gebhart/patrepeval huggingface dataset:
Long-Term Therapy of Myoclonus and Other Neurologic Disorders with L-5-Hydroxytryptophan and Carbidopa (1977)

We evaluated the therapeutic effect of L-5-hydroxytryptophan (L-5HTP), the precursor of serotonin (5-hydroxytryptamine), combined with carbidopa, a peripheral decarboxylase inhibitor, in patients with intention myoclonus and examined the serotonin metabolites in spinal fluid, blood and urine before and during therapy. In 18 patients with intention myoclonus due to anoxia or other brain damage, 11 derived more than 50% overall improvement during treatment with L-5HTP and carbidopa. Spinal-fluid 5-hydroxyindoleacetic acid was 35% lower in patients with intention myoclonus than in controls (P less than 0.05). Therapy with L-5HTP and carbidopa increased the concentration of serotonin metabolites in urine and spinal fluid. We postulate that a deficiency of brain serotonin is causally related to intention myoclonus and that the therapeutic effect of L-5HTP and carbidopa may be due to the repletion of serotonin in regions of the brain where serotoninergic neurons have degenerated.
Synthetic Attractants for Some Dipteran Species1 (1972)

Uploaded by Plazi for TaxoDros. We do not have abstracts.
Phospholipase D signaling pathway is involved in lung cancer-derived IL-8 increased osteoclastogenesis (2010)

Bone is a frequent target of lung cancer metastasis, which is associated with significant morbidity and a dismal prognosis. This study analyzed the soluble factors secreted by lung cancer cells, which are responsible for increasing osteoclast differentiation. Addition of recombinant human interleukin-8 (rhIL-8), present in large amounts in A549-conditioned medium (CM) and NCI-H460-CM, mimicked the inductive effect of A549-CM and NCI-H460-CM on osteoclastogenesis. In contrast, depletion of interleukin-8 (IL-8) from A549-CM and NCI-H460-CM decreased the osteoclastogenesis-inductive properties of A549-CM and NCI-H460-CM. Induction of osteoclast differentiation by lung cancer-derived-CM and rhIL-8 was associated with increased phospholipase D (PLD) activation, and the activations of protein kinase C (PKC) alpha/betaII, extracellular signal-regulated kinase (ERK) 1/2 and AKT/the mammalian target of rapamycin (mTOR). Blocking PLD by a specific inhibitor significantly decreased osteoclast formation by inhibiting PKCs activation and subsequently attenuating the phosphorylation of ERK1/2. PLD inhibitor also completely decreased AKT and mTOR phosphorylation, whereas phosphatidylinositol-3-kinase (PI3K) inhibitor only partially decreased mTOR phosphorylation, suggesting that mTOR activation by PLD is through both PI3K/AKT-dependent and PI3K/AKT-independent manner. In addition, blocking AKT and ERK1/2 by a specific inhibitor also suppressed lung cancer-derived-CM and rhIL-8-induced osteoclast differentiation. Moreover, treatment of peripheral blood mononuclear cells with sera from invasive lung cancer patients increased the formation of osteoclasts. Our study suggests that IL-8 or IL-8-mediated PLD/PKC/ERK1/2 or PLD/AKT signaling is an attractive therapeutic target for osteolytic bone metastases in lung cancer patients.
Inhibition of mutant huntingtin expression by RNA duplex targeting expanded CAG repeats (2011)

The specific silencing of the gene of interest is the major objective of RNA interference technology; therefore, unique sequences but not abundant sequence repeats are targeted by silencing reagents. Here, we describe the targeting of expanded CAG repeats that occur in transcripts derived from the mutant allele of the gene implicated in Huntington's disease (HD) in the presence of the normal allele and other human mRNAs containing CAG and CUG repeat tracts. We show that a high degree of silencing selectivity may be achieved between the repeated sequences. We demonstrate preferential suppression of the mutant huntingtin allele and concomitant activation of the normal huntingtin allele in cell lines derived from HD patients that were transfected with short RNA duplexes composed of CAG and CUG repeats containing mutations at specific positions. These effects may lead to promising therapeutic modalities for HD, a condition for which no therapy presently exists.
Degradation of Corticosteroids. III.1,2 Catalytic Hydrogenation of Cortisol (1959)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTDegradation of Corticosteroids. III.1,2 Catalytic Hydrogenation of CortisolELIAHU CASPICite this: J. Org. Chem. 1959, 24, 5, 669–673Publication Date (Print):May 1, 1959Publication History Published online1 May 2002Published inissue 1 May 1959https://pubs.acs.org/doi/10.1021/jo01087a027https://doi.org/10.1021/jo01087a027research-articleACS PublicationsRequest reuse permissionsArticle Views138Altmetric-Citations10LEARN 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
Application of a response surface method to the design of tip jet driven stopped rotor/wing concepts (1995)

