Journal articles: 'SK'

1

Liu, Yingfan, Jiangtao Cui, Zi Huang, Hui Li, and Heng Tao Shen. "SK-LSH." Proceedings of the VLDB Endowment 7, no. 9 (May 2014): 745–56. http://dx.doi.org/10.14778/2732939.2732947.

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2

Brueckner, Anthony. "∼K∼SK." Philosophical Issues 21, no. 1 (October 2011): 74–89. http://dx.doi.org/10.1111/j.1533-6077.2011.00198.x.

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3

Tsukamoto, K. "SK-896." Drugs of the Future 26, no. 3 (2001): 239. http://dx.doi.org/10.1358/dof.2001.026.03.610452.

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4

YASUDA, HIROSHI, and Rob Kirschbaum. "Dyneema SK-60." Sen'i Gakkaishi 43, no. 4 (1987): P139—P142. http://dx.doi.org/10.2115/fiber.43.4_p139.

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5

Sugaya, E. "SK-TJ-960." Drugs of the Future 12, no. 4 (1987): 360. http://dx.doi.org/10.1358/dof.1987.012.04.54029.

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6

Shi, G. Y., B. I. Chang, S. M. Chen, D. H. Wu, and H. L. Wu. "Function of streptokinase fragments in plasminogen activation." Biochemical Journal 304, no. 1 (November 15, 1994): 235–41. http://dx.doi.org/10.1042/bj3040235.

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Several peptide fragments of streptokinase (SK) were prepared by incubating SK with immobilized human plasmin (hPlm) and purified by h.p.l.c. with a reverse-phase phenyl column. The N-terminal sequences, amino acid compositions and molecular masses of these peptide fragments were determined. The SK peptide fragment of 36 kDa consisting of Ser60-Lys387 (SK-p), was the only peptide fragment that could be tightly bound to immobilized hPlm. Another three large SK peptide fragments, SK-m, SK-n and SK-o, with molecular masses of 7 kDa, 18 kDa and 30 kDa, and consisting of Ile1-Lys59, Glu148-Lys333, Ser60-Lys333 respectively, were also obtained from the supernatant of the reaction mixture. The purified SK-p had high affinity with hPlm and could activate human plasminogen (hPlg) with a kPlg one-sixth that of the native SK. SK-o had low affinity with hPlm and could also activate hPlg, although the catalytic constant was less than 1% of the native SK. SK-n, as well as SK-m, which is the N-terminal 59 amino acid peptide of the native SK, had no activator activity. However, SK-m could enhance the activator activity of both SK-o and SK-p and increase their second-order rate constants by two- and six-fold respectively. It was concluded from these studies that (1) SK-o, the Ser60-Lys333 peptide of SK, was essential for minimal SK activator activity, (2) the C-terminal peptide of SK-p, Ala334-Lys387, was essential for high affinity with hPlm, and (3) the N-terminal 59-amino-acid peptide was important in maintaining the proper conformation of SK to have its full activator activity.

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7

Breuning, L., J. Tvedskov, and S. Munkvad. "Anti-streptokinase (SK) IgG remains low following local SK-therapy compared to intravenous coronary thrombolysis with SK." Fibrinolysis 8, no. 3 (May 1994): 189–91. http://dx.doi.org/10.1016/s0268-9499(05)80018-9.

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8

LAWLEY, Wendy J., Sue FLETCHER, Iain B. SQUIRE, Kent L. WOODS, and Colin R. A. HEWITT. "T-cell recognition of discrete regions of the thrombolytic drug streptokinase." Clinical Science 99, no. 3 (August 23, 2000): 239–46. http://dx.doi.org/10.1042/cs0990239.

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Streptokinase (SK) is a bacterial protein used clinically as a thrombolytic agent in humans. Administration of SK causes a rapid increase in the frequency of anti-SK T cells and the titre of specific anti-SK antibodies that, on subsequent administration of SK, may neutralize the activity of the drug or elicit allergic-type reactions. By locating and modifying the immunogenic T-cell epitopes within the SK protein, it is possible that an agent with reduced immunogenicity but equal efficacy may be produced. We have investigated the T-cell epitopes within SK using nine non-overlapping, recombinant peptide fragments of SK. We investigated the proliferative T-cell response of peripheral blood mononuclear cells obtained from patients before and 6 days after administration of SK for myocardial infarction. We also examined the response of cultured anti-SK T-cell lines derived from patients 6 days after treatment with SK. Before administration of SK, peripheral blood mononuclear cells from six of nine patients showed a proliferative response to SK. The response was significantly higher 6 days after administration of SK (P = 0.0004). Cultured T-cell lines showed similar proliferative responses to clinical-grade SK and recombinant SK. Marked differences in T-cell responses were apparent in response to each recombinant SK fragment (P = 0.04). The mean proliferative response exceeded background to only two peptides, peptide 2 (P = 0.04) and peptide 3 (P = 0.009). Peptide 3, representing amino acids 100–150 of mature SK, was recognized preferentially in the majority of assays. Marked variation in the T-cell response to SK following treatment with this agent was observed between subjects. Despite these differences, peptides 2 and 3 induced T-cell proliferation at a level significantly above background in the majority of subjects. These epitopes may represent a region of enhanced immunogenicity within SK.

