, and was shown to elicit antiviral activity on cultured cells. This antiviral activity was not eliminated in the presence of neutralizing monoclonal antibodies to IFN-alpha, -beta and -gamma, and a low concentration of soluble type I IFN receptor, suggesting that it was not due to IFN contamination or the induction of endogenous IFNs by SYR6. This peptide might be a potent agonist to provide a mechanism of activating heterodimeric cytokine receptors.
Detection of glutamine synthetase in the cerebrospinal fluid of Alzheimer diseased patients: a potential diagnostic biochemical marker. (1992)

In this report, 8- and 2-azidoadenosine 5'-[gamma-32P]triphosphate were used to examine cerebrospinal fluid (CSF) samples for the presence of an ATP binding protein unique to individuals with Alzheimer disease (AD). A 42-kDa ATP binding protein was found in the CSF of AD patients that is not observed in CSF from normal patients or other neurological controls. The photolabeling is saturated with 30 microM 2-azidoadenosine 5'-[gamma-32P]triphosphate. Photoinsertion can be totally prevented by the addition of 25 microM ATP. Photoinsertion of 2-azidoadenosine 5'-triphosphate into the protein is only weakly protected by other nucleotides such as ADP and GTP, indicating that this is a specific ATP binding protein. A total of 83 CSF samples were examined in a blind manner. The 42-kDa protein was detected in 38 of 39 AD CSF samples and in only 1 of 44 control samples. This protein was identified as glutamine synthetase [GS; glutamate-ammonia ligase; L-glutamate:ammonia ligase (ADP-forming), EC 6.3.1.2] based on similar nucleotide binding properties, comigration on two-dimensional gels, reaction with a polyclonal anti-GS antibody, and the presence of significant GS enzyme activity in AD CSF. In brain, GS plays a key role in elimination of free ammonia and also converts the neurotransmitter and excitotoxic amino acid glutamate to glutamine, which is not neurotoxic. The involvement of GS, if any, in the onset of AD is unknown. However, the presence of GS in the CSF of terminal AD patients suggests that this enzyme may be a useful diagnostic marker and that further study is warranted to determine any possible role for glutamate metabolism in the pathology of AD.
CHILDREN WITH AIDS (1989)

Hundreds of children with AIDS are suffering or dying prematurely because they are unable to obtain AZT, a drug that could prolong and improve the quality of their lives.... Experts say AZT, or azidothymidine, the only AIDS drug approved for use in adults and teen-agers, has been tested in children and shown to be just as active in them, prolonging life and even dramatically reversing mental deterioration. Yet the Burroughs Wellcome Company, the drug's manufacturer, has not yet applied for approval to market AZT to children under the age of 12 or to make it available to them under "compassionate use" procedures before marketing approval is granted. As a result, AZT is not available in a pediatric dose, except in clinical trials, and insurance companies and government programs will not pay for its use in children... A company official said Burroughs Wellcome was working as fast as possible to prepare material needed for Federal approval. But Dr. Samuel Broder, director of the National Cancer Institute, who was a key figure in demonstrating that AZT could slow the spread of the AIDS virus, said he was "very disturbed" that Burroughs Wellcome had not applied for approval to market the drug to children.... Nearly, 1,800 cases of children under 12 with AIDS have been reported to the Federal Centers for Disease Control, but experts say many more have gone unreported. About 800 of these children have died. About 300 children are enrolled in clinical trials...
Uroplakin gene expression in normal human tissues and locally advanced bladder cancer (2002)

The uroplakins are widely regarded as urothelium-specific markers of terminal urothelial cytodifferentiation. This study investigated the expression of the four uroplakin genes, UPIa, UPIb, UPII and UPIII, in a wide range of normal human tissues to determine tissue specificity and in advanced transitional cell carcinoma (TCC) to examine gene expression in primary and metastatic disease. In the urinary tract, all four uroplakins were expressed by urothelium and UPIII was also expressed by prostatic glandular epithelium. UPIa and UPII appeared to be urothelium-specific, but UPIb was detected in several non-urothelial tissues, including the respiratory tract, where it was associated with squamous metaplasia of tracheal and bronchial epithelia. The ten cases of primary TCC and corresponding lymph node metastases demonstrated that each uroplakin gene could be expressed at the mRNA level. No single uroplakin gene was expressed in all primary tumours or metastases, but 80% of the primary tumours and 70% of the lymph node metastases expressed at least one uroplakin gene. UPIII mRNA was often expressed in the absence of UPIII protein. These results confirm that in human tissues the expression of UPIa and UPII genes is highly specific to urothelium and suggest that the tight differentiation-restricted expression of uroplakin genes in normal urothelium is lost following malignant transformation.
The Sheep Erythrocyte Receptor and Both α and β Chains of the Human T‐Lymphocyte Antigen Receptor Bind the Mitogenic Lectin (Phytohaemagglutinin) from Phaseolus vulgaris (1986)