Presented at the 1st AIAA Aircraft Engineering, Technology, and Operations Congress, Anaheim, CA, September 19-21, 1995.
A new neural network for solving linear programming problems and its application (1996)

Presents a new neural network which improves existing neural networks for solving general linear programming problems. The network, without setting parameter, uses only simple hardware in which no analog multipliers are required, and is proved to be completely stable to the exact solutions. Moreover, using this network the author can solve linear programming problems and its dual simultaneously, and cope with problems with nonunique solutions whose set is allowed to be unbounded.
Lymphosarcoma and persistent feline leukemia virus infection of pet cats: a system to study responses during extracorporeal treatments. (1984)

Pet cats, persistently infected with feline leukemia virus and having lymphosarcoma, were treated by extracorporeal immunoadsorption using Staphylococcus aureus Cowan I (which has protein A on its surface) to remove immunoglobulin G and circulating immune complexes. Complete viral clearance and long-lasting tumor regression were achieved following such treatments in 9 of 16 cats. In addition, in vitro immunologic assays have been developed that are useful in the clinical evaluation of cats during treatment.
Operating-system directed power reduction (2000)

this paper presents a new approach for power reduction by taking a global, software-centric view. It analyzes the sources of power consumption: tasks that require services from hardware components. When a component is not used by any task, it can enter a sleeping state to save power. Operating systems have detailed information about tasks; therefore, OS is the best place for identifying hardware idleness and shutting down unused components. We implement this technique in Linux and show that it can save more than 50% power compared to traditional hardware-centric shutdown techniques.
Purification of chick nuclear thyroid‐hormone‐receptor protein (1984)

A crude nuclear thyroid-hormone-receptor protein preparation from chick liver (an ammonium sulfate fractionation of high-ionic-strength-solubilized chromatin proteins) binds both triiodothyronine and thyroxine with high affinity. This crude preparation has characteristics similar to preparations from a variety of animal tissues, reported by several different laboratories, and is used for the further purification of the receptor protein. For this purification an affinity chromatography medium, 4-[N-(3,5,3'-triiodothyronine)-2-amino-3-hydroxypropoxy]-butylpropoxy -Sepharose ether, is used to take advantage of the observation that hydroxymercuribenzoic acid causes a reversible dissociation of the complex between triiodothyronine and the receptor protein. The hydroxymercuribenzoate treatment greatly increases this rate of dissociation at low temperatures compared with other methods, such as free triiodothyronine competition or an increase in ionic strength or pH. This procedure results a in purified fraction (1000-10000-fold with respect to binding triiodothyronine), which has a molecular mass of approximately 65 kDa and which retains a high degree of the original thyroid-hormone-binding activity.
Increased CD4+ expression and decreased IL-10 in the anterior chamber in idiopathic uveitis. (1999)

The results suggest a selective recruitment of CD4+ T cells within aqueous humor but only in idiopathic uveitis. In both disease groups there was a decrease in the immunoregulatory cytokine interleukin-10, which might enable an immune response to occur in an otherwise highly immunosuppressive microenvironment. Increases in activated CD4+ T cells combined with depressed interleukin-10 levels could partially explain why, for example, in acute anterior uveitis, the inflammatory disease is often more severe.
Production and Characterization of Recombinant Human Neutrophil Chemotactic Factor (1989)

A putative mature human neutrophil chemotactic factor (NCF) corresponding to the C-terminal 72 amino acids of its precursor was directly produced in Escherichia coli by recombinant DNA technology. Human NCF was present in both the soluble and insoluble protein fractions of the homogenate of host cells, and it was partially purified as a water-soluble polypeptide from both fractions, separately. The partially purified NCF preparation was highly purified to an endotoxin-free homogeneous polypeptide by means of CM-Sepharose CL-6B column chromatography and gel filtration on Toyopearl HW-55. No difference between the human NCF preparations purified from both starting materials could be found concerning purity, primary structure, solubility, molecular weight, and chemotactic activity for human neutrophils. The amino acid sequence of recombinant human NCF was identical to the sequence deduced from the cDNA sequence. A methionine residue due to the translation initiation codon was removed. Recombinant human NCF was found to be biologically active and to exhibit chemotactic activity for human neutrophils in vitro and cause a neutrophil infiltration in vivo in mice.
Constitutive expression of human double-stranded RNA-activated p68 kinase in murine cells mediates phosphorylation of eukaryotic initiation factor 2 and partial resistance to encephalomyocarditis virus growth (1992)

The cDNA encoding interferon-induced human double-stranded RNA-activated p68 kinase was expressed in murine NIH 3T3 cells by using the pcDNA1/neo vector. Several stable clones were selected which expressed either the wild-type kinase or an inactive mutant possessing a single amino acid substitution in the invariant lysine 296 in the catalytic domain II. The transfected wild-type kinase showed properties similar to those of the natural kinase, such as subcellular ribosomal localization and dependence on double-stranded RNA for autophosphorylation. Upon infection with encephalomyocarditis virus (EMCV), wild-type- but not mutant-expressing clones were found to partially resist virus growth. Such natural antiviral activity was virus specific, since no inhibition was observed in the case of vesicular stomatitis virus infection. In accord with EMCV inhibition, the wild-type p68 kinase was found to be highly phosphorylated during infection. Furthermore, its natural substrate, the small subunit of protein synthesis initiation factor eIF2, was phosphorylated. These results demonstrate that p68 kinase is activated during EMCV infection, leading to reduced virus production.
Potency Trends of Δ9-THC and Other Cannabinoids in Confiscated Marijuana from 1980–1997 (2000)

The analysis of 35,312 cannabis preparations confiscated in the USA over a period of 18 years for delta-9-tetrahydrocannabinol (delta9-THC) and other major cannabinoids is reported. Samples were identified as cannabis, hashish, or hash oil. Cannabis samples were further subdivided into marijuana (loose material, kilobricks and buds), sinsemilla, Thai sticks and ditchweed. The data showed that more than 82% of all confiscated samples were in the marijuana category for every year except 1980 (61%) and 1981 (75%). The potency (concentration of delta9-THC) of marijuana samples rose from less than 1.5% in 1980 to approximately 3.3% in 1983 and 1984, then fluctuated around 3% till 1992. Since 1992, the potency of confiscated marijuana samples has continuously risen, going from 3.1% in 1992 to 4.2% in 1997. The average concentration of delta9-THC in all cannabis samples showed a gradual rise from 3% in 1991 to 4.47% in 1997. Hashish and hash oil, on the other hand, showed no specific potency trends. Other major cannabinoids [cannabidiol (CBD), cannabinol (CBN), and cannabichromene (CBC)] showed no significant change in their concentration over the years.
Improving Healthcare Accessibility through Point-of-Care Technologies (2007)

NIBIB has developed a funding initiative to establish a Point-of-Care Technologies Research Network that will work to bridge the technology/clinical gap and provide the partnerships necessary for the application of technologies to pressing clinical needs in POC testing.
DNA Damage and Repair Biomarkers of Immunotherapy Response (2017)