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Goldstein, Joel, Gary R. Matsueda, and Shyh-Yu Shaw. "A Chimeric Streptokinase with Unexpected Fibrinolytic Selectivity." Thrombosis and Haemostasis 76, no. 03 (1996): 429–38. http://dx.doi.org/10.1055/s-0038-1650595.

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SummaryChimeric 59D8-SK was designed to confer fibrin-selectivity to streptokinase by fusion of the Fab fragment of anti-fibrin antibody 59D8 to the N-terminus of streptokinase (SK: Ile1-Lys414). It was expressed in a mouse hybridoma cell line and purified by affinity chromatography on a 59D8-antigen column. Chimeric 59D8-SK is a disulfide-linked heterodimer composed of an antibody light chain (Mr 27,000) and a N-glycosylated chimeric heavy chain (Mr 90,000). The fibrin targeting by 59D8 increased plasma clot lysis by 2-fold, but connecting 59D8 to SK has provided 59D8-SK several unique properties: (i) 59D8-SK activated human Glu-plasminogen with a significant lag period that coincided with limited proteolysis of 59D8-SK similar to that observed for wild-type SK. In a kinetic study, both gave very similar kinetic parameters for the activation of Glu-plasminogen even though 59D8-SK was N-glycosylated in its SK portion; (ii) 59D8-SK was relatively inactive in human plasma, compared to SK, but it became activated in the presence of clots; (iii) 59D8-SK lysed clots slowly but completely whereas SK lysed clots rapidly but incompletely. Even though the mechanism behind these new properties is not fully understood, they are characteristics of a second-generation plasminogen activator.

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10

Brucato, FH, and SV Pizzo. "Catabolism of streptokinase and polyethylene glycol-streptokinase: evidence for transport of intact forms through the biliary system in the mouse." Blood 76, no. 1 (July 1, 1990): 73–79. http://dx.doi.org/10.1182/blood.v76.1.73.73.

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Abstract The catabolism of streptokinase (SK) and polyethylene glycol derivatives of SK (PEG-SK) were studied in mice. The clearance and catabolism of SK:plasmin (SK:Pm) and PEG-SK:Pm activator complexes were also investigated. Native 125I-SK cleared rapidly (t1/2 = 15 minutes) from the circulation, with the majority of the ligand accumulating in the liver and gastrointestinal (GI) tract and a substantial fraction also localizing in the kidneys. SK, which was removed from the plasma by the liver, was secreted into bile and then the GI tract. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) demonstrated that 125I-SK recovered from liver and bile was homogeneous and of the same molecular weight (mol wt approximately 50,200) as native SK. PEG-125I-SK cleared slowly (t1/2 greater than 200 minutes), with more than 80% of the preparation localizing in liver and GI tract. The PEG-125I-SK secreted into the bile was also intact. The bile containing 125I-SK was incubated with stoichiometric amounts of plasminogen and electrophoresed under nondenaturing conditions. This study demonstrated that the secreted SK was able to form SK:Pg complexes. SDS-PAGE also showed activation of 125I-Pg that was incubated with recovered bile containing the SK. 125I-SK:Pm catabolism was also studied. In these experiments, the mol wt approximately 42,000 fragment obtained when SK is cleaved by plasmin was found in the bile. This fragment of 125I-SK was not recovered as part of a complex with plasmin, consistent with our previous observations that catabolism of SK:Pm involves transfer of the plasmin to plasma proteinase inhibitors while SK is catabolized independently. By contrast, when PEG-125I-SK:Pm was injected into mice, only intact PEG-125I-SK was found in the bile, consistent with our previous observations that the PEG derivatization blocks its degradation by plasmin.

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Brucato, FH, and SV Pizzo. "Catabolism of streptokinase and polyethylene glycol-streptokinase: evidence for transport of intact forms through the biliary system in the mouse." Blood 76, no. 1 (July 1, 1990): 73–79. http://dx.doi.org/10.1182/blood.v76.1.73.bloodjournal76173.

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The catabolism of streptokinase (SK) and polyethylene glycol derivatives of SK (PEG-SK) were studied in mice. The clearance and catabolism of SK:plasmin (SK:Pm) and PEG-SK:Pm activator complexes were also investigated. Native 125I-SK cleared rapidly (t1/2 = 15 minutes) from the circulation, with the majority of the ligand accumulating in the liver and gastrointestinal (GI) tract and a substantial fraction also localizing in the kidneys. SK, which was removed from the plasma by the liver, was secreted into bile and then the GI tract. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) demonstrated that 125I-SK recovered from liver and bile was homogeneous and of the same molecular weight (mol wt approximately 50,200) as native SK. PEG-125I-SK cleared slowly (t1/2 greater than 200 minutes), with more than 80% of the preparation localizing in liver and GI tract. The PEG-125I-SK secreted into the bile was also intact. The bile containing 125I-SK was incubated with stoichiometric amounts of plasminogen and electrophoresed under nondenaturing conditions. This study demonstrated that the secreted SK was able to form SK:Pg complexes. SDS-PAGE also showed activation of 125I-Pg that was incubated with recovered bile containing the SK. 125I-SK:Pm catabolism was also studied. In these experiments, the mol wt approximately 42,000 fragment obtained when SK is cleaved by plasmin was found in the bile. This fragment of 125I-SK was not recovered as part of a complex with plasmin, consistent with our previous observations that catabolism of SK:Pm involves transfer of the plasmin to plasma proteinase inhibitors while SK is catabolized independently. By contrast, when PEG-125I-SK:Pm was injected into mice, only intact PEG-125I-SK was found in the bile, consistent with our previous observations that the PEG derivatization blocks its degradation by plasmin.

