gebhart/patrepeval huggingface dataset:
The tetraspanin protein, CD9, is expressed by progenitor cells committed to oligodendrogenesis and is linked to β1 integrin, CD81, and Tspan‐2 (2002)

Previous studies identified the tetraspanin protein CD9 in myelinating oligodendrocytes. The present report extends these observations by identifying CD9 in a subpopulation of oligodendrocyte progenitor cells (OPCs) and in premyelinating oligodendrocytes in rodents. NG2-positive cells expressed CD9 in a temporal and spatial pattern during development that was consistent with CD9 expression in OPCs just prior to their differentiation into premyelinating oligodendrocytes. NG2-positive cells in mature brains were CD9-negative. CD9 expression during oligodendrocyte development in vitro supported this hypothesis, as all CD9-positive cells became O4-positive when switched to oligodendrocyte differentiating media. CD9 immunoreactivity was enriched in myelinating oligodendrocytes and their processes, and the outer aspects of myelin internodes. Immunoprecipitation of CD9 from postnatal rat cerebrum coprecipitated beta1 integrin, CD81, and Tspan-2, another tetraspanin protein recently identified in oligodendrocytes. Following surface biotinylation of oligodendrocytes in vitro, biotinylated beta1 integrin was identified in a CD9 immunoprecipitate. These data support a molecular link between surface integrins and a CD9, Tspan-2 molecular web during the differentiation of oligodendrocytes. Oligodendrocyte production and myelination appears to be normal in CD9-deficient mice. These data support the hypothesis that CD9 helps form the tetraspanin web beneath the plasma membranes of progenitor cells committed to oligodendrogenesis, but that CD9 is not essential for oligodendrogenesis and myelination.
Glycated hemoglobin. Reaction and biokinetic studies. Clinical application of hemoglobin A1c in the assessment of metabolic control in children with diabetes mellitus. (1985)

The introduction briefly describes the necessity of maintaining a good metabolic control in children with diabetes mellitus. Thereupon, the object of the study is defined, viz. the wish to elucidate glycation of hemoglobin by means of reaction and biokinetic studies and to evaluate the applicability of the glycated hemoglobin fraction HbA1c in the clinical control of children with diabetes mellitus. In the subsequent historical section the most important studies on glycated hemoglobin are reviewed, with a particular view to the formation of this hemoglobin fraction and its clinical applicability. A brief description follows of the pathway in which hemoglobin A, via condensation with glucose, first forms a labile intermediate adduct, designated HbA1d, which is thereafter rearranged to the more stable HbA1c form. The methods used for determining glycated hemoglobin are described and their specificity assessed. In addition, an account is given of the reasons for choosing isoelectric focusing for a further elucidation of the glycation of hemoglobin. Among the results of the present studies it may be mentioned that by using the method of isoelectric focusing for separation of hemoglobin it is possible to: separate HbA1d and HbA1c and to determine the rate and equilibrium constants for the formation and dissociation of these glycated hemoglobin fractions; calculate, by the use of a biokinetic model, that HbA1c reflects the mean blood glucose concentration of the preceding 4 weeks; ascertain that HbA1c is preferable to HbA1 as a parameter for assessing the glycemic control; demonstrate that in children with newly diagnosed diabetes mellitus HbA1c is a useful index for defining the start and cessation of the remission period and for predicting the length of this period; demonstrate that HbA1c in children with diabetes mellitus is positively correlated to the clinical control and negatively correlated to linear growth; demonstrate a seasonal variation in the HbA1c substance fraction which shows the lowest level in the months of June and July; demonstrate that the transport of glucose across the erythrocyte membrane in children with diabetes mellitus is not notably affected by the glycemic control. The final section deals with the possibility whether glycation of hemoglobin and of other proteins can be a contributory cause of long-term diabetic complications.
Two Lineages of Mannose-Binding Lectin-Associated Serine Protease (MASP) in Vertebrates (1998)

