gebhart/patrepeval huggingface dataset:
Macromolecular Trafficking Indicated by Localization and Turnover of Sucrose Transporters in Enucleate Sieve Elements (1997)

The leaf sucrose transporter SUT1 is essential for phloem loading and long-distance transport of assimilates. Both SUT1 messenger RNA (mRNA) and protein were shown to be diurnally regulated and to have high turnover rates. SUT1 protein was detected by immunolocalization in plasma membranes of enucleate sieve elements (SEs) in tobacco, potato, and tomato. Analysis by in situ hybridization showed that SUT1 mRNA localizes mainly to the SE and is preferentially associated with plasmodesmata. Antisense inhibition of SUT1 expression under control of a companion cell (CC)-specific promoter indicated synthesis of SUT1 mRNA in the CC. These results provide evidence for targeting of plant endogenous mRNA and potentially SUT1 protein through phloem plasmodesmata and for sucrose loading at the plasma membrane of SE.
Glial Tumor Invasion: A Role for the Upregulation and Cleavage of BEHAB/Brevican (2001)

Glial tumors, gliomas, are the most common primary intracranial tumors. Their distinct ability to invade the normal surrounding tissue makes them difficult to control and nearly impossible to completely remove surgically, and it accounts for the extraordinarily high lethality associated with gliomas. The ability of these transformed glial cells to invade the normal surrounding tissue is relatively unique in the adult CNS, which under most circumstances, is inhibitory to cell movement. The extracellular matrix (ECM) can modulate, in part, the permissiveness of a tissue to cell movement. Accordingly, the ability of gliomas to modify the ECM of the CNS may mediate the invasiveness of these cells. One ECM molecule that shows dramatic upregulation in gliomas is BEHAB (brain enriched hyaluronan binding)/brevican, a brain-specific chondroitin sulfate proteoglycan. BEHAB/brevican expression is also upregulated during periods of increased glial cell motility in development and following brain injury. Experimental evidence suggests that in glioma, in addition to upregulation of BEHAB/brevican, proteolytic processing of the full-length protein also may contribute to invasion. Here, the authors present a review of the literature on glial tumor invasion by modulation of the ECM and propose a two-step model for BEHAB/brevican's role in this process.
Field Tests of Specially Selected Air Conditioners for Hot Dry Climates (2008)

This paper presents the results of three field studies of residential air conditioners in Hot Dry Climates. These air conditioners were production units. The combinations of single speed outdoor condensing units, indoor coils, and furnaces were selected to meet specific performance criteria at hot dry conditions present in the southwestern United States. Eight manufacturers' units were tested in a pre-retrofit, post-retrofit experimental design. Each home was monitored over half a cooling season with a standard SEER 13 unit. The units were replaced with the Hot Dry units and monitoring continued for at least the second half of the summer. Most of the units performed sufficiently better than the baseline units to meet the goal of 20% energy savings and up to 34% peak reduction at system critical peak times. Characteristics common to the best performing units were brushless DC variable speed fan motors, more efficient heat exchangers, higher sensible heat ratio, and furnace fan control modifications.
The Impact of Treatment-Resistant Depression on Health Care Utilization and Costs (2002)

Treatment-resistant depression is costly and associated with extensive use of depression-related and general medical services. These findings underscore the need for early identification and effective long-term maintenance treatment for treatment-resistant depression.
Evolution and ecology of influenza A viruses (1992)