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12

Raju, N. B., and D. D. Perkins. "Expression of meiotic drive elements Spore killer-2 and Spore killer-3 in asci of Neurospora tetrasperma." Genetics 129, no. 1 (September 1, 1991): 25–37. http://dx.doi.org/10.1093/genetics/129.1.25.

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Abstract It was shown previously that when a chromosomal Spore killer factor is heterozygous in Neurospora species with eight-spored asci, the four sensitive ascospores in each ascus die and the four survivors are all killers. Sk-2K and Sk-3K are nonrecombining haplotypes that segregate with the centromere of linkage group III. No killing occurs when either one of these killers is homozygous, but each is sensitive to killing by the other in crosses of Sk-2K x Sk-3K. In the present study, Sk-2K and Sk-3K were transferred by recurrent backcrosses from the eight-spored species Neurospora crassa into Neurospora tetrasperma, a pseudohomothallic species which normally makes asci with four large spores, each heterokaryotic for mating type and for any other centromere-linked genes that are heterozygous in the cross. The action of Sk-2K and Sk-3K in N. tetrasperma is that predicted from their behavior in eight-spored species. A sensitive nucleus is protected from killing if it is enclosed in the same ascospore with a killer nucleus. Crosses of Sk-2K x Sk-2S, Sk-3K x Sk-3S, and Sk-sK x Sk-3K all produce four-spored asci that are wild type in appearance, with the ascospores heterokaryotic and viable. The Eight-spore gene E, which shows variable penetrance, was used to obtain N. tetrasperma asci in which two to eight spores are small and homokaryotic. When killer and sensitive alleles are segregating in the presence of E, only those ascospores that contain a killer allele survive. Half of the small ascospores are killed. In crosses of Sk-2K x Sk-3K (with E heterozygous), effectively all small ascospores are killed. The ability of N. tetrasperma to carry killer elements in cryptic condition suggests a possible role for Spore killers in the origin of pseudohomothallism, with adoption of the four-spored mode restoring ascospore viability of crosses in which killing would otherwise occur.

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13

Shadi, Milud, Piotr Janusz, Paweł Koczewski, Michał Walczak, Joanna Kraśny, and Tomasz Kotwicki. "Skin necrosis after SUPERknee procedure – typical versus modified surgical approach." Journal of Medical Science 88, no. 2 (March 9, 2019): 75–81. http://dx.doi.org/10.20883/jms.337.

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Introduction. SUPERknee procedure (SK) is a treatment for complex knee instability in children with congenital deformations. Due to wide surgical approach and long time of surgery (ST) the skin around the knee is in risk of ischemic necrosis (SN) or healing complications (HC). Aim. The purpose of the study is to compare incidence of SN in SK using typical and modified approach.Material and Methods. Sixteen patients underwent SK since 2015 till 2016, in mean age 8.1 (4.3–12.7) y.o. In 8 cases SK and in 8 SK combined with SUPERhip (SK+SH) was performed. In 6 patients (3 SK and 3 SK+SH) the approach was performed from one incision (OIA). In 10 patients (5 SK and 5 SK+SH) a modified approach was performed, involving additional skin incision (DIA). The occurrence of SN, ST and risk factors of HC were evaluated. Results. SN appeared in 2 cases treated with OIA (33%). There was no SN in DIA (0%). With this number of patients the difference was below level of significance, p = 0.1250, OR = 11.7. In one patient treated with SK+SH area of SN was 17.5 cm2. In the other patient treated with SK 35 cm2. Mean ST in SK was 3.4h (2.5–4.0) and in SK+SH 4.6h (4.0–5.5). ST of the surgery with OIA was 4.1h (2.5–5.5) and in DIA 3.7h (3.0–4.5), p = 0.4746. No additional risk factor relevant to SN was found. Keywords: SUPERknee, SUPERhip, super knee, super hip, healing complications, skin necrosis.

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14

Nita, Gelu M., Jack Hickish, David MacMahon, and Dale E. Gary. "EOVSA Implementation of a Spectral Kurtosis Correlator for Transient Detection and Classification." Journal of Astronomical Instrumentation 05, no. 04 (December 2016): 1641009. http://dx.doi.org/10.1142/s2251171716410099.

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We describe in general terms the practical use in astronomy of a higher-order statistical quantity called spectral kurtosis (SK), and describe the first implementation of SK-enabled firmware in the Fourier transform-engine (F-engine) of a digital FX correlator for the Expanded Owens Valley Solar Array (EOVSA). The development of the theory for SK is summarized, leading to an expression for generalized SK that is applicable to both SK spectrometers and those not specifically designed for SK. We also give the means for computing both the [Formula: see text] estimator and thresholds for its application as a discriminator of RFI contamination. Tests of the performance of EOVSA as an SK spectrometer are shown to agree precisely with theoretical expectations, and the methods for configuring the correlator for correct SK operation are described.