We have studied the interaction of mitogenic lectins such as phytohaemagglutinin (PHA) and concanavalin A (Con A) with both surface molecules which, by the use of monoclonal antibodies, are known to trigger T-cell mitogenesis. Monoclonal antibodies recognizing the T-lymphocyte receptor for antigen (Ti) and/or its associated structure, CD3, activate T cells. More recently, a second pathway of activation has been described which involves the sheep erythrocyte binding glycoprotein CD2, a surface molecule distinct from Ti-CD3. Lysates from surface-iodinated T-leukaemia cell lines were treated with lectin and affinity purified anti-lectin antibodies coupled to protein A-Sepharose. We have shown that eluates from Con A/anti-Con A or PHA/anti-PHA immunoprecipitates contained Ti, since a rabbit anti-T alpha serum, which recognizes the native and denatured forms of the constant region of the alpha chain, immunoprecipitated Ti from these eluates. Furthermore, Ti immunoprecipitated by anti-T alpha serum from lysates of surface iodinated E+ lymphocytes was binding to PHA after elution from the immunoprecipitate. When the purified Ti molecule was reduced and alkylated, allowing the permanent dissociation of its alpha and beta subunits, PHA interacted with both chains, whereas anti-T alpha serum immunoprecipitated the alpha chain only. Altogether, these results demonstrate that PHA interacts with both chains of the T cell receptor for antigen on human peripheral T lymphocytes. With the HPB-ALL tumour line, a similar approach showed that both alpha and beta chains of Ti bind to Con A and Ulex europaeus 1 but not Helix pomatia. Affinity chromatography on immobilized lectins and immunoprecipitation with lectin/anti-lectin antibodies were employed to test whether CD2 binds to PHA and Con A. The results show that CD2 from human peripheral T lymphocytes binds both lectins but with a lower affinity for PHA than Con A.
Production and characterization of a monoclonal antibody able to discriminate galectin-1 from galectin-2 and galectin-3 (1998)

Antisera raised against galectin-1 exhibit crossreactivities with other galectins or related molecules. In order to overcome this problem, a monoclonal antibody to human brain galectin-1 was obtained by selecting clones without reactivity toward galectin-3. This mAb specifically bound galectin-1 of various animal origins but neither galectin-2 nor galectin-3. Western-blotting analysis of soluble human brain extracts after 2D gel electrophoresis revealed only the two most acidic isoforms of galectin-1. The ability of this mAb to bind galectin-1/asialofetuin complexes indicates that its epitope is not localized in the carbohydrate recognition domain of galectin-1. This particularity induces with efficiency its monospecificity.
Novel mutations in KvLQT1 that affect Iks activation through interactions with Isk (2000)

Novel mutations are described that induce a voltage shift of the channel activation only in the presence of IsK. They appear associated with a milder cardiac phenotype.
The Effects of Increased Prosthetic Ankle Motions on the Gait of Persons with Bilateral Transtibial Amputations (2009)

Both the subjective and objective results suggest that prosthetic foot and ankle components that allow for greater sagittal and transverse plane rotations provide substantial benefit during walking and should be considered for persons with bilateral transtibial amputations. Nonetheless, clinicians should perform individual and appropriate assessments of patients to ensure that they are capable of using components that may improve mobility while possibly sacrificing some degree of stability.
THE MATERIAL BONE: Structure-Mechanical Function Relations (1998)

▪ Abstract The term bone refers to a family of materials, all of which are built up of mineralized collagen fibrils. They have highly complex structures, described in terms of up to 7 hierarchical levels of organization. These materials have evolved to fulfill a variety of mechanical functions, for which the structures are presumably fine-tuned. Matching structure to function is a challenge. Here we review the structure-mechanical relations at each of the hierarchical levels of organization, highlighting wherever possible both underlying strategies and gaps in our knowledge. The insights gained from the study of these fascinating materials are not only important biologically, but may well provide novel ideas that can be applied to the design of synthetic materials.
Phosphodiesterase-4D Knock-Out and RNA Interference-Mediated Knock-Down Enhance Memory and Increase Hippocampal Neurogenesis via Increased cAMP Signaling (2011)