In this review we examine the hypothesis that aquatic birds are the primordial source of all influenza viruses in other species and study the ecological features that permit the perpetuation of influenza viruses in aquatic avian species. Phylogenetic analysis of the nucleotide sequence of influenza A virus RNA segments coding for the spike proteins (HA, NA, and M2) and the internal proteins (PB2, PB1, PA, NP, M, and NS) from a wide range of hosts, geographical regions, and influenza A virus subtypes support the following conclusions. (i) Two partly overlapping reservoirs of influenza A viruses exist in migrating waterfowl and shorebirds throughout the world. These species harbor influenza viruses of all the known HA and NA subtypes. (ii) Influenza viruses have evolved into a number of host-specific lineages that are exemplified by the NP gene and include equine Prague/56, recent equine strains, classical swine and human strains, H13 gull strains, and all other avian strains. Other genes show similar patterns, but with extensive evidence of genetic reassortment. Geographical as well as host-specific lineages are evident. (iii) All of the influenza A viruses of mammalian sources originated from the avian gene pool, and it is possible that influenza B viruses also arose from the same source. (iv) The different virus lineages are predominantly host specific, but there are periodic exchanges of influenza virus genes or whole viruses between species, giving rise to pandemics of disease in humans, lower animals, and birds. (v) The influenza viruses currently circulating in humans and pigs in North America originated by transmission of all genes from the avian reservoir prior to the 1918 Spanish influenza pandemic; some of the genes have subsequently been replaced by others from the influenza gene pool in birds. (vi) The influenza virus gene pool in aquatic birds of the world is probably perpetuated by low-level transmission within that species throughout the year. (vii) There is evidence that most new human pandemic strains and variants have originated in southern China. (viii) There is speculation that pigs may serve as the intermediate host in genetic exchange between influenza viruses in avian and humans, but experimental evidence is lacking. (ix) Once the ecological properties of influenza viruses are understood, it may be possible to interdict the introduction of new influenza viruses into humans.
Metformin Increases AMP-Activated Protein Kinase Activity in Skeletal Muscle of Subjects With Type 2 Diabetes (2002)

Metformin is an effective hypoglycemic drug that lowers blood glucose concentrations by decreasing hepatic glucose production and increasing glucose disposal in skeletal muscle; however, the molecular site of metformin action is not well understood. AMP-activated protein kinase (AMPK) activity increases in response to depletion of cellular energy stores, and this enzyme has been implicated in the stimulation of glucose uptake into skeletal muscle and the inhibition of liver gluconeogenesis. We recently reported that AMPK is activated by metformin in cultured rat hepatocytes, mediating the inhibitory effects of the drug on hepatic glucose production. In the present study, we evaluated whether therapeutic doses of metformin increase AMPK activity in vivo in subjects with type 2 diabetes. Metformin treatment for 10 weeks significantly increased AMPK alpha2 activity in the skeletal muscle, and this was associated with increased phosphorylation of AMPK on Thr172 and decreased acetyl-CoA carboxylase-2 activity. The increase in AMPK alpha2 activity was likely due to a change in muscle energy status because ATP and phosphocreatine concentrations were lower after metformin treatment. Metformin-induced increases in AMPK activity were associated with higher rates of glucose disposal and muscle glycogen concentrations. These findings suggest that the metabolic effects of metformin in subjects with type 2 diabetes may be mediated by the activation of AMPK alpha2.
Increased Incidence of Acute Kidney Injury with Aprotinin Use during Cardiac Surgery Detected with Urinary NGAL (2008)

Postoperative urinary NGAL - a novel marker for renal injury - is increased in cardiac surgical patients receiving aprotinin compared to patients receiving epsilon amino-caproic acid. These results further support the hypothesis that aprotinin may cause renal injury. The substantial rise of urinary NGAL associated with aprotinin use may in part be due to aprotinin blocking the uptake of NGAL by megalin/gp330 receptors in the proximal tubules.
Alarm Processing in Electrical Power Systems Through a Neuro-Fuzzy Approach (2004)

This work presents a methodology that combines the use of artificial neural networks and fuzzy logic for alarm processing and identification of faulted components in electrical power systems. Fuzzy relations are established and form a database employed to train artificial neural networks. The artificial neural networks inputs are alarm patterns, while each output neuron is responsible for estimating the degree of membership of a specific system component into the class of faulted components. The proposed method allows good interpretation of the results, even in the presence of difficult corrupted alarm patterns. Tests are performed with a test system and with part of a real Brazilian system.
Genetic Mechanisms in Apc-Mediated Mammary Tumorigenesis (2009)