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15

Terentyev, Dmitry, Jennifer A. Rochira, Radmila Terentyeva, Karim Roder, Gideon Koren, and Weiyan Li. "Sarcoplasmic reticulum Ca2+ release is both necessary and sufficient for SK channel activation in ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 5 (March 1, 2014): H738—H746. http://dx.doi.org/10.1152/ajpheart.00621.2013.

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SK channels are upregulated in human patients and animal models of heart failure (HF). However, their activation mechanism and function in ventricular myocytes remain poorly understood. We aim to test the hypotheses that activation of SK channels in ventricular myocytes requires Ca2+ release from sarcoplasmic reticulum (SR) and that SK currents contribute to reducing triggered activity. SK2 channels were overexpressed in adult rat ventricular myocytes using adenovirus gene transfer. Simultaneous patch clamp and confocal Ca2+ imaging experiments in SK2-overexpressing cells demonstrated that depolarizations resulted in Ca2+-dependent outward currents sensitive to SK inhibitor apamin. SR Ca2+ release induced by rapid application of 10 mM caffeine evoked repolarizing SK currents, whereas complete depletion of SR Ca2+ content eliminated SK currents in response to depolarizations, despite intact Ca2+ influx through L-type Ca2+ channels. Furthermore, voltage-clamp experiments showed that SK channels can be activated by global spontaneous SR Ca2+ release events Ca2+ waves (SCWs). Current-clamp experiments revealed that SK overexpression reduces the amplitude of delayed afterdepolarizations (DADs) resulting from SCWs and shortens action potential duration. Immunolocalization studies showed that overexpressed SK channels are distributed both at external sarcolemmal membranes and along the Z-lines, resembling the distribution of endogenous SK channels. In summary, SR Ca2+ release is both necessary and sufficient for the activation of SK channels in rat ventricular myocytes. SK currents contribute to repolarization during action potentials and attenuate DADs driven by SCWs. Thus SK upregulation in HF may have an anti-arrhythmic effect by reducing triggered activity.

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TAKEUCHI, YASUO. "SOLAR NEUTRINO RESULTS FROM SUPER-KAMIOKANDE." International Journal of Modern Physics A 18, no. 22 (September 10, 2003): 3777–87. http://dx.doi.org/10.1142/s0217751x03017178.

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The solar neutrino results from 1496days of measurement from Super-Kamiokande-I (SK-I) are reported. The accident at SK-I, rebuilding of SK-II detector, and some prospects for SK-II are also reported briefly.

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Kostyliovienė, Silva, Gintarė Žiobaitė, Laura Urbonavičiūtė-Mikelkevičienė, Alina Vaškelytė, and Dovilė Grinkevičiūtė. "SLAUGYTOJŲ ŽINIOS APIE VAIKŲ SKAUSMO VERTINIMĄ." Visuomenės sveikata 27, no. 6 (December 28, 2017): 179–86. http://dx.doi.org/10.5200/sm-hs.2017.116.

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Skausmas yra vienas iš dažniausių simptomų, su kuriuo susiduria slaugytojai, slaugydami vaikus ligoninėse. Slaugytojams reikia turėti kompetencijos nuspręsti, kokį skausmo vertinimo instrumentą taikyti, į kokius aspektus atsižvelgti skausmo vertinimo metu. Mokslinių tyrimų rezultatai rodo, kad slaugytojų žinios apie vaikų skausmo vertinimą yra nepakankamos. Šio tyrimo tikslas buvo išanalizuoti slaugytojų žinias apie vaikų skausmo vertinimą. Anketinė apklausa atlikta 2016 m. vienoje iš didžiausių Lietuvos ligoninių vaikų chirurgijos (v. ch.) ir dviejuose vaikų ligų (v. l.) skyriuose. Tyrime dalyvavo 61 slaugytojas. Rezultatai. Buvo nustatyta, kad didesnė dalis respondentų, dirbančių I v. l. sk. (87,5 proc.) ir II v. l. sk. (66,7 proc.), teigė, jog skausmo intensyvumą tiksliausia įvardins pats pacientas, tačiau taip nurodė apie pusę (54,5 proc.) v. ch. sk. dirbančių respondentų (p=0,042). Dauguma (70,0 proc.) respondentų, dirbančių I v. l. sk. nurodė skausmo vertinimui naudojantys skales, tuo tarpu arti pusės (44,0 proc.) II v. l. sk. ir arti trečdalio (36,0 proc.) v. ch. sk. dirbančių respondentų skausmo skales naudojo reikalui esant (p=0,003). Didesnė dalis respondentų, dirbančių II v. l. sk. (80,0 proc.) ir v. ch. sk. (63,6 proc.), naudojo žodinę skausmo skalę, tuo tarpu tik apie pusė (45,8 proc.) I v. l. sk. dirbančių respondentų nurodė naudojantys šią skausmo skalę. Wong - Bakker veidelių išraiškos skalę skausmo vertinimui naudojo reikšmingai didesnė dalis respondentų, dirbančių I v. l. sk. (70,8 proc.) ir v. ch. sk. (54,5 proc.), lyginant su II v. l. sk. (13,3 proc.) dirbančiaisiais (p=0,003).

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Döll, Frauke, Josef Pfeilschifter, and Andrea Huwiler. "Prolactin upregulates sphingosine kinase-1 expression and activity in the human breast cancer cell line MCF7 and triggers enhanced proliferation and migration." Endocrine-Related Cancer 14, no. 2 (June 2007): 325–35. http://dx.doi.org/10.1677/erc-06-0050.