Phosphodiesterase-4 (PDE4) plays an important role in mediating memory via the control of intracellular cAMP signaling; inhibition of PDE4 enhances memory. However, development of PDE4 inhibitors as memory enhancers has been hampered by their major side effect of emesis. PDE4 has four subtypes (PDE4A-D) consisting of 25 splice variants. Mice deficient in PDE4D displayed memory enhancement in radial arm maze, water maze, and object recognition tests. These effects were mimicked by repeated treatment with rolipram in wild-type mice. In addition, similarly as rolipram-treated wild-type mice, PDE4D-deficient mice also displayed increased hippocampal neurogenesis and phosphorylated cAMP response element-binding protein (pCREB). Furthermore, microinfusion of lentiviral vectors that contained microRNAs (miRNAs) targeting long-form PDE4D isoforms into bilateral dentate gyri of the mouse hippocampus downregulated PDE4D4 and PDE4D5, enhanced memory, and increased hippocampal neurogenesis and pCREB. Finally, while rolipram and PDE4D deficiency shortened α2 adrenergic receptor-mediated anesthesia, a surrogate measure of emesis, miRNA-mediated PDE4D knock-down in the hippocampus did not. The present results suggest that PDE4D, in particular long-form PDE4D, plays a critical role in the mediation of memory and hippocampal neurogenesis, which are mediated by cAMP/CREB signaling; reduced expression of PDE4D, or at least PDE4D4 and PDE4D5, in the hippocampus enhances memory but appears not to cause emesis. These novel findings will aid in the development of PDE4 subtype- or variant-selective inhibitors for treatment of disorders involving impaired cognition, including Alzheimer's disease.
S-LAYER POSITIVE MOTILE AEROMONADS ISOLATED FROM CHANNEL CATFISH (1991)

Motile aeromonads are ubiquitous aquatic bacteria that can cause motile aeromonad septicemia (MAS), a disease which affects channel catfish and can produce significant economic loss. Motile aeromonads isolated from commercially-raised channel catfish were screened for production of S-layer protein in order to evaluate its potential role in natural epizootics. The S-layer protein was produced by 14 of 24 (58%) isolates from epizootics evaluated in this study. Concomitant infections with other internal pathogens were detected in 10 of the 24 cases used in this study, and only one of those 10 isolates (10%) produced the S-layer protein. When Aeromonas sp. was the only internal pathogen diagnosed, 13 of 14 (93%) isolates produced the S-layer protein.
Adoptive transfer of tumor-infiltrating lymphocytes in patients with sarcomas, ovarian, and pancreatic cancers. (2019)

TPS2650 Background: Adoptive cell therapy (ACT) with tumor-infiltrating lymphocytes (TIL) has a long history of efficacy in metastatic melanoma, and is being increasingly considered across other solid tumors. Preclinical data generated at MD Anderson Cancer Center has demonstrated the ability to grow TIL from a variety of tumor types including various types of sarcomas, ovarian and pancreas cancers. We are testing the efficacy of TIL across multiple tumor types using two different manufacturing protocols. Methods: We are conducting two ongoing investigator initiated basket TIL therapy trials. The first (NCT03449108) includes cohorts with poorly differentiated soft tissue and bone sarcomas, osteosarcoma, and platinum resistant ovarian cancer. The TIL product used in this trial is an investigational cell product (LN-145, Iovance Biotherapeutics, Inc.). The second trial (NCT03610490) includes cohorts of osteosarcoma, platinum resistant ovarian cancer, and pancreatic cancer (who have progressed on, or received maximal benefit from, front-line therapy). For this trial, TIL are manufactured at MD Anderson Cancer Center using a protocol that includes the use of urelumab (an agonistic anti-CD137 antibody) combined with T cell receptor activation during TIL expansion. In both trials eligible subjects undergo tumor harvest using a surgical excisional biopsy of the tumor for TIL manufacturing, receive a modified cyclophosphamide and fludarabaine lymphodepletion regimen and up to six doses of IL-2 (600,000 IU/kg) following TIL infusion. No intervening therapy is allowed between tumor harvest and initiation of lymphodepletion. The primary endpoint for each cohort is ORR as assessed by investigators using RECIST 1.1 criteria. The Simon’s two stage design is used to monitor the efficacy of each cohort independently. In the first stage, 10 patients will be treated per cohort. If there is no confirmed response in these 10 evaluable patients, the cohort will be terminated. If the cohort moves forward to Stage II, an additional 8 patients will be treated leading to a total of 18 patients. Three or more responders out of 18 treated patients for the cohort will be considered clinically relevant to justify further investigation. Enrollment is ongoing in all cohorts in both trials. An accrual update will be provided at the annual meeting. Clinical trial information: NCT03449108, NCT03610490.
In vivo degradation of tungsten embolisation coils. (2000)

