gebhart/patrepeval huggingface dataset:
Nerve biopsy and conduction studies in diabetic neuropathy. (1977)

Morphological findings in sural nerves were related to nerve conduction in 12 patients with diabetic neuropathy, five with mainly sensory involvement, four with severe, symmetrical sensory-motor polyneuropathy, and three with multiple mononeuropathy. All had loss of large and small myelinated and of unmyelinated fibres, even early in the disease; segmental remyelination was the most prominent myelin alteration in teased fibres, segmental demyelination was found in only a few fibres. Axonal degeneration and Schwann cell damage seem to proceed independently of each other. The relation between recorded conduction velocity and that expected from the diameter of the largest fibres indicated that slowing of 20 to 30% was due to causes other than fibre loss; a grossly diminished conduction velocity was caused mainly by fibre loss. Electrophysiological findings in the sural nerve were largely representative of findings in other nerves, though abnormalities were less marked in the median nerve. In half the endoneurial vessels from diabetic neuropathy the perivascular space was thickened or contained more layers of basal laminae than normal. The same abnormalities were found in one-quarter of the endoneurial vessels from other acquired neuropathies.
The Genus Nocardiopsis Represents a Phylogenetically Coherent Taxon and a Distinct Actinomycete Lineage: Proposal of Nocardiopsaceae fam. nov. (1996)

The genus Nocardiopsis was shown to be phylogenetically coherent and to represent a distinct lineage within the radiation of the order Actinomycetales. The closest relatives of the genus Nocardiopsis are members of the genera Actinomadura, Thermomonospora, Streptosporangium, and Microtetraspora. The intrageneric structure of the genus Nocardiopsis is shown to consist of a highly related species group containing Nocardiopsis dassonvillei, Nocardiopsis alborubida, and Nocardiopsis antarctica and a second group of less highly related species comprising Nocardiopsis alba subsp. alba, Nocardiopsis alba subsp. prasina, and Nocardiopsis listeri. Nocardiopsis lucentensis occupies a position intermediate between the two species groups. The results of a 16S ribosomal DNA sequence analysis are generally consistent with the available chemotaxonomic, phenotypic, and DNA-DNA hybridization data. The phylogenetic position and the morpho- and chemotaxonomic properties of Nocardiopsis species support the creation of a family for the genus Nocardiopsis, Nocardiopsaceae fam. nov.
Studies on 3-substituted 1,2-benzisoxazole derivatives. I. (1976)

3-Amidinomethyl- (8), 3-imidazolinylmethyl- (9) and 3-tetrahydropyrimidinylmethyl-1, 2-benzisoxazole (10) were synthesized from 1, 2-benzisoxazole-3-acetonitrile (4) via iminoether (7). 3-Tetrazolylmethyl-1, 2-benzisoxazole (5) and 1, 2-benzisoxazole-3-acetamide oxime (11) were also prepared from 4. 3-Aminoethyl-1, 2-benzisoxazole (25), a tryptamine analogue of 1, 2-benzisoxazole, was synthesized from 3-chloroethyl-1, 2-benzisoxazole (20). The bromination of 1, 2-benzisoxazole-3-acetic acid (1) with one molar equivalent of bromine afforded α-bromo-1, 2-benzisoxazole-3-acetic acid (27), which was decarboxylated to give 3-bromomethyl-1, 2-benzisoxazole (30). The amination of 30 afforded 3-amino-methyl-1, 2-benzisoxazole (31). The bromination of 1 with excess of bromine gave 3-tribromomethyl-1, 2-benzisoxazole (28). N-Substituted 1, 2-benzisoxazolylglycine ester (32) was synthesized from methyl α-bromo-1, 2-benzisoxazole-3-acetate (29) which was obtained by the bromination of methyl 1, 2-benzisoxazole-3-acetate (2).
Vascular disease : molecular biology and gene therapy protocols (1999)

In Vascular Disease: Molecular Biology and Gene Therapy Protocols, Andrew Baker and a noted panel of expert investigators describe today's most powerful molecular methods for investigating the pathogenesis of vascular disease. These detailed, easy-to-follow techniques range from methods that have been used successfully to identify specific mutations involved in cardiovascular disorders, to those for transferring genes associated with cardiovascular disease into various vascular cell types by in vitro and in vivo routes. There are methods to identify novel genes and generate full-length cDNAs, to study gene transcription and promoter activity easily and effectively, and to ascertain precisely gene expression levels within the individual cell types in different pathophysiological conditions. Accurate methods to quantify apoptosis in both cultured cells and pathological specimens are also given. Vascular Disease: Molecular Biology and Gene Therapy Protocols offers today's vascular biologist and gene therapist an unprecedented ability to study the pathogenesis of vascular disease and readily to probe the potential for gene-based therapies. Powerful and productive, the techniques presented here operate across a wide range of exciting research areas, and promise spectacular therapeutic breakthroughs in the ongoing battle against vascular disease
Prevention of Rejection in Cardiac Transplantation by Blockade of the Interleukin-2 Receptor with a Monoclonal Antibody (2000)

Induction therapy with daclizumab safely reduces the frequency and severity of cardiac-allograft rejection during the induction period.
Selective group II glutamate metabotropic receptor agonist LY354740 attenuates pentetrazole- and picrotoxin-induced seizures. (2000)

There are several data indicating the involvement of metabotropic glutamate receptors (mGluR) in seizures and epileptogenesis. In the present experiments, the selective group II mGluR agonist (+)-2-aminobicyclo-[3.1.0]hexane-2,6-dicarboxylic acid (LY 354740) at doses from 4 to 16 mg/kg) administered prior to the injection of pentetrazole (80 mg/kg) or picrotoxin (3.2 mg/kg) produced a dose-dependent decrease in the number of mice exhibiting clonic convulsions. Our data suggest that group II mGluR agonist LY 354740 possesses antiseizure activity.
Isolation of chromosome 18-specific brain transcripts as positional candidates for bipolar disorder (1997)

Several studies have proposed the existence of susceptibility loci for bipolar disorder on chromosome 18. To identify possible candidate genes for this disease, we isolated brain-expressed transcripts by direct cDNA selection on chromosome 18-specific biotinylated cosmid clones. Longer cognate cDNA clones of the selected cDNAs were isolated from a normalized infant brain cDNA library. Physical mapping by PCR on a panel of somatic cell hybrids was conducted by the use of primers derived from partial sequences on either the 5' or 3' ends of the clones. In our initial analysis, 48 cDNA clones were found to be chromosome 18-specific, mapping to different subchromosomal regions. Sequence redundancy among these clones yielded 30 unique transcripts, five of which were represented in previously known genes. Further sequencing of the remaining 25 unique cDNA clones confirmed the absence of significant homology to known genes, indicating that these transcripts represented novel genes. Mapping with the use of a radiation hybrid panel positioned the brain cDNAs to within = 100 to 1100 kb from reference sequence tag sites (STSs) and assembled them into six high resolution linkage groups. The majority of the transcripts were found to cluster to discrete locations on 18p and 18q, previously hypothesized as susceptibility regions for bipolar disorder, identifying them as positional candidate genes.
Enhancement of human B cell proliferation and differentiation by tumor necrosis factor-alpha and interleukin 1. (1987)