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Sphingosine kinases (SK) catalyze the formation of sphingosine-1-phosphate (S1P) which plays a crucial role in cell growth and survival. Here, we show that prolactin (PRL) biphasically activates the SK-1, but not the SK-2 subtype, in the breast adenocarcinoma cell-line MCF7. A first peak occurs after minutes of stimulation and is followed by a second delayed activation after hours of stimulation. A similar biphasic effect on SK-1 activity is seen for 17β-estradiol (E2). The delayed activation of SK-1 derives from an upregulated mRNA and protein expression and is due to increased SK-1 promoter activity and mechanistically involves STAT5 activation as well as protein kinase C and the classical mitogen-activated protein kinases. Furthermore, glucocorticoids also block both hormone-induced SK-1 expression and activity. Functionally, long-term stimulation of MCF7 cells with PRL or E2 is well known to trigger increased cell proliferation and migration. Both hormone-induced cell responses critically involve SK-1 activation since the depletion of SK-1, but not SK-2, by siRNA transfection abolishes the hormone-induced cell proliferation and migration. In summary, our data show that PRL and E2 cause a pronounced delayed SK-1 activation which is due to increased gene transcription, and critically determines the capability of cells to grow and move. Thus, the SK-1 may represent a novel attractive target for anti-tumor therapy.

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19

Kim, Wonki. "SK Headquarters Building, Seoul." Structural Engineering International 11, no. 1 (February 2001): 28–29. http://dx.doi.org/10.2749/101686601780324359.

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., Shanaz Ansari Wahid, Norris Sookoo ., and Ashok Sahai . "Lattices of SK-Partitions." Journal of Applied Sciences 7, no. 16 (August 1, 2007): 2366–70. http://dx.doi.org/10.3923/jas.2007.2366.2370.

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MOTEGI, Shujun. "avibhagad vaisvarupyasya (SK 15)." JOURNAL OF INDIAN AND BUDDHIST STUDIES (INDOGAKU BUKKYOGAKU KENKYU) 43, no. 1 (1994): 453–47. http://dx.doi.org/10.4259/ibk.43.453.

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Sharma, S. "Reply to SK Goyal." Journal of the Operational Research Society 57, no. 6 (June 2006): 748. http://dx.doi.org/10.1057/palgrave.jors.2602054.

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Adelman, John P. "SK channels and calmodulin." Channels 10, no. 1 (May 5, 2015): 1–6. http://dx.doi.org/10.1080/19336950.2015.1029688.

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Diaz, E., GR Goldberg, WA Coward, and AM Prentice. "Reply to SK Kumar." American Journal of Clinical Nutrition 54, no. 3 (September 1, 1991): 608–9. http://dx.doi.org/10.1093/ajcn/54.3.608a.

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Kraggerud, Egil. "Ennius Ann. 579 Sk." Symbolae Osloenses 89, no. 1 (January 2015): 54–59. http://dx.doi.org/10.1080/00397679.2015.1030896.

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Hay, D. W. P., J. F. Newton, T. J. Torphy, and J. G. Gleason. "SK&F-104353." Drugs of the Future 15, no. 3 (1990): 240. http://dx.doi.org/10.1358/dof.1990.015.03.115228.

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Badger, A. M., and D. A. Schwartz. "SK&F-105685." Drugs of the Future 16, no. 9 (1991): 815. http://dx.doi.org/10.1358/dof.1991.016.09.148126.

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Ife, R. J. "SK&F-96067." Drugs of the Future 17, no. 9 (1992): 796. http://dx.doi.org/10.1358/dof.1992.017.09.182872.

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Bagder, A., and C. S. Wright. "SK&F-106615." Drugs of the Future 20, no. 9 (1995): 893. http://dx.doi.org/10.1358/dof.1995.020.09.311577.

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30

Xu, Liang, Benlong Shi, Yong Qiu, Zhonghui Chen, Xi Chen, Song Li, Changzhi Du, Qingshuang Zhou, Zezhang Zhu, and Xu Sun. "How does the cervical spine respond to hyperkyphosis correction in Scheuermann’s disease?" Journal of Neurosurgery: Spine 31, no. 4 (October 2019): 493–500. http://dx.doi.org/10.3171/2019.3.spine1916.

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OBJECTIVEThis study aimed to quantify the response of the cervical spine to the surgical correction of Scheuermann’s kyphosis (SK) and to postoperative proximal junctional kyphosis (PJK).METHODSFifty-nine patients (mean age 14.6 ± 2.3 years) were enrolled in the study: 35 patients in a thoracic SK (T-SK) group and 24 in a thoracolumbar SK (TL-SK) group. The mean follow-up period was 47.2 ± 17.6 months. Radiographic data, PJK-related complications, and patient-reported outcomes were compared between groups.RESULTSThe global kyphosis significantly decreased postoperatively, and similar correction rates were observed between the two groups (mean 47.1% ± 8.6% [T-SK] vs 45.8% ± 9.4% [TL-SK], p = 0.585). The cervical lordosis (CL) in the T-SK group notably decreased from 21.4° ± 13.3° to 13.1° ± 12.4° after surgery and was maintained at 14.9° ± 10.7° at the latest follow-up, whereas in the TL-SK group, CL considerably increased from 7.2° ± 10.7° to 11.7° ± 11.1° after surgery and to 13.8° ± 8.9° at the latest follow-up. PJK was identified in 16 patients (27.1%). Its incidence in the TL-SK group was notably higher than it was in the T-SK group (41.6% [n = 10] vs 17.1% [n = 6], p = 0.037). Compared with non-PJK patients, PJK patients had greater CL and lower pain scores on the Scoliosis Research Society–22 questionnaire (p < 0.05).CONCLUSIONSHyperkyphosis correction eventually resulted in reciprocal changes in the cervical spine, with CL notably decreased in the T-SK group but significantly increased in the TL-SK group. Patients developing PJK have increased CL, which seems to have a negative effect on patients’ health-related quality of life.