Many components of Wnt/beta-catenin signaling pathway also play critical roles in mammary tumor development, yet the role of the tumor suppressor gene APC (adenomatous polyposis coli) in breast oncongenesis is unclear. To better understand the role of Apc in mammary tumorigenesis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-cre and WAP-cre transgenic mice that express Cre-recombinase in mammary progenitor cells and lactating luminal cells, respectively. Only the K14-cre-mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological heterogeneity, suggesting the multilineage progenitor cell origin of these tumors. These tumors harbored truncation mutation in a defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of beta-catenin signaling. Activating mutations at codons 12 and 61 of either H-Ras or K-Ras were also found in a subset of these tumors. Expression profiles of acinar-type mammary tumors from K14-cre; Apc(CKO/+) mice showed luminal epithelial gene expression pattern, and clustering analysis demonstrated more correlation to MMTV-neu model than to MMTV-Wnt1. In contrast, neither WAP-cre-induced Apc heterozygous nor homozygous mutations resulted in predisposition to mammary tumorigenesis, although WAP-cre-mediated Apc deficiency resulted in severe squamous metaplasia of mammary glands. Collectively, our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of beta-catenin signaling optimal for mammary tumor development and explain partially the colon- but not mammary-specific tumor development in patients that carry germline mutations in APC.
Protein geranylgeranyltransferase of Saccharomyces cerevisiae is specific for Cys-Xaa-Xaa-Leu motif proteins and requires the CDC43 gene product but not the DPR1 gene product. (1991)

Protein prenylation occurs by modification of proteins with one of at least two isoprenoids, the farnesyl group and the geranylgeranyl group. Protein farnesyltransferases have been identified, but no such enzyme has been identified for geranylgeranylation. We report the identification of an activity in crude soluble yeast extracts that catalyzes the transfer of a geranylgeranyl moiety from geranylgeranyl pyrophosphate to proteins having the C-terminal sequence Cys-Ile-Ile-Leu or Cys-Val-Leu-Leu but not to a similar protein ending with Cys-Ile-Ile-Ser. This activity is dependent upon the CDC43/CAL1 gene, which is involved in budding and the control of cell polarity, but does not require the DPR1/RAM1 gene, which is known to be required for the farnesylation of Ras proteins. These results indicate that the protein geranylgeranyltransferase activity is distinct from the protein farnesyltransferase activity and that its specificity depends in part on the extreme C-terminal leucine in the protein to be prenylated.
Making the diagnosis of Alzheimer's disease. A primer for practicing pathologists. (1993)

There is demand on community pathologists to perform autopsies to confirm the clinical diagnosis of Alzheimer's disease, the most common cause of dementia in our increasingly aging society. Yet many pathologists are reluctant to examine autopsy brains because they have little experience with neuropathology and with the common histopathologic staining methods needed to evaluate dementia cases. This article provides interested pathologists with a simple, practical protocol to use in meeting this demand. While there is no absolute diagnostic gold standard for Alzheimer's disease and the histopathologic diagnosis remains imperfect, the guidelines presented are adapted from those used by many neuropathologists at Alzheimer's disease research centers participating in CERAD, the Consortium to Establish a Registry for Alzheimer's Disease. Recipes for appropriate stains and specific case examples are provided for convenience.
Development of a multi-behavior based mobile robot for remote supervisory control through the Internet (2000)

We review the networked mobile robot systems and suggest taxonomy based on the three levels of control commands. The performance analysis result shows that direct control has potential difficulty for implementation due to the unpredicted transmission delay of the network. To tackle this problem, we have suggested the behavior-programming control concept to avoid disturbances of the Internet latency. For this purpose, primitive local intelligence of the mobile robot is grouped into motion planner, motion executor, and motion assistant, where each of a group is treated as an agent. They are integrated by centralized control architecture based on multi-agent concept, communicated through a center information memory. The event-driven concept is applied on the robot to switch the behaviors to accommodate the unpredicted mission autonomously. We have successfully demonstrated experimentally the feasibility and reliability for system through a performance comparison with direct remote control.
Mechanism of action of hydroxyurea. (1992)

Hydroxyurea is well absorbed after oral administration, converted to a free radical nitroxide in vivo, and transported by diffusion into cells where it quenches the tyrosyl free radical at the active site of the M2 protein subunit of ribonucleotide reductase, inactivating the enzyme. The entire replitase complex, including ribonucleotide reductase, is inactivated and DNA synthesis is selectively inhibited, producing cell death in S phase and synchronization of the fraction of cells that survive. Repair of DNA damaged by chemicals or irradiation is also inhibited by hydroxyurea, offering potential synergy between hydroxyurea and radiation or alkylating agents. Hydroxyurea renders cells sensitive to bleomycin because the quenched tyrosyl free radical no longer stabilizes the adjacent iron center, making it more susceptible to the chelating properties of bleomycin, which then produces active oxygen. Synergy has also been observed between hydroxyurea and a number of other chemotherapeutic agents, including cytarabine and etoposide. Recently, two new effects of hydroxyurea have been observed: hydroxyurea increases the level of fetal hemoglobin, leading to a reduction in the incidence of vasoocclusive crises in sickle cell anemia, and hydroxyurea selectively reduces the level of episomal DNA and thus potentially may reduce drug resistance associated with duplicated genes retained as episomes. Further exploration of the efficacy of hydroxyurea in combination with other therapeutic agents is warranted.
Ott1 ( Rbm15 ) has pleiotropic roles in hematopoietic development (2007)