It has been suggested that tungsten embolisation coils in intracranial aneurysms may dissolve in situ. These coils are also used, in much larger quantities, for the occlusion of larger vessels outside the cranium. This study was performed to investigate whether tungsten embolisation coils may become degraded in vivo and to examine whether this is radiographically evident on medium-term follow-up. 10 patients who had undergone aortic stent-graft repair of an abdominal aortic aneurysm (8 male and 2 female, mean age 69.7 years) and 10 age- and sex-matched controls were studied. The study group had also received an average of 64 cm of tungsten coil either to prevent or to treat an endoleak. Whole blood, serum and urine tungsten levels were assayed. Immediate post-operative and follow-up abdominal radiographs were reviewed by two consultant vascular radiologists to detect visible changes in the coils. Whole blood, serum and urine levels of tungsten were highly and significantly elevated (p < 0.001) in the study group compared with the controls. No radiographic changes in the coils were seen at an average of 16.7 months. In conclusion, tungsten embolisation coils dissolve in humans but radiographic changes are not apparent on medium-term follow-up. The clinical significance of these findings is uncertain but long-term follow-up is needed.
A tutorial on Reed-Solomon coding for fault-tolerance in RAID-like systems (1997)

It is well-known that Reed-Solomon codes may be used to provide error correction for multiple failures in RAID-like systems. The coding technique itself, however, is not as well-known. To the coding theorist, this technique is a straightforward extension to a basic coding paradigm and needs no special mention. However, to the systems programmer with no training in coding theory, the technique may be a mystery. Currently, there are no references that describe how to perform this coding that do not assume that the reader is already well-versed in algebra and coding theory. This paper is intended for the systems programmer. It presents a complete specification of the coding algorithm plus details on how it may be implemented. This specification assumes no prior knowledge of algebra or coding theory. The goal of this paper is for a systems programmer to be able to implement Reed-Solomon coding for reliability in RAID-like systems without needing to consult any external references. © 1997 John Wiley & Sons, Ltd.
Multiplication of Human Chondrocytes with Low Seeding Densities Accelerates Cell Yield without Losing Redifferentiation Capacity (2004)

To treat a cartilage defect with tissue-engineering techniques, multiplication of donor cells is essential. However, during this multiplication in monolayer expansion culture chondrocytes will lose their phenotype and produce matrix of inferior quality (dedifferentiation). Dedifferentiation occurs more extensively with low seeding densities and passaging. To obtain cartilage of good quality it is important that the multiplicated cells regain their cartilaginous phenotype (redifferentiation capacity). A "gold standard" for the multiplication of chondrocytes in monolayer, with respect to seeding density and passaging, is lacking. In numerous available studies, various cell densities have been used, making comparison of the results of these studies difficult. Therefore, we performed a comparative study to gain insight concerning the effect of seeding density and passaging on the capacity of cells to redifferentiate. From the resulting data we deduced the seeding density in monolayer culture for which cell expansion is both sufficient and fast, while the cells retain a capacity to redifferentiate. As a guideline we calculated that, at minimum, 20-fold multiplication is needed to fill an average cartilage defect of 4 cm(2) with the amount of donor chondrocytes we obtained. For this study we used isolated ear chondrocytes from five children. Four different seeding densities in monolayer culture were used, ranging from 3500 to 30000 cells/cm(2). The cells were cultured for four passages. The capacity of the expanded chondrocytes to redifferentiate (redifferentiation capacity) was studied after an additional 3-week culture in alginate beads and was assessed by glycosaminoglycan production and immunohistochemical stainings for collagen type I, collagen type II, elastin, and a fibroblast marker (11-fibrau). In general, we found that both passaging and decreasing seeding density yielded an increase in expanded chondrocytes, but at the same time decreased the dedifferentiation capacity. In further analyzing our data according to the proposed guidelines we found that with lower seeding densities sufficient multiplication (20 times) was reached in less time and with less passaging than at higher seeding densities. Importantly, the redifferentiation capacity of these chondrocytes was preserved. It was equal to or even surpassed that of chondrocytes multiplied 20 times at higher seeding densities, which required more time and more passages in monolayer culture. Thus, for cartilage tissue-engineering purposes we propose that expansion culture with low seeding densities is preferable.