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Campbell, Joseph L., and Barbara C. Turner. "Recombination block in the Spore killer region of Neurospora." Genome 29, no. 1 (February 1, 1987): 129–35. http://dx.doi.org/10.1139/g87-022.

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Spore killers Sk-2K and Sk-3K are chromosomal meiotic drive factors in Neurospora. In heterozygous crosses, ascospores not contining the Spore killer die. Sk-2K and Sk-3K, which differ in killing specificity, were found to be associated with suppression of recombination in a centromere-spanning region of linkage group III, and investigation of that recombination block is reported here. The block covers a region that is normally 30 to 40 map units long. A locus (r(Sk-2)) conferring resistance to Sk-2K maps to the left end of the recombination block. Recombination is normal in r(Sk-2) × Sk sensitive but blocked in Sk-2K × r(Sk-2); so the block does not depend upon killing. By selective plating, SkK stocks carrying genetic markers within the block were obtained at frequencies on the order of 10−5 or 10−6. Since this tight block is far beyond what has been observed for genetic reduction of recombination, a structural basis is assumed. No evidence of chromosome rearrangement was obtained. Crosses homozygous for Sk-2K show normal crossing-over and map order for the flanking markers cum and his-7 and three included markers (acr-7, acr-2, and leu-1). Results would be consistent with a divergence of sequence great enough to interfere with homologous pairing. Key words: meiotic drive, Neurospora, crossover suppressor.

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Bergelin, N., T. Blom, J. Heikkilä, C. Löf, C. Alam, S. Balthasar, J. P. Slotte, A. Hinkkanen, and K. Törnquist. "Sphingosine Kinase as an Oncogene: Autocrine Sphingosine 1-Phoshate Modulates ML-1 Thyroid Carcinoma Cell Migration by a Mechanism Dependent on Protein Kinase C-α and ERK1/2." Endocrinology 150, no. 5 (October 30, 2008): 2055–63. http://dx.doi.org/10.1210/en.2008-0625.

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Sphingosine 1-phosphate (S1P) induces migration of the human thyroid follicular carcinoma cell line ML-1 by activation of S1P1 and S1P3 receptors, Gi proteins, and the phosphatidylinositol 3-kinase-Akt pathway. Because sphingosine kinase isoform 1 (SK) recently has been implicated as an oncogene in various cancer cell systems, we investigated the functions of SK in the migration, proliferation and adhesion of the ML-1 cell line. SK overexpressing ML-1 cells show an enhanced secretion of S1P, which can be attenuated, by inhibiting SK activity and a multidrug-resistant transport protein (ATP-binding cassette transporter). Furthermore, overexpression of SK enhances serum-induced migration of ML-1 cells, which can be attenuated by blocking ATP-binding cassette transporter and SK, suggesting that the migration is mediated by autocrine signaling through secretion of S1P. Inhibition of protein kinase Cα, with both small interfering RNA (siRNA) and small molecular inhibitors attenuates migration in SK overexpressing cells. In addition, SK-overexpressing cells show an impaired adhesion, slower cell growth, and an up-regulation of ERK1/2 phosphorylation, as compared with cells expressing a dominant-negative SK. Taken together, we present evidence suggesting that SK enhances migration of ML-1 cells by an autocrine mechanism and that the S1P-evoked migration is dependent on protein kinase Cα, ERK1/2, and SK.

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Hancock, Jane, Andrew F. James, Jules C. Hancox, and Neil V. Marrion. "Effects of SK Channel Blockers on Atrial Myocytes Suggest SK Channel Heterogeneity." Biophysical Journal 104, no. 2 (January 2013): 283a. http://dx.doi.org/10.1016/j.bpj.2012.11.1585.

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Li, Xiaochun, Milena Stankovic, Claudine S. Bonder, Christopher N. Hahn, Michelle Parsons, Stuart M. Pitson, Pu Xia, Richard L. Proia, Mathew A. Vadas, and Jennifer R. Gamble. "Basal and angiopoietin-1–mediated endothelial permeability is regulated by sphingosine kinase-1." Blood 111, no. 7 (April 1, 2008): 3489–97. http://dx.doi.org/10.1182/blood-2007-05-092148.