OTT1(RBM15) was originally described as a 5' translocation partner of the MAL(MKL1) gene in t(1,22)(p13;q13) infant acute mega karyocytic leukemia. OTT1 has no established physiological function, but it shares homology with the spen/Mint/SHARP family of proteins defined by three amino-terminal RNA recognition motifs and a carboxyl-terminal SPOC (Spen paralog and ortholog carboxyl-terminal) domain believed to act as a transcriptional repressor. To define the role of OTT1 in hematopoiesis and help elucidate the mechanism of t(1,22) acute megakaryocytic leukemia pathogenesis, a conditional allele of Ott1 was generated in mice. Deletion of Ott1 in adult mice caused a loss of peripheral B cells due to a block in pro/pre-B differentiation. There is myeloid and megakaryocytic expansion in spleen and bone marrow, an increase in the Lin(-)Sca-1(+)c-Kit(+) compartment that includes hematopoietic stem cells, and a shift in progenitor fate toward granulocyte differentiation. These data show a requirement for Ott1 in B lymphopoiesis, and inhibitory roles in the myeloid, megakaryocytic, and progenitor compartments. The ability of Ott1 to affect hematopoietic cell fate and expansion in multiple lineages is a novel attribute for a spen family member and delineates Ott1 from other known effectors of hematopoietic development. It is plausible that dysregulation of Ott1-dependent hematopoietic developmental pathways, in particular those affecting the megakaryocyte lineage, may contribute to OTT1-MAL-mediated leukemogenesis.
Simultaneous Analysis of 9-THC and its Major Metabolites in Urine, Plasma, and Meconium by GC-MS Using an Immunoaffinity Extraction Procedure (2000)

A simple extraction procedure for delta9-tetrahydrocannabinol (delta9-THC) and its metabolites from various biological specimens was developed based on immunoaffinity chromatography. Using the affinity resin prepared by immobilization of THC antibody onto cyanogen bromide-activated Sepharose 4B, delta9-THC and its major metabolites including 11-nor-delta9-THC-9-carboxylic acid (delta9-THCCOOH), 11-hydroxy-delta9-THC (11-OH-delta9-THC), and 8beta,11-dihydroxy-delta9-THC (8beta,11-diOH-delta9-THC) were extracted simultaneously from plasma or urine after enzyme hydrolysis. The samples were derivatized as TMS derivatives and analyzed by gas chromatography-mass spectrometry in EI mode with SIM monitoring. Greater than 87% extraction recovery of the four analytes was obtained from both plasma and urine at 5 and 50 ng/mL concentration levels. The method was also used for meconium analysis with some modification. The extraction recovery from meconium, however, was lower than that of plasma and urine, ranging from 52 to 72% at the 10-ng/g level. All compounds showed good linearity within the tested ranges up to 100 ng/mL (g). The limits of detection ranged from 0.5 to 2.5 ng/mL in plasma and urine, and from 1.0 to 2.5 ng/g in meconium. Analysis of 24 meconium specimens showed that 11-OH-delta9-THC is indeed an important metabolite in meconium.
Synthesis and biological evaluation of 5-substituted O4-alkylpyrimidines as CDK2 inhibitors (2010)