Mannose-binding lectin-associated serine protease (MASP) is a newly identified member of the serine protease superfamily. MASP is involved in host defense against pathogens through a novel system of complement activation, designated the lectin pathway. To elucidate the origin of the lectin pathway and the molecular evolution of MASP, we cloned six MASP cDNAs from five vertebrate species going from mammal to cyclostome. An alignment of the amino acid sequences deduced from the cDNAs revealed the presence of two different lineages of the MASP gene. This classification was supported by the precise correlation with two types of exon organization for the protease domain. One of the two lineages is unique in that a single exon encodes the protease domain, unlike most other serine proteases. All members of this group, termed the AGY type, have an AGY codon at the active site serine. A phylogenetic tree suggests that the AGY type diverged from another lineage, termed the TCN type, before the emergence of primitive vertebrates. Furthermore, the presence of MASP or MASP-like sequences in most vertebrate species suggests that the lectin pathway functions extensively in vertebrates and that its origin is traced back to the invertebrate stage.
The Carbon-13 NMR Spectra and Electronic Structure of 3H-Phenothiazin-3-one and Its Methyl Derivatives (1984)

Abstract The 13C NMR chemical shifts of 3H-phenothiazin-3-one (1) and eleven of its methyl derivatives are reported. The effect of including sulfur 3d orbitals is discussed in relation to the 13C chemical shifts. The chemical shifts of 1 can be explained in terms of both the successive polarization of the long π-conjugated framework promoted by the carbonyl group and the contribution of the sulfur d-orbitals. The 13C chemical shifts gave a better correlation with the CNDO/2 π- and total electron densities calculated by means of the sp-basis set than by means of the spd-basis set, but an improved correlation was obtained by reducing the extent of d-orbital participation on sulfur. From the correlation of the 13C chemical shifts with the CNDO/2 sp π- and the total electron densities of all the carbons of 1 and monomethyl derivatives, the proportionality constants of −300 and −180 ppm/e respectively were obtained.
Fas-ligand (CD178) and TRAIL synergistically induce apoptosis of CD40-activated chronic lymphocytic leukemia B cells (2004)

Chronic lymphocytic leukemia (CLL) B cells become sensitive to Fas (CD95)-mediated apoptosis 3 to 5 days after CD40 ligation. However, CD4+ cytotoxic T lymphocytes (CTLs) can kill CLL B cells via a Fas-ligand (CD178)-dependent process within 24 hours after CD40 cross-linking, when ligation of CD95 alone is insufficient to induce apoptosis. In addition to CD95, CD40-activated CLL cells also express DR5, a receptor for tumor-necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) that is expressed by CD4+ CTL. In addition, CD40 ligation in vitro and in vivo induces CLL cells to express the proapoptotic protein, BH3 interacting domain death agonist (Bid), which can facilitate crosstalk between mitochondrial-dependent, apoptosis-inducing pathways and death receptors, such as death receptor 5 (DR5). To evaluate whether ligation of CD95 and/or DR5 can induce apoptosis of CD40-activated CLL cells, we generated artificial cytotoxic effector cells that express both human TRAIL and CD178 (Chinese hamster ovary [CHO]-CD178/TRAIL) or only TRAIL (CHO-TRAIL) or CD178 (CHO-CD178). CHO-CD178/TRAIL cells were significantly more effective in killing CD40-activated CLL cells than either CHO-TRAIL or CHO-CD178 and, unlike the latter, could kill CLL cells 24 hours after CD40 ligation. We conclude that CD40 ligation induces CLL cells to express the proapoptotic molecule Bid and the death receptors CD95 and DR5, the latter of which can act synergistically to induce caspase-dependent apoptosis of CD40-activated CLL B cells.
Adenovirus‐mediated gene transfer into tendon and tendon sheath (1996)

In this study, we successfully transferred the Escherichia coli beta-galactosidase gene. LacZ, into the chicken tendon and tendon sheath by a recombinant adenovirus. The recombinant adenovirus Adv-beta gal that carried the E. coli LacZ gene was constructed by homologous recombination in 293 cells (human transformed embryonic kidney) between the expressing vector and the ClaI large fragment of adenovirus 5 genome. Each chicken received a 10 microliters injection containing 10(5) plaque-forming units of recombinant virus Adv-beta gal. into the tendon sheath of the long toe Samples of tendon and tendon sheath were harvested at 3.30, and 75 days after the injection. The LacZ gene transfer was detected for its coding product beta-galactosidase by staining with X-gal solution. The results showed that all tendon and tendon sheath samples from the three harvest times stained positive (blue). The tendon sheath samples were more extensively stained; staining of the tendon was limited to the epitenon layer. These data suggest that a functional exogenous gene can potentially be transferred into the tendon and tendon sheath by similar techniques; such techniques may be used to improve healing and reduce adhesion formation.
Gene Targeting by Triple Helix‐Forming Oligonucleotides (2003)