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Abstract Endothelial cells (ECs) regulate the barrier function of blood vessels. Here we show that basal and angiopoietin-1 (Ang-1)–regulated control of EC permeability is mediated by 2 different functional states of sphingosine kinase-1 (SK-1). Mice depleted of SK-1 have increased vascular leakiness, whereas mice transgenic for SK-1 in ECs show attenuation of leakiness. Furthermore, Ang-1 rapidly and transiently stimulates SK-1 activity and phosphorylation, and induces an increase in intracellular sphingosine-1-phosphate (S1P) concentration. Overexpression of SK-1 resulted in inhibition of permeability similar to that seen for Ang-1, whereas knockdown of SK-1 by small interfering RNA blocked Ang-1-mediated inhibition of permeability. Transfection with SKS225A, a nonphosphorylatable mutant of SK-1, inhibited basal leakiness, and both SKS225A and a dominant-negative SK-1 mutant removed the capacity of Ang-1 to inhibit permeability. These effects were independent of extracellular S1P as knockdown or inhibition of S1P1, S1P2, or S1P3, did not affect the Ang-1 response. Thus, SK-1 levels in ECs powerfully regulate basal permeability in vitro and in vivo. In addition, the Ang-1–induced inhibition of leakiness is mediated through activation of SK-1, defining a new signaling pathway in the Ang-1 regulation of permeability.

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Zhang, Xiao-Dong, Phung N. Thai, Deborah K. Lieu, and Nipavan Chiamvimonvat. "Cardiac small-conductance calcium-activated potassium channels in health and disease." Pflügers Archiv - European Journal of Physiology 473, no. 3 (February 23, 2021): 477–89. http://dx.doi.org/10.1007/s00424-021-02535-0.

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AbstractSmall-conductance Ca2+-activated K+ (SK, KCa2) channels are encoded by KCNN genes, including KCNN1, 2, and 3. The channels play critical roles in the regulation of cardiac excitability and are gated solely by beat-to-beat changes in intracellular Ca2+. The family of SK channels consists of three members with differential sensitivity to apamin. All three isoforms are expressed in human hearts. Studies over the past two decades have provided evidence to substantiate the pivotal roles of SK channels, not only in healthy heart but also with diseases including atrial fibrillation (AF), ventricular arrhythmia, and heart failure (HF). SK channels are prominently expressed in atrial myocytes and pacemaking cells, compared to ventricular cells. However, the channels are significantly upregulated in ventricular myocytes in HF and pulmonary veins in AF models. Interests in cardiac SK channels are further fueled by recent studies suggesting the possible roles of SK channels in human AF. Therefore, SK channel may represent a novel therapeutic target for atrial arrhythmias. Furthermore, SK channel function is significantly altered by human calmodulin (CaM) mutations, linked to life-threatening arrhythmia syndromes. The current review will summarize recent progress in our understanding of cardiac SK channels and the roles of SK channels in the heart in health and disease.

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Hrabě, Petr, Viktor Kolář, Abraham Kabutey, and Aleš Sedláček. "Welding materials used to increase service life of agricultural machinery processing soil." MATEC Web of Conferences 244 (2018): 01002. http://dx.doi.org/10.1051/matecconf/201824401002.

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Intensive abrasive wear occurs in soil-treatment machines. This article is focused on increasing the service life of ploughs by the welding material. The welding material is applied at a 45° angle to the tool. This material is abrasive wear resistant. The welding material was applied parallel to the head of ploughshares with spacing of 60 mm. Carbide materials were used (SK 258 TiC-O, SK 900-O, SK A43-O, SK 299- O, SK A45-O, OK TUBRODUR 15.82, SK 258 TiC-O). The tested ploughshare variants were wearing the same when were used the welding material and the standard.

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Abdelouahed, Mustapha, Mohamed Hatmi, Gérard Helft, Sharareh Emadi, Ismaïl Elalamy, and Meyer Michel Samama. "Comparative Effects of Recombinant Staphylokinase and Streptokinase on Platelet Aggregation." Thrombosis and Haemostasis 77, no. 05 (1997): 0815–17. http://dx.doi.org/10.1055/s-0038-1656058.

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SummaryRecombinant staphylokinase (RSTA) has been shown to offer promise as a thrombolytic agent. In contrast to streptokinase (SK), few studies have been devoted to possible effects of RSTA on platelets. We have compared the capacity of RSTA and SK to trigger platelet aggregation and to modify ADP (2.5 µM) response in platelet-rich plasma (PRP) of 25 healthy subjects. Thus, exposure of PRP to SK (40 to 50 µg/ml) induced platelet aggregation in 6 out of 25 subjects. However, under the same conditions, RSTA failed to induce platelet aggregation in all cases (25 out of 25 subjects). In contrast to RSTA, SK (0.4 to 50 µg/ml) greatly reduced ADP-induced platelet aggregation in 12 out of 25 subjects. Preincubation of plasma with SK is associated with a decrease in the fibrinogen concentration. Furthermore, there was a good correlation between SK-induced fibrinogenolysis and SK- induced platelet aggregation defect (r2 = 0.9; p = 0.001). No fibrino genolysis was observed when different amounts of RSTA (0.4 to 50 µg/ml) were incubated in plasma for one min. However, there was a marked decrease in fibrinogen level (about 50%) when the plasma was incubated for five min with a very high concentration of RSTA. SK markedly enhanced the platelet response to ADP in 13 out of 25 subjects. In PRP of 6 out of 25 subjects, SK induces platelet aggregation and potentiates platelet response to ADP, however in PRP of 7 out of 25 subjects, SK caused only the increase of platelet response to ADP. The monoclonal antibody anti-FcγRIIal, IV-3 (2 [µ/ml), abolished SK-induced platelet aggregation and SK-enhanced ADP-induced platelet aggregation. In all cases (25 out of 25 subjects), RSTA failed to potentiate platelet response to ADP.These findings confirm that RSTA has a lesser fibrinogenolytic ability than SK and suggest its negligeable effect on platelet function.