CDK2 inhibitory structure-activity relationships have been explored for a range of 5-substituted O(4)-alkylpyrimidines. Variation of the 5-substituent in the 2,6-diaminopyrimidine series confirmed the 5-nitroso substituent as optimal, and showed that 5-formyl and 5-acetyl substituents were also tolerated at this position. A series of O(4)-alkyl-N(2)-aryl-5-substituted-6-aminopyrimidines revealed interesting structure-activity relationships. In the 5-nitroso series, the optimum O(4)-alkyl substituents were cyclohexylmethyl or sec-butyl, combined with a 2-sulfanilyl group. By contrast, in the N(2)-arylsulfonamido-5-formyl series, the cyclohexylmethyl compound showed relatively poor activity compared with the sec-butyl derivative (22j, (R)-4-(4-amino-6-sec-butoxy-5-formylpyrimidin-2-ylamino)benzenesulfonamide; CDK2 IC(50) = 0.8 nM). Similarly, in the N(2)-arylsulfonamido-5-(hydroxyiminomethyl) series the O(4)-sec-butyl substituent conferred greater potency than the cyclohexylmethyl (23c, (rac)-4-(4-amino-6-sec-butoxy-5-(hydroxyiminomethyl)pyrimidin-2-ylamino)benzenesulfonamide; CDK2 IC(50) = 7.4 nM). The 5-formyl derivatives show selectivity for CDK2 over other CDK family members, and are growth inhibitory in tumour cells (e.g. 22j, GI(50) = 0.57 microM).
Epidemiology of Bovine Venereal Campylobacteriosis: Geographic Distribution and Recent Advances in Molecular Diagnostic Techniques (2009)

Bovine venereal campylobacteriosis (BVC) is a major cause of economic loss to the cattle industries in different parts of the world. Camplylobacter fetus subsp. venerealis (Cfv), the main causative agent of BVC, is highly adapted to the genital tract of cattle and is transmitted by carrier bulls. However, infertility and abortions can also be caused by the intestinal pathogens C. fetus subsp. fetus (Cff), and C. jenuni, which are not venereally transmitted. Bovine venereal campylobacteriosis, caused by Cfv associated with lowered fertility, embryo mortality and abortion, repeated returns to service, reduced pregnancy rates and extended calving intervals, has the highest prevalence in developing countries where natural breeding in cattle is widely practised. The epidemiology, pathogenesis and diagnosis of the disease have been the subject of previous reviews. The main focus of this review is to highlight the epidemiology of this disease with particular reference to geographical distribution and recent advances in molecular diagnostic techniques. It is hoped that further research interest of scientists will be stimulated with a view to finding lasting solutions to the reproductive problems associated with the disease for better livestock productivity, particularly in developing endemic countries.
Tumor Necrosis Factor-α Regulation of Glucose Transporter (GLUT1) mRNA Turnover (1997)

In the current study we report on the contribution of the GLUT1 3'-untranslated region (UTR) to the stability of the GLUT1 mRNA. To facilitate these investigations, a hybrid construct was prepared by insertion of the GLUT1 3'-UTR into a normally stable reporter gene coding for preproinsulin. The GLUT1 3'-UTR conferred lability to the otherwise long lived construct and transferred an ability to be stabilized in response to treatment with the cytokine, tumor necrosis factor-alpha (TNF). The destabilizing element has been mapped to a region located between bases 2242 and 2347 of the GLUT1 3'-UTR; this same region also mediates the stabilization response to TNF. In vitro RNA-protein binding assays using protein extracts from control and TNF-treated cells demonstrated that two proteins, one of 37 kDa and the other of 40 kDa, recognized sequence elements within the stability-determining region and were up-regulated in response to TNF treatment. The RNA-binding activity of these proteins coincides with the stabilization of the GLUT1 message, suggesting that they may be involved in regulation of the turnover of this message.
Involvement of Inflammation in a Mouse Model of Inherited Pigmentary Glaucoma (2008)

Our understanding of the biology of human glaucoma has been enhanced by the study of animal models of glaucoma. Animal models allow experiments not possible in human and facilitate testing of potential treatments to establish proof-of-principle before human testing. The generation of mutant and transgenic mice that mimic specific events of human glaucoma makes these mice an important model because such models of glaucoma are not available in other model systems. Many forms of glaucoma are known to have genetic components. Some types of human glaucoma are associated with anterior segment abnormalities, such as pigment dispersion syndrome (PDS), a unique syndrome characterized by radial defects of the iris pigment epithelium which are visible on retroillumination, and by the liberation and the deposition of melanin granules on the corneal endothelium (Krukenberg spindle), on the posterior lens capsule, and in the anterior chamber and in aqueous humor drainage structures. PDS is frequently associated with secondary open-angle glaucoma, also referred to as