gebhart/patrepeval huggingface dataset:
TRPM8 in prostate cancer cells: a potential diagnostic and prognostic marker with a secretory function? (2006)

During the past 5 years it has emerged that the transient receptor potential (TRP) family of Ca(2+)-and Na(+)-permeable channels plays a diverse and important role in cell biology and in pathology. One member of this family, TRPM8, is highly expressed in prostate cancer cells but the physiological and pathological functions of TRPM8 in these cells are not known. Here we address these questions, and the issue of whether or not TRPM8 is an effective diagnostic and prognostic marker in prostate cancer. TRPM8 is known to be activated by cool stimuli (17-25 degrees C) and cooling compounds such as menthol. The activation mechanism(s) involves voltage sensing of membrane potential, phosphatidylinositol 4,5-bisphosphate and Ca(2+). In addition to prostate cancer cells, TRPM8 is expressed in sensory neurons where it acts as a sensor of cold. In prostate epithelial cells, expression of TRPM8 is regulated by androgen and is elevated in androgen-sensitive cancerous cells compared with normal cells. While there is some evidence that in prostate cancer cells Ca(2+) and Na(+) inflow through TRPM8 is necessary for survival and function, including secretion at the apical membrane, the function of TRPM8 in these cells is not really known. It may well differ from the role of TRPM8 as a cool sensor in sensory nerve cells. Androgen unresponsive prostate cancer is difficult to treat effectively and there are limited diagnostic and prognostic markers available. TRPM8 is a potential tissue marker in differential diagnosis and a potential prognostic marker for androgen-unresponsive and metastatic prostate cancer. As a consequence of its ability to convey Ca(2+) and Na(+) and its expression in only a limited number of cell types, TRPM8 is considered to be a promising target for pharmaceutical, immunological and genetic interventions for the treatment of prostate cancer.
Intravesicular Localization and Exocytosis of α-Synuclein and its Aggregates (2005)

Alpha-synuclein (alpha-syn), particularly in its aggregated forms, is implicated in the pathogenesis of Parkinson's disease and other related neurological disorders. However, the normal biology of alpha-syn and how it relates to the aggregation of the protein are not clearly understood. Because of the lack of the signal sequence and its predominant localization in the cytosol, alpha-syn is generally considered exclusively an intracellular protein. Contrary to this assumption, here, we show that a small percentage of newly synthesized alpha-syn is rapidly secreted from cells via unconventional, endoplasmic reticulum/Golgi-independent exocytosis. Consistent with this finding, we also demonstrate that a portion of cellular alpha-syn is present in the lumen of vesicles. Importantly, the intravesicular alpha-syn is more prone to aggregation than the cytosolic protein, and aggregated forms of alpha-syn are also secreted from cells. Furthermore, secretion of both monomeric and aggregated alpha-syn is elevated in response to proteasomal and mitochondrial dysfunction, cellular defects that are associated with Parkinson's pathogenesis. Thus, intravesicular localization and secretion are part of normal life cycle of alpha-syn and might also contribute to pathological function of this protein.
Lectins as Bioactive Plant Proteins: A Potential in Cancer Treatment (2005)

Plant lectins, a unique group of proteins and glycoproteins with potent biological activity, occur in foods like wheat, corn, tomato, peanut, kidney bean, banana, pea, lentil, soybean, mushroom, rice, and potato. Thus, dietary intakes by humans can be significant. Many lectins resist digestion, survive gut passage, and bind to gastrointestinal cells and/or enter the circulation intact, maintaining full biological activity. Several lectins have been found to possess anticancer properties in vitro, in vivo, and in human case studies; they are used as therapeutic agents, preferentially binding to cancer cell membranes or their receptors, causing cytotoxicity, apoptosis, and inhibition of tumor growth. These compounds can become internalized into cells, causing cancer cell agglutination and/or aggregation. Ingestion of lectins also sequesters the available body pool of polyamines, thereby thwarting cancer cell growth. They also affect the immune system by altering the production of various interleukins, or by activating certain protein kinases. Lectins can bind to ribosomes and inhibit protein synthesis. They also modify the cell cycle by inducing non-apoptotic G1-phase accumulation mechanisms, G2/M phase cell cycle arrest and apoptosis, and can activate the caspase cascade. Lectins can also downregulate telomerase activity and inhibit angiogenesis. Although lectins seem to have great potential as anticancer agents, further research is still needed and should include a genomic and proteomic approach.
Pregnancy by Means of Tubal Insemination and Subsequent Spontaneous Pregnancy in Rabbits (1992)