The role of tumor necrosis factor-alpha (TNF-alpha) in human B cell responses was examined and compared with that of interleukin (IL) 1 by assessing the ability of each cytokine to support proliferation and differentiation. Recombinant TNF-alpha (rTNF-alpha) and recombinant IL-1 (rIL-1) each enhanced the generation of immunoglobulin-secreting cells (ISC) in cultures of pokeweed mitogen-stimulated B cells incubated with T cells. To examine the direct effect of rTNF-alpha and rIL-1 on the responding B cell, highly purified peripheral blood B cells were stimulated with Cowan I Staphylococcus aureus (SA). In the absence of T cell factors, proliferation was minimal and there was no generation of ISC. Recombinant IL-2 (rIL-2) supported both responses. Although rTNF-alpha alone did not support SA-stimulated generation of ISC, it did increase SA-stimulated B cell DNA synthesis by two- to eightfold. In addition, rTNF-alpha augmented B cell proliferation in rIL-2 supported SA-stimulated cultures. Moreover, rTNF-alpha enhanced the generation of ISC stimulated by rIL-2 alone or rIL-2 and SA. rIL-1 also augmented DNA synthesis and generation of ISC by B cells stimulated with SA and rIL-2. However, rTNF-alpha enhanced proliferation and ISC generation in SA + rIL-2-stimulated cultures even when they were supplemented with saturating concentrations of rIL-1. Utilizing a two-stage culture system, it was found that the major effect of rTNF-alpha was to enhance responsiveness of SA-activated B cells to rIL-2, whereas it exerted only a minimal effect during initial stimulation. These results indicate that TNF-alpha as well as IL-1 augment B cell responsiveness. Moreover, the ability of rTNF-alpha to enhance B cell responsiveness was not an indirect effect resulting from the induction of Il-1 production by contaminating monocytes, but rather resulted from the delivery of a signal by rTNF-alpha directly to the responding B cell that promoted both proliferation and differentiation after initial activation. The data therefore indicate that human B cell responsiveness can be independently regulated by the action of two separate monocyte-derived cytokines.
Globus pallidus internus deep brain stimulation for dystonic conditions: A prospective audit (2003)

In the current era of functional surgery for movement disorders, deep brain stimulation (DBS) of the globus pallidus internus (GPi) is emerging as the favoured target in the treatment of patients with dystonia. The results of 25 consecutive patients with medically intractable dystonia (12 with generalised dystonia, 7 with spasmodic torticollis, and 6 with other types of dystonia) treated with GPi stimulation are reported. Although comparisons were limited by differences in their respective neurological rating scales, chronic DBS benefited all groups, resulting in clear and progressive improvements in their condition. This study clearly demonstrates that DBS of the GPi provides amelioration of intractable dystonia.
Proton-transfer steps in Steglich esterification: a very practical new method for macrolactonization (1985)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTProton-transfer steps in Steglich esterification: a very practical new method for macrolactonizationEugene P. Boden and Gary E. KeckCite this: J. Org. Chem. 1985, 50, 13, 2394–2395Publication Date (Print):June 1, 1985Publication History Published online1 May 2002Published inissue 1 June 1985https://pubs.acs.org/doi/10.1021/jo00213a044https://doi.org/10.1021/jo00213a044research-articleACS PublicationsRequest reuse permissionsArticle Views6653Altmetric-Citations402LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Loss of Catheter Locking Solution Caused by Fluid Density (2005)

The avoidance of clotting in catheter lumina between treatments usually entails locking with an anticoagulant solution such as heparin. In a previous work, it was shown that approximately 20% of locking solution flows from the catheter during instillation of the lock equal in volume to the lumen volume. Furthermore, the locking solution may spill into the blood stream under the influence of gravity. This work investigates the influence of density and viscosity of the locking solution on the volume and speed of locking solution loss from the catheter lumen. A large fraction of the catheter locking solution spills under the influence of gravity if the locking solution's density is higher than the fluid it spills to (blood). Locking solution lost is replaced by blood. Viscosity delays this process, but at 90 minutes after injection, the loss is completed even when highly viscous lock solutions are used. Slow administration of the lock has negligible influence upon the dynamics of the loss.
Localization of immunoreactive epidermal growth factor receptors in human nervous system. (1988)