Abstract DNA-damaging agents are widely used in clinical oncology and exploit deficiencies in tumor DNA repair. Given the expanding role of immune checkpoint blockade as a therapeutic strategy, the interaction of tumor DNA damage with the immune system has recently come into focus, and it is now clear that the tumor DNA repair landscape has an important role in driving response to immune checkpoint blockade. Here, we summarize the mechanisms by which DNA damage and genomic instability have been found to shape the antitumor immune response and describe clinical efforts to use DNA repair biomarkers to guide use of immune-directed therapies. Significance: Only a subset of patients respond to immune checkpoint blockade, and reliable predictive biomarkers of response are needed to guide therapy decisions. DNA repair deficiency is common among tumors, and emerging experimental and clinical evidence suggests that features of genomic instability are associated with response to immune-directed therapies. Cancer Discov; 7(7); 675–93. ©2017 AACR.
Dynamics of infection of the blood stream and internal organs of white mice withSalmonella typhiby intraperitoneal injection (1962)

An LD 50 dose S. typhi (strain Ty was injected intraperitoneally into white mice, and the number of micro-organisms was determined after 1 min. and subsequently, in the blood, and after 3 hr. and subsequently, in the spleen and liver. The course of the infection was observed for 34 days. The number of bacteria gradually increased in the blood stream during the first post-infective hours. It was possible to differentiate by external signs from the sixth post-infective hour and onwards between sick animals and recovering ones. This difference corresponded to the bacterial concentration in the blood stream and internal organs. In the sick animals the increase in the bacterial count of blood stream continued till 9–10 hr. after the inoculation, when it reached its first peak. During the following 8 hr. a clear decrease in the blood count was evident which was attributed to the ‘clearing mechanism’ of the blood. The onset of a new bacterial rise in the blood stream appeared 18 hr. after the inoculation and reached a second peak during the further 6–8 hr. In contrast to the observed decrease in the bacterial blood count, a steady and gradual increase in the count of the internal organs was seen; it was steadily progressive till the exitus. In the recovering animals a steady decrease in the bacterial blood count was recorded. Between 24 and 26 hr. the number of micro-organisms in the blood and spleen was found to be 400 times less in the recovering animals than in the moribund ones. From 48 hr. and onwards a slow and gradual decrease in the bacterial count of the surviving animals was observed. The blood became sterile after 25 days. In the spleen and liver of the surviving animals after 48 hr. a new increase in the bacterial count is evident, accompanied by hyperplasia of the spleen. The number of bacteria reached a new peak in the liver on the third day and in the spleen on the fourth day after the infection. Subsequently a slow and gradual decrease in the bacterial count was observed in both organs, but even after 34 days a small number of persisting bacteria in the spleen and liver tissue may be found.
Regulation of the Mannan-Binding Lectin Pathway of Complement on Neisseria gonorrhoeae by C1-Inhibitor and α2-Macroglobulin (2002)

We examined complement activation by Neisseria gonorrhoeae via the mannan-binding lectin (MBL) pathway in normal human serum. Maximal binding of MBL complexed with MBL-associated serine proteases (MASPs) to N. gonorrhoeae was achieved at a concentration of 0.3 microg/ml. Preopsonization with MBL-MASP at concentrations as low as 0.03 microg/ml resulted in approximately 60% killing of otherwise fully serum-resistant gonococci. However, MBL-depleted serum (MBLdS) reconstituted with MBL-MASP before incubation with organisms (postopsonization) failed to kill at a 100-fold higher concentration. Preopsonized organisms showed a 1.5-fold increase in C4, a 2.5-fold increase in C3b, and an approximately 25-fold increase in factor Bb binding; enhanced C3b and factor Bb binding was classical pathway dependent. Preopsonization of bacteria with a mixture of pure C1-inhibitor and/or alpha(2)-macroglobulin added together with MBL-MASP, all at physiologic concentrations before adding MBLdS, totally reversed killing in 10% reconstituted serum. Reconstitution of MBLdS with supraphysiologic (24 microg/ml) concentrations of MBL-MASP partially overcame the effects of inhibitors (57% killing in 10% reconstituted serum). We also examined the effect of sialylation of gonococcal lipooligosaccharide (LOS) on MBL function. Partial sialylation of LOS did not decrease MBL or C4 binding but did decrease C3b binding by 50% and resulted in 80% survival in 10% serum (lacking bacteria-specific Abs) even when sialylated organisms were preopsonized with MBL. Full sialylation of LOS abolished MBL, C4, and C3b binding, resulting in 100% survival. Our studies indicate that MBL does not participate in complement activation on N. gonorrhoeae in the presence of "complete" serum that contains C1-inhibitor and alpha(2)-macroglobulin.
Reply to: A Critical Appraisal of the Lens Circulation Model—An Experimental Paradigm for Understanding the Maintenance of Lens Transparency? (2010)

The authors of the Point article clearly describe the fluid circulation model (FCM) in its current form. The two articles present contrasting views of lens physiology. In the view of Donaldson et al., mature fiber cells in the adult lens are metabolically active, requiring a steady supply of substrates and removal of metabolic end products. If this view were correct, robust circulation of intracellular fluid might be needed. Our perspective, which is supported by several published studies not considered by proponents of the FCM, is that mature fiber cells have little or no metabolic activity. They depend on superficial fiber cells to maintain their ionic balance and to preserve a reducing environment in their cytoplasm. The movement of ions and reducing agents such as glutathione (GSH) to and from the lens core occurs by simple diffusion across the gap junctions of mature fiber cells, not by an internal circulatory system.

The data we present suggest that the FCM is unlikely to be valid. To test whether the FCM is an accurate view of lens physiology, it should be sufficient to perform only two experiments. One would be to repeat the study cited in Figure 1 of our Counterpoint article on adult lenses, while monitoring extralenticular currents. Displacement of a gap-junction–permeable dye, relative to an impermeant marker, would directly measure fluid flow in the intact lens, if it exists. The second experiment should test whether homogenates of adult human nuclear fiber cells transform a substantial amount of labeled glucose into pyruvate and amino acid precursors into reduced glutathione. The first directly measures flow in the lens, and the second tests whether GSH can be synthesized and reduced in mature fiber cells.

Figure 4 of our Counterpoint article shows that unidirectional flow from the center to the periphery of the lens would impede the diffusion of small molecules such as GSH, in the opposite direction. Therefore, the FCM requires that sufficient metabolism persist in the nucleus to generate ATP from glucose and reduced glutathione from amino acids and NADPH. For this reason, flow and metabolism are inextricably linked. If flow cannot be demonstrated or GSH cannot be synthesized and reduced by local metabolism in the lens nucleus, the FCM hypothesis is untenable.
Detection and identification of Treponema hyodysenteriae by using oligodeoxynucleotide probes complementary to 16S rRNA (1990)

Oligodeoxynucleotide probes (17 and 28 bases long) complementary to a unique region of Treponema hyodysenteriae 16S rRNA were developed. These probes bound specifically to partially purified rRNA and whole-cell rRNA of T. hyodysenteriae. No binding to partially purified rRNA or whole-cell rRNA of Treponema innocens, Treponema succinifaciens, Treponema bryantii, or Escherichia coli occurred under stringent conditions. The 28-base probe was 5 to 10 times more sensitive than the 17-base probe when hybridized with T. hyodysenteriae rRNA. The 28-base probe detected T. hyodysenteriae in the feces of experimentally inoculated pigs exhibiting clinical signs of swine dysentery.
Lung alveoli: endogenous programmed destruction and regeneration (2002)

Mammalian alveoli, complex architectural and cellular units with dimensions that are linked to the organism's O2 consumption (VO2), are thought to be destroyed only by disease and not to spontaneously regenerate. Calorie restriction of adult mammals lowers VO2, and ad libitum refeeding returns VO2 to pre-calorie-restriction values. We took advantage of these relationships and tested the hypothesis in adult mice that calorie restriction (two-thirds reduction for 2 wk) followed by ad libitum refeeding (3 wk) would cause alveolar destruction and regeneration, respectively. Calorie restriction diminished alveolar number 55% and alveolar surface area 25%. Refeeding fully reversed these changes. Neither manipulation altered lung volume. Within 72 h, calorie restriction increased alveolar wall cell apoptosis and diminished lung DNA (approximately 20%). By 72 h of refeeding, alveolar wall cell replication increased and lung DNA rose to amounts in mice that were never calorie restricted. We conclude that adult mice have endogenous programs to destroy and regenerate alveoli, thereby raising the danger of inappropriate activation but the possibility of therapeutic induction, if similar programs exist in humans.