The purpose of the study was to determine whether or not physical stimulation by tubal insemination had any unfavourable influences upon the tubal fimbria. Tubal insemination was carried out on 14 rabbits and subsequent pregnancy results were monitored. After a period of 69-123 days following tubal insemination, 10 of the rabbits were mated spontaneously and these rabbits were then monitored for pregnancy. Newborn were obtained, with normal gestation periods in six out of the 14 rabbits, following tubal insemination and all 10 of the rabbits that were mated spontaneously with males following tubal insemination subsequently delivered. It is concluded that physical stimulation by tubal insemination does not produce adhesive changes on the tubal fimbria.
Transforming variant of Met receptor confers serum independence and anti-apoptotic property and could be involved in the mouse thymic lymphomagenesis (2004)

Met tyrosine kinase receptor, the receptor of hepatocyte growth factor/scatter factor (HGF/SF), is present in mouse tissues as two major isoforms differing by a 47-aminoacid segment in the juxtamembrane domain via alternative splicing of exon 14. We found that the smaller isoform of Met (Sm-Met) was highly transformable in both in vitro and in vivo tumorigenesis assays. In this report, close examination of the transforming activity of the Sm-Met showed that the expression of Sm-Met conferred the cells serum independence and anti- apoptotic property when treated with doxorubicin. These properties of Sm-Met seemed to be originated from its far longer maintenance of tyrosine kinase activity after the binding of HGF/SF. Interestingly, the longer maintenance of activated status was accompanied with more increase of tyrosine phosphorylation of Stat3 protein. Moreover, we have tried to find (an) animal tumorigenesis model(s) showing the increase in the expression of this transforming variant of Met. In gamma-ray-induced mouse thymic lymphoma model, the expression of the mRNAs for Sm-Met was significantly increased as well as those of wild type Met and HGF/SF, suggesting a possible role of the Sm-Met in tumorigenesis in vivo.
Superficial Bladder Cancer Therapy (2004)

Bladder cancer treatment remains a challenge despite significant improvements in preventing disease progression and improving survival. Intravesical therapy has been used in the management of superficial transitional cell carcinoma (TCC) of the urinary bladder (i.e. Ta, T1, and carcinoma in situ) with specific objectives which include treating existing or residual tumor, preventing recurrence of tumor, preventing disease progression, and prolonging survival. The initial clinical stage and grade remain the main determinant factors in survival regardless of the treatment. Prostatic urethral mucosal involvement with bladder cancer can be effectively treated with Bacillus Calmette-Guerin (BCG) intravesical immunotherapy. Intravesical chemotherapy reduces short-term tumor recurrence by about 20%, and long-term recurrence by about 7%, but has not reduced progression or mortality. Presently, BCG immunotherapy remains the most effective treatment and prophylaxis for TCC (Ta, T1, CIS) and reduces tumor recurrence, disease progression, and mortality. Interferons, Keyhole-limpet hemocyanin (KLH), bropirimine and Photofrin-Photodynamic Therapy (PDT) are under investigation in the management of TCC and early results are encouraging. This review highlights and summarizes the recent advances in therapy for superficial TCC.
Mutations in the SH3 domain of the src oncogene which decrease association of phosphatidylinositol 3'-kinase activity with pp60v-src and alter cellular morphology (1992)

To analyze the signaling pathways utilized in malignant transformation by pp60v-src, we have isolated and characterized src mutants which possess normal levels of protein tyrosine kinase activity but which cause only a partially transformed phenotype. Our hypothesis is that such mutants are partially defective for transformation because they are defective in their ability to activate specific components of the cellular signaling machinery while still activating others. In this communication, we report on the molecular and biochemical characterization of one such mutant, CU12 (D. D. Anderson, R. P. Beckmann, E. H. Harms, K. Nakamura, and M. J. Weber, J. Virol. 37:455-458, 1981). Cells infected with this mutant are capable of anchorage-independent growth, but rather than exhibiting the rounded and refractile morphology characteristic of wild-type-infected cells, they display an extremely elongated, fusiform morphology. The morphological properties of this mutant src could be accounted for entirely by a single mutation in the SH3 domain (lysine 106 to glutamate). Other mutations were constructed in this region by in vitro mutagenesis, both in a v-src and in an activated c-src background, and several of them also induced a fusiform morphology. All of the mutations inducing fusiform morphology also resulted in decreased association of pp60src with phosphatidylinositol 3'-kinase activity. In addition, association of pp60src with some tyrosine-phosphorylated proteins was altered. We propose that the SH3 domain participates (along with the SH2 domain) in the interaction of pp60src with cellular signaling proteins, and we speculate that the association with phosphatidylinositol 3'-kinase plays an important role in the regulation of cellular morphology.
A neutralizing antibody-inducing peptide of the V3 domain of feline immunodeficiency virus envelope glycoprotein does not induce protective immunity (1994)