Epidermal growth factor is a well-defined peptide which stimulates cell growth and elicits cell responses in a variety of tissues by binding to specific receptors, EGF-R. A specific antiserum against the EGF receptor, which has previously been used to characterize EGF-R in human skin, fibroblasts, and smooth muscle, was used to survey the distribution of EGF-R in human nervous system. Portions of formalin-fixed, paraffin-embedded autopsy specimens were examined by use of immunohistochemical staining (PAP technique) with EGF-R antiserum. Many types of nerve cells, e.g., cerebral cortical pyramidal cells, hippocampal pyramidal cells, Purkinje cells, anterior horn cells, and dorsal root ganglion neurons, contained immunoreactive EGF-R. However, immunoreactive EGF-R were not detected in astrocytes, oligodendrogliocytes, and other small neurons such as granule cells. Intense immunostaining for EGF-R was also detected in ependymal cells from choroidal and extrachoroidal locations. Although immunoreactive EGF-R is widely distributed in human nervous system, the functional role of EGF and its receptor in the nervous system remains unknown.
Advancing the Molecular Diagnosis of Thyroid Nodules: Defining Benign Lesions by Molecular Profiling (2005)

Background: Thyroid nodules are common and most are benign. Previous data from our laboratory and others has suggested that gene profiling can accurately distinguish between benign and malignant thyroid nodules and provide new leads in the study of thyroid tumorigenesis. Current preoperative techniques do not permit distinction between neoplastic and hyperplastic follicular neoplasms. These studies were undertaken to determine whether benign follicular tumors could be subcategorized by molecular profiling. Methods: Molecular profiles of 8 follicular adenomas and 8 hyperplastic nodules were analyzed by oligonucleotide microarray analysis. A list of 402 differentially expressed genes was produced based on a comparison of these two groups. Seven additional benign follicular lesions were then added to the analysis. A hierarchical clustering analysis was performed on all 23 samples, utilizing the gene list generated from the test set, to examine the groups for potential differences and the ability of the gene list to distinguish tumor types. Results: Cluster analysis of all 23 samples produced two distinct groups, one containing the adenomas and one containing the hyperplastic lesions. The analysis was able to identify follicular adenomas with a sensitivity of 84.6% and a specificity of 100%. Conclusions: These data indicate that benign thyroid lesions can be separated into distinct groups through molecular profiling. Analysis of the gene list may help further the understanding of thyroid tumorigenesis. Expression profiling may ultimately allow us to distinguish potentially malignant from benign follicular nodules.
On the role of the incretin hormones GIP and GLP-1 in the pathogenesis of Type 2 diabetes mellitus. (2004)

BACKGROUND In 1906, extracts of mucosa from the porcine upper small intestine were used by Moore et al. as a treatment for diabetes, hoping that “the pancreas secretion might be stimulated by the substance of the nature of a hormone yielded by the duodenal mucosa membrane” (1). In 1932, La Barre named the unidentified substance thought to exert this effect “incretin” (2). Thirty years later, McIntyre et al. demonstrated that gut derived factors have a potentiating effect on insulin secretion after ingestion of glucose (3). Some years later, a polypeptide was discovered and named gastric inhibitory polypeptide (GIP) because of its inhibitory effect on gastric acid secretion in dogs (4). Eventually, it was shown to be insulinotropic at elevated glucose concentrations (5-7). Its gastric inhibitory effects were weak (8, 9) and it was, therefore, suggested that GIP should be renamed “glucose-dependent insulinotropic polypeptide” (5-7). Today, both names are still in use. Later, experimental and clinical studies suggested that the gut produces more than a single insulinotropic hormone (10, 11). In 1983, the gene encoding the human pancreatic hormone, glucagon, was cloned, and the structure of its precursor, proglucagon, was deduced and shown to include the sequence of two glucagon-like peptides, in addition to glucagon itself (12). The gene was found to be expressed in both the pancreatic α-cells and the intestinal L-cells. The primary transcripts and translation products of the gene in the two types of cells are identical (13), but the post-translational processing differs markedly in these two tissues (14-16). In the pancreas proglucagon is cleaved to glucagon, glicentin-related pancreatic peptide (GRPP) and a major proglucagon fragment (14). Apart from glucagon, all of these fragments seem to be biologically inactive (17). In contrast, in the intestinal L-cells, the molecule is processed to GLP-1 (glucagon-like peptide-1), GLP-2 (glucagon-like peptide-2) (18) and glicentin (19) (Figure 1). GLP-1 was found to be strongly insulinotropic (20, 21) and GLP-2 to be a key regulator of small bowel growth (22). Today, therefore, we have two major incretin hormones: glucosedependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), which together are thought to be responsible for the incretin effect. The incretin effect is quantitated by comparison of the insulin response after oral and intravenous glucose, administered in such a way that identical blood glucose concentrations are obtained (23-26) .
Immunohistochemical Analysis of MUC5B Apomucin Expression in Breast Cancer and Non-malignant Breast Tissues (2005)