Effective gene targeting reagents would have widespread utility for genomic manipulation including transgenic cell and animal construction and for gene therapy. They would also be useful in basic research as probes of chromatin structure, and as tools for studying the repair and mutagenesis of targeted DNA damage. We are developing triple helix-forming oligonucleotides (TFOs) for gene targeting in living mammalian cells. Challenges to TFO bioactivity include the impediments to the biochemistry of triplex formation presented by the physiological environment and the charge repulsion between the duplex and the third strand. In addition, there are biological constraints to target access imposed by mammalian chromatin structure. Here we describe the oligonucleotide modification format that appears to support biological activity of TFOs. In addition we show that manipulation of the cell biology, specifically the cell cycle, has a dramatic influence on TFO bioactivity.
Characterization of human cardiac myosin heavy chain genes (1989)

Micro-nano plastics originating from the prevalent usage of plastics have raised increasingly alarming concerns worldwide. However, there remains a fundamental knowledge gap in nanoplastics because of the lack of effective analytical ...Plastics are now omnipresent in our daily lives. The existence of microplastics (1 µm to 5 mm in length) and possibly even nanoplastics (<1 μm) has recently raised health concerns. In particular, nanoplastics are believed to be more toxic since their ...
Could chronic pain and spread of pain sensation be induced and maintained by glial activation? (2006)

An injury often starts with acute physiological pain, which becomes inflammatory or neuropathic, and may sometimes become chronic. It has been proposed recently that activated glial cells, astrocytes and microglia within the central nervous system could maintain the pain sensation even after the original injury or inflammation has healed, and convert it into chronic by altering neuronal excitability. Glial cell activation has also been proposed to be involved in the phenomenon of spread of pain sensation ipsilaterally or to the contralateral side (i.e. mirror image pain). Substance P and calcitonin gene-related peptide, released due to an inflammatory process, interact with the endothelial cells of the blood-spinal cord and blood-brain barriers. The barriers open partially and substances may influence adjacent glial cells. Such substances are also released from neurones carrying the 'pain message' all the way from the injury to the cerebral cortex. Pro-inflammatory cytokines may be released from the microglial cells, and astroglial Ca2+-transients or oscillations may spread within the astroglial networks. One theory is that Ca2+-oscillations could facilitate the formation of new synapses. These new synapses could establish neuronal contacts for maintaining and spreading the pain sensation. If this theory holds true, it is possible that Ca2+ waves, production of cytokines and growth factors could be modified by selective anti-inflammatory drugs to achieve a balance in the activities of the different intercellular and intracellular processes. This paper reviews current knowledge about glial mechanisms underlying the phenomena of chronic pain and spread of the pain sensation.
Novel approaches to treatment of advanced colorectal cancer with anti‐EGFR monoclonal antibodies (2006)

The standard treatment of metastatic colorectal cancer (mCRC) is combination of 5- fluorouracil/folinic acid with irinotecan or oxaliplatin-based chemotherapy. Epidermal growth factor receptor (EGFR) is overexpressed in 70%-80% of colorectal cancers (CRC). EGFR overexpression is known to be involved in carcinogenic processes, such as cell proliferation, apoptosis, angiogenesis and metastasis. Monoclonal antibodies targeting EGFR have shown antitumor activity and improved the efficacy of chemotherapy. Cetuximab is a chimeric immunoglobulin (Ig) G1 anti-EGFR monoclonal antibody (MoAb). Several clinical studies have shown cetuximab, either as a single agent or in combination with irinotecan, having promising efficacy in patients with metastatic CRC. Cetuximab with 5-fluorouracil/LV (leucovorin) plus irinotecan or oxaliplatin-based chemotherapy has shown higher response rate and longer time to progression as first-line treatment of mCRC. Currently, there are no data showing that addition of cetuximab would prolong overall survival in randomized studies. Panitumumab, a fully human IgG2 monoclonal antibody, has also shown antitumor activity against EGFR-expressing mCRC with less allergic reaction. Anti-EGFR MoAbs are well tolerated and have limited overlapping toxicities in combination with other cytotoxic drugs. The most common side effect of anti-EGFR MoAb is an acneform skin rash, which is a surrogate marker of efficacy of treatment with MoAbs. In this review, we will discuss the use of anti-EGFR MoAbs in the treatment of mCRC, with focus on cetuximab and panitumumab.
<title>Nuclear Magnetic Resonance (NMR) Imaging At Hammersmith Hospital</title> (1981)

Preliminary results have been obtained with two NMR imaging machines. High resolution images of anatomical cross sections can be produced with good soft tissue contrast and several tissue characteristics can be measured quantitatively. Functional studies are possible using paramagnetic materials as contrast agents, and blood flow effects can be readily demonstrated. NMR imaging therefore combines several features of other imaging methods in a single technique, which promises to make it a versatile tool for radiology.
Involvement of the mutated M protein in altered budding polarity of a pantropic mutant, F1-R, of Sendai virus (1996)

Wild-type Sendai virus buds at the apical plasma membrane domain of polarized epithelial MDCK cells, whereas a pantropic mutant, F1-R, buds at both the apical and basolateral domains. In F1-R-infected cells, polarized protein transport and the microtubule network are impaired. It has been suggested that the mutated F and/or M proteins in F1-R are responsible for these changes (M. Tashiro, J. T. Seto, H.-D. Klenk, and R. Rott, J. Virol. 67:5902-5910, 1993). To clarify which gene or mutation(s) was responsible for the microtubule disruption which leads to altered budding of F1-R, MDCK cell lines containing the M gene of either the wild type or F1-R were established. When wild-type M protein was expressed at a level corresponding to that synthesized in virus-infected cells, cellular polarity and the integrity of the microtubules were affected to some extent. On the other hand, expression of the mutated F1-R M protein resulted in the formation of giant cells about 40 times larger than normal MDCK cells. Under these conditions, the effects on the microtubule network were enhanced. The microtubules were disrupted and polarized protein transport was impaired as indicated by the nonpolarized secretion of gp80, a host cell glycoprotein normally secreted from the apical domain, and bipolar budding of wild-type and F1-R Sendai viruses. The mutated F glycoprotein of F1-R was transported bipolarly in cells expressing the F1-R M protein, whereas it was transported predominantly to the apical domain when expressed alone or in cells coexpressing the wild-type M protein. These findings indicate that the M protein of F1-R is involved in the disruption of the microtubular network, leading to impairment of cellular polarity, bipolar transport of the F glycoprotein, and bipolar budding of the virus.
Enantioselective syntheses of vinblastine, leurosidine, vincovaline and 20'-epi-vincovaline (1991)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTEnantioselective syntheses of vinblastine, leurosidine, vincovaline and 20'-epi-vincovalineMartin E. Kuehne, Patricia A. Matson, and William G. BornmannCite this: J. Org. Chem. 1991, 56, 2, 513–528Publication Date (Print):January 1, 1991Publication History Published online1 May 2002Published inissue 1 January 1991https://pubs.acs.org/doi/10.1021/jo00002a008https://doi.org/10.1021/jo00002a008research-articleACS PublicationsRequest reuse permissionsArticle Views1697Altmetric-Citations117LEARN 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-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
trans-10, cis-12 Conjugated Linoleic Acid Decreases Lipogenic Rates and Expression of Genes Involved in Milk Lipid Synthesis in Dairy Cows (2002)