Specific-pathogen-free cats, immunized with a 22-amino-acid synthetic peptide designated V3.3 and derived from the third variable region of the envelope glycoprotein of the Petaluma isolate of feline immunodeficiency virus (FIV), developed high antibody titers to the V3.3 peptide and to purified virus, as assayed by enzyme-linked immunoassays, as well as neutralizing antibodies, as assayed by the inhibition of syncytium formation in Crandell feline kidney cells. V3.3-immunized animals and control cats were challenged with FIV and then monitored for 12 months; V3.3 immunization failed to prevent FIV infection, as shown by virus isolation, anti-whole virus and anti-p24 immunoglobulin G antibody responses, and positive PCRs for gag and env gene fragments. Sequence analysis of the V3 region showed no evidence for the emergence of escape mutants that might have contributed to the lack of protection. The sera of the V3.3-hyperimmunized cats and two anti-V3.3 monoclonal antibodies neutralized FIV infectivity for Crandell feline kidney cells at high antibody dilutions but paradoxically failed to completely neutralize FIV infectivity at low dilutions. Moreover, following FIV challenge, V3.3-immunized animals developed a faster and higher antiviral antibody response than control cats. This was probably due to enhanced virus replication, as also suggested by quantitative PCR data.
High-power pseudospark and BLT switches (1988)

A review is presented of recent developments in a new group of high-power hollow-electrode switches, including the pseudospark and the backlighted thyratron (BLT). Experiments demonstrate that for several key high-power switching performance factors, the pseudospark and BLT switches are superior to either high-pressure spark gap switches or thyratrons or, in some cases, both. High performance has been demonstrated in peak current (>100 kA), current rate of rise (>10/sup 12/ A/s), switching precision, trigger efficiency, current reversal (100%), and recovery time. Several electrical and optical trigger methods have been demonstrated and are described.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Blasenentleerungsstörungen bei Encephalomyelitis disseminata - medikamentöse und interventionelle Therapieoptionen (1995)

Patients with disseminated encephalomyelitis have various urological presentations, ranging from pollakisuria to urge incontinence. After detailed evaluation (neuro-urological examination, urodynamic investigation) drug therapy and various interventional methods must be adapted to the individual manifestations. Patients with detrusor hyperreflexia are treated with oral anticholinergic agents (oxybutynin, trospium chloride, propiverine). Patients with urinary retention are recommended to be managed with clean intermittent (self)-catheterisation. The various interventional therapeutic options (bladder denervation, electrostimulation, local treatment with botulinum toxin) and the surgical therapy (sacral deafferentation and anterior root stimulation, bladder neck closure and cystostomy, sphincterotomy or augmentation cystoplasty) must be reserved for special cases.
l-Ornithine affects peripheral clock gene expression in mice (2016)

The peripheral circadian clock is entrained by factors in the external environment such as scheduled feeding, exercise, and mental and physical stresses. In addition, recent studies in mice demonstrated that some food components have the potential to control the peripheral circadian clock during scheduled feeding, although information about these components remains limited. l-Ornithine is a type of non-protein amino acid that is present in foods and has been reported to have various physiological functions. In human trials, for example, l-ornithine intake improved a subjective index of sleep quality. Here we demonstrate, using an in vivo monitoring system, that repeated oral administration of l-ornithine at an early inactive period in mice induced a phase advance in the rhythm of PER2 expression. By contrast, l-ornithine administration to mouse embryonic fibroblasts did not affect the expression of PER2, indicating that l-ornithine indirectly alters the phase of PER2. l-Ornithine also increased plasma levels of insulin, glucose and glucagon-like peptide-1 alongside mPer2 expression, suggesting that it exerts its effects probably via insulin secretion. Collectively, these findings demonstrate that l-ornithine affects peripheral clock gene expression and may expand the possibilities of L-ornithine as a health food.
Antitumour and antimicrobial activities of endophytic streptomycetes from pharmaceutical plants in rainforest (2008)

These endophytic streptomycetes are precious resources obtained from rainforests, and they could be a promising source for bioactive agents.
A Prospective Study to Determine Whether Cover Gowns in Addition to Gloves Decrease Nosocomial Transmission of Vancomycin-Resistant Enterococci in an Intensive Care Unit (2002)

Our data lend support to current HICPAC recommendations for the use of cover gowns to decrease nosocomial transmission of VRE.
Two‐Photon Excitation of Quantum‐Dot‐Based Fluorescence Resonance Energy Transfer and Its Applications (2007)

Nonradiative fluorescence resonance energy transfer (FRET) between a luminescent quantum dot (QD) donor and a proximal dye brought in close proximity of the QD surface via conjugation with a dye-labeled peptide (or a protein) is shown (see figure). The system is excited with near IR irradiation (well below the absorption band of the QD), via a fast two-photon process, which produces a FRET signal with very low background contribution due to a substantially reduced nonlinear direct excitation of the dye. Supporting information for this article is available on the WWW under http://www.wiley-vch.de/contents/jc_2089/2007/c2036_s.pdf or from the author. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Nitric oxide regulates nitric oxide synthase-2 gene expression by inhibiting NF-κB binding to DNA (1997)

Treatment of astroglial cells with interleukin 1beta and interferon gamma transcriptionally activates the nitric oxide synthase (NOS)-2 gene. The duration of mRNA expression is brief because of transcript instability. In addition, NO donors reduce the expression of NOS-2 mRNA dramatically by reducing the rate of transcription. In this study we observed that the NO donor, spermine NONOate did not inhibit the activation and translocation of NF-kappaB, a key transcription factor in the induction of NOS-2, but inhibited formation of the NF-kappaB-DNA complex. This effect was reversed by methaemoglobin (acting as an NO trap) and by the reducing agent dithiothreitol. Formation of the interferon-regulatory factor-DNA complex was unaffected by NO. These results suggest that NO can modulate its own production by interfering with NF-kappaB interaction with the promoter region of the NOS gene, a negative feedback effect that may be important for limiting NO production in vivo.
Cytogenetic deletion maps of hematologic neoplasms: Circumstantial evidence for tumor suppressor Loci (1993)

Research in oncogenetics has led to the identification of two major classes of tumor-associated genes, oncogenes and tumor suppressor genes. In a wide variety of solid tumor types, mutations of both groups of genes have been implicated in the tumorigenic process. In hematologic neoplasms, on the other hand, most attention has focused on illegitimate activation of oncogenes, e.g., deregulation leading to disturbed transcriptional activity and structural rearrangements resulting in hybrid genes. Whether loss or mutational inactivation of tumor suppressor genes also plays an essential role in the genesis of tumors of the hematopoietic system has received less attention. Because such inactivation can be the result of karyotypically detectable loss of chromosomal material, cytogenetic studies may prove helpful in pinpointing genomic sites that harbor tumor suppressor genes. The present study is based on a total of 12,473 cytogenetically abnormal hematologic neoplasms reported in the literature to date. Among these, we selected the 6,422 cases with sole clonal chromosomal abnormalities in order to include only aberrations of importance in the genesis, rather than in the progression, of these neoplasms. All tumors with monosomies or structural abnormalities resulting in loss of chromosomal material were compiled, and for every such structural aberration, i.e., deletion, unbalanced translocation, isochromosome, and ring chromosome, the chromosome bands lost were ascertained. This cytogenetic deletion mapping revealed that the most commonly lost chromosomes were Y and 7 in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and chronic myeloproliferative disorders (MPD); X, Y, 7, 20, and 21 in acute lymphocytic leukemia (ALL); X, Y, and 17 in chronic lymphoproliferative disorders (LPD); and X and Y in non-Hodgkin's lymphoma (NHL). Chromosome segments/bands lost due to unbalanced structural abnormalities in at least 5% of the cases were 5q13-33, 7q22-36, 9q13-31, 11q23-25, 12p12-13, 17p11-13, and 20q11-13 in AML; 5q13-35 and 20q11-13 in MDS; 5q22-23, 7q22, 13q12-22, 17p11-13, and 20q11-13 in MPD; 6q15-27, 9p11-24, 12p12-13, and 19p13 in ALL; 6q16-27, 11q21-25, 13q13-14, and 14q32 in LPD; and 6q21-27, 11q13-25, and 14q24-32 in NHL. Based on these findings, three conclusions can be drawn. First, there is no good correspondence between total and partial monosomies, the only exception being -7 and 7q-, both of which are common in myeloid neoplasms. This indicates different pathogenetic effects of total and partial losses.(ABSTRACT TRUNCATED AT 400 WORDS)
Age-related changes in expression of neural cell adhesion molecule (NCAM) in heart: a comparative study of newborn, adult and aged rats. (1993)

The neural cell adhesion molecule (NCAM) has been implicated in cellular interactions involved in cardiac morphogenesis and innervation. In this study, expression of NCAM mRNA and protein was characterized in rat heart during postnatal development and aging (postnatal days 1, 10, 40, 270, and 730). Alternative splicing of NCAM mRNA was analyzed by Northern blotting using DNA oligonucleotide probes designed for demonstration of certain exons or exon combinations. Total NCAM mRNA was downregulated during postnatal development followed by upregulation in the aging heart. Three major NCAM mRNA classes of 6.7, 5.2 and 2.9 kb were expressed in newborn heart in approximately equal proportions. At all other ages, the mRNAs of 5.2 and 2.9 kb were more predominant than the 6.7 kb mRNA. During postnatal development and aging, expression of exon VASE was selectively downregulated in the 6.7 kb NCAM mRNA class, whereas it was clearly detectable in NCAM mRNA classes of 5.2 and 2.9 kb. Insertion of exons a and AAG between exons 12 and 13 was more pronounced in the 5.2 and 2.9 kb NCAM mRNAs than in the 6.7 kb mRNA at all ages. Insertions at the 12/13 junctions decreased in the 6.7 kb mRNA as compared to the 5.2 and 2.9 kb mRNAs during postnatal development. Quantification of NCAM protein by enzyme-linked immunosorbent assay showed that NCAM protein amount decreased from a level of 0.93 microgram NCAM/mg total protein at birth to postnatal day 40 where a level of 0.21 microgram NCAM/mg total protein was found. During aging, NCAM increased again to 0.34 micrograms NCAM/mg total protein at postnatal day 730. NCAM isoforms were studied by immunoblotting analysis. At all ages, the major NCAM isoforms of 190, 145 and 120 kDa were observed in heart, the 145 kDa isoform being predominant.(ABSTRACT TRUNCATED AT 250 WORDS)
Intersubband absorption in a modulation-doped Ga0.47In0.53As/Al0.48In0.52As multiple quantum well structure (1988)

We observe strong intersubband absorption at a wavelength of 8.4 μm in an n-type modulation-doped Ga0.47In0.53As/Al0.48In0.52As multiple quantum well structure with a well thickness of 8.2 nm. An oscillator strength of the corresponding dipole transition of 21.0 is measured. The dependence of the intersubband absorption on the polarization of the incident light and on lattice temperature is investigated in detail.
The Yeast SPC22/23 Homolog Spc3p Is Essential for Signal Peptidase Activity (1997)

In eucaryotic cells signal sequences of secretory and membrane proteins are cleaved by the signal peptidase complex during their transport into the lumen of the endoplasmic reticulum. The signal peptidase complex in yeast consists of four subunits. To date, three of these subunits have been functionally characterized. One of them, the Sec11p, is essential for viability of yeast cells. It shows significant homology to the mammalian SPC18 and SPC21 as well as to bacterial leader peptidases. Two other subunits, Spc1p and Spc2p, have been shown to be homologous to mammalian SPC12 and SPC25, respectively, and are not essential for protein translocation or signal peptide cleavage. We have purified and analyzed the fourth subunit of yeast signal peptidase, Spc3p. The protein is essential for viability of yeast cells. Depletion of SPC3 leads to accumulation of precursors of secretory proteins in vivo and to the loss of the signal peptidase activity in vitro. Therefore, in contrast to the bacterial leader peptidases, yeast signal peptidase requires a second subunit for its function.