A deregulation of several MUC genes (MUC1, MUC2, MUC3, MUC5AC, and MUC6) was previously demonstrated in breast carcinomas. Considering that recently we found the "non-mammary" MUC5B mRNA in primary breast tumors (Berois et al. 2003), we undertook the present study to evaluate the expression profile of MUC5B protein product in breast tissues, using LUM5B-2 antisera raised against sequences within the non-glycosylated regions of this apomucin. Expression of MUC5B by breast cancer cells was confirmed by immunocytochemistry, in situ hybridization, and Western blot on MCF-7 cancer cells. Using an immunohistochemical procedure, MUC5B apomucin was detected in 34/42 (81%) primary breast tumors, in 13/14 (92.8%) samples of non-malignant breast diseases, in 8/19 (42.1%) samples of normal-appearing breast epithelia adjacent to cancer, and in 0/5 normal control breast samples. The staining pattern of MUC5B was very different when comparing breast cancer cells (cytoplasmic) and non-malignant breast cells (predominantly apical and in the secretory material). We analyzed MUC5B mRNA expression using RT-PCR in bone marrow aspirates from 22/42 patients with breast cancer to compare with MUC5B protein expression in the primary tumors. Good correlation was observed because the six MUC5B-positive bone marrow samples also displayed MUC5B expression in the tumor. Our results show, for the first time at the protein level, that MUC5B apomucin is upregulated in breast cancer. Its characterization could provide new insights about the glycobiology of breast cancer cells.
An evaluation of four methods for measuring cholesterol absorption by the intestine in man (1971)

Critical comparisons have been made in 12 patients of four methods for measuring cholesterol absorption from the intestine. Methods I-III depend on the use of labeled cholesterol (intravenously or continuous labeling orally) in conjunction with sterol balance measurements; Method IV can be carried out with only a single test dose containing labeled cholesterol plus labeled beta-sitosterol. In the latter technique absorption is calculated as the loss of cholesterol relative to beta-sitosterol during intestinal transit. Method III (isotopic steady-state method) proved to be undependable because of uncertainties in determining the existence of an isotopic steady state. However, Method IV gave good agreement with Methods I and II, and it appears to have certain practical as well as theoretical advantages. Although Method IV requires collections of stools for up to 8 days, it is nevertheless the most rapid and the simplest of all the methods for estimating absorption. It can also be used in certain situations, such as in fur-licking animals, when Methods I and II are inadequate. Therefore, this method would seem to be a valuable addition to other isotopic techniques for estimating cholesterol absorption in man.
Novel glutamic acid-derived cholecystokinin receptor ligands (1990)

Novel aryl amide analogues of glutamic acid dialkylamide have been synthesized to test for a possible structural analogy between glutamic acid and benzodiazepine CCK antagonists such as compounds 2 and 24 (lorglumide and MK-329, respectively). In support of the structural model, certain of these hybrid compounds are more potent in pancreas CCK radioligand binding assays than corresponding lorglumide-type reference compounds. Modifications previously found in the benzodiazepine antagonists to result in brain CCK/gastrin receptor selectivity were also incorporated to produce an aryl urea series of glutamic acid analogues. None of these compounds were brain CCK/gastrin selective; however, one was potent and selective in the pancreas binding assay. The model appears to be most useful in the design of selective ligands for the pancreas type CCK receptor.