Feeding conjugated linoleic acid (CLA) reduces milk fat synthesis in lactating dairy cows, and the effect has been shown to be specific for the trans-10, cis-12 CLA isomer. Our objectives were to examine potential mechanisms by which trans-10, cis-12 CLA inhibits milk fat synthesis. Multiparous Holstein cows (n = 4) in late lactation were used in a balanced 2 x 2 crossover design. Treatments consisted of a 5 d abomasal infusion of either skim milk (control) or purified trans-10, cis-12 CLA (13.6 g/d) emulsified in skim milk. On d 5 of infusion, mammary gland biopsies were performed and a portion of the tissue analyzed for mRNA expression of acetyl CoA carboxylase, fatty acid synthetase, delta 9-desaturase, lipoprotein lipase, fatty acid binding protein, glycerol phosphate acyltransferase and acylglycerol phosphate acyltransferase. Lipogenic capacity was evaluated with another portion of the tissue. Infusion of trans-10, cis-12 CLA decreased milk fat content and yield 42 and 48%, respectively and increased the trans-10, cis-12 CLA content in milk fat from < 0.1 to 4.9 mg/g. Reductions in milk fat content of C4 to C16 fatty acids contributed 63% to the total decrease in milk fat yield (molar basis). Analysis of the ratios of specific fatty acid pairs indicated trans-10, cis-12 CLA also shifted fatty acid composition in a manner consistent with a reduction in delta 9-desaturase. Mammary explant incubations with radiolabeled acetate established that lipogenic capacity was decreased 82% and acetate oxidation to CO2 was reduced 61% when cows received trans-10, cis-12 CLA. Infusing trans-10, cis-12 CLA also decreased the mRNA expression of all measured enzymes by 39 to 54%. Overall, data demonstrated the mechanism by which trans-10, cis-12 CLA inhibits milk fat synthesis includes decreasing expression of genes that encode for enzyme involved in circulating fatty acid uptake and transport, de novo fatty acid synthesis, desaturation of fatty acids and triglyceride synthesis.
Sensitisation to airborne moulds and severity of asthma: cross sectional study from European Community respiratory health survey (2002)

Sensitisation to moulds is a powerful risk factor for severe asthma in adults. This should be taken into account in primary prevention, management, and patients' education.
A simple subtractive hybridization technique employing photoactivatable biotin and phenol extraction (1988)

We report a simple method for nucleic acid subtractive hybridization, that involves hybridization of untreated and photobiotinylated DNA or RNA. After treatment with streptavidin and phenol, hybrids and single-stranded biotinylated material are sequestered to the aqueous/ organic interface while unhybridized material remains in the aqueous supematant. This procedure is simpler than published methods using either hydroxyapatite (HAP) chromatography (eg 1) or cupric-iminodiacetic acid agarose chromatography of biotinylated nucleic acid (2). The protocol given here is for subtraction of cDNA with RNA, but any combination of nucleic acid may be used.
Sodium cyanoborohydride in the immobilization of proteins to glutaraldehyde‐activated aminoalkyl silica (1983)

Abstract No Absrtact.
[Experimental study of acute spinal cord injury: a study of spinal blood flow]. (1993)

It is well known that the worsening of neurological findings after spinal cord injury is due to the secondary progression of pathological changes which may be caused by spinal cord blood flow disturbance. We measured spinal blood flow of 5mm rostrally and caudally distant portions from the injured point, using the laser Doppler flowmeter experimentally. Forty rats were used. Ten of these were used as a control group. And thirty animals were injured at the level of the tenth thoracic cord with a 50g epidural one minute compression method and measured continuously from 30 minutes before the injury to 6 hours after the injury. Twenty two surviving animals were evaluated. In the control group, spinal blood flow was stable. But in the injured group, spinal blood flow dropped by 30.6 + 9.8% on the rostral side and 37.3 + 17.6% on the caudal side in comparison with the resting value soon after the injury. Although the flow improved to 89.3 + 11.1 and 71.3 + 17.8% respectively 15 minutes later, it dropped again gradually and reached 42.8 + 14.1 and 66.2 + 16.4% respectively 6 hours after the injury had been inflicted. Lastly, in the animals, carbon perfusion was performed through the left ventricle. The normal figured vasculature in the preparation of the injured and measured portion was calculated with a microcomputer imaging analyzer and compared with control groups. The number of the normal vessels was significantly more abundant on the caudal side than on the rostral side (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)