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Trübestein, G. "Die Fibrinolysetherapie von Becken- und Beinvenenthrombosen." Hämostaseologie 12, no. 04 (October 1992): 142–48. http://dx.doi.org/10.1055/s-0038-1660332.

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ZusammenfassungDie fibrinolytische Therapie der Becken- und Beinvenenthrombosen ist ein anerkanntes therapeutisches Prinzip und wird überwiegend mit Streptokinase (SK) und Urokinase (UK) durchgeführt. Als Therapieschemata haben sich die konventionelle SK-Therapie mit 100000 IE SK/h über 3-6 Tage und die ultrahohe SK (UHSK)-Therapie mit 1,5 Mio. IE SK/h über 6 Stunden in 1-3 Zyklen sowie die konventionelle UK-Therapie mit 100000 IE UK/h über 7-14 Tage bewährt. Bei den konventionellen SK- und UK-Dosierungsschemata wird Heparin simultan verabreicht. Die Eröffnungsrate ist bei der konventionellen SK- und UK-Therapie am höchsten. Die Nebenwirkungsrate ist bei der konventionellen UK-Therapie und der UHSK-Therapie am geringsten. Neuere Fibrinolyse-Aktivatoren, wie der Gewebe-Plasminogenaktivator (rt-PA) und die Pro-Urokinase (SCUPA) stehen bei dieser Indikation in klinischer Erprobung.

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LANTERMAN, Margaret M., and Julie D. SABA. "Characterization of sphingosine kinase (SK) activity in Saccharomyces cerevisiae and isolation of SK-deficient mutants." Biochemical Journal 332, no. 2 (June 1, 1998): 525–31. http://dx.doi.org/10.1042/bj3320525.

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Sphingosine kinase (SK) catalyses the phosphorylation of sphingosine to generate sphingosine 1-phosphate, which is a second messenger involved in the proliferative responses of mammalian cells. Although the yeast Saccharomyces cerevisiae has similar phosphorylated sphingoid bases which appear to be involved in growth regulation and the response to stress, SK activity had not been previously demonstrated in yeast. In this study, an in vitro system was set up to characterize yeast SK activity. Activity was detected in the cytosol at neutral pH and 37 °C. Yeast SK phosphorylated the sphingoid bases sphingosine, dihydrosphingosine and phytosphingosine. (d,l)-threo-dihydrosphingosine, an inhibitor of mammalian SK, did not inhibit the yeast enzyme. Unique properties of yeast SK were an optimal temperature of 43 °C, and in vivo activation during nutrient deprivation. Spontaneous mutants with diminished SK activity were isolated utilizing a screen for resistance to sphingosine in a sphingosine-phosphate-lyase deletion background. Abnormal growth and heat sensitivity were observed in these mutants. These findings suggest that SK may function as a stress-response protein in yeast.

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Fay, William P., and Lakshmi V. Bokka. "Functional Analysis of the Amino- and Carboxyl-Termini of Streptokinase." Thrombosis and Haemostasis 79, no. 05 (1998): 985–91. http://dx.doi.org/10.1055/s-0037-1615107.

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SummaryStreptokinase (SK) is a 414 amino acid bacterial protein that activates human plasminogen. Streptokinase fragments derived from the central portion of the protein bind plasminogen, but are inactive, indicating that the amino- and/or carboxyl-termini are required for normal plasminogen activator activity. To better define the function of the N- and C-termini of SK we generated and characterized 21 N-terminal and 20 C-terminal deletion mutants. All mutants lacking ≥18 N-terminal or ≥51 C-terminal amino acids exhibited markedly reduced plasminogen activator activity, while mutants lacking ≤12 N-terminal or ≤40 C-terminal residues were fully active. The decrease in SK activity with N-terminal deletion appeared to result not from loss of plasminogen binding capacity, but rather from increased susceptibility of deletion mutants to degradation by plasmin. Point mutations at positions 13 (SK V13D) or 20 (SK V20D) produced functional abnormalities similar to those observed in N-terminal deletion mutants, with SK V13D exhibiting delayed amidolytic activity and SK V20D exhibiting only 1% plasminogen activator activity and marked sensitivity to degradation by plasmin. C-terminal deletion mutants lacking ≥51 amino acids also bound plasminogen, but did not induce significant amidolytic activity in plasminogen or activator activity in plasmin. Prevention of cleavage at position 59 of SK had no effect on plasminogen activator activity, suggesting that the rapid hydrolysis of this bond that occurs after SK-plasminogen complex formation is not required for normal function of the N-terminus. These results suggest that residues within or near positions 13-20 of SK are important determinants of its capacity to generate amidolytic activity and are a critical determinant of the stability of SK, while residues within or near position 364-374 are required for generating amidolytic activity and for conferring plasminogen activator activity to plasmin(ogen). These results also suggest that SK fragments significantly smaller than SK 13-374 are unlikely to be effective thrombolytic agents.

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Wei, Yuan, ZhiJian Wang, Elisa Babilonia, Hyacinth Sterling, Peng Sun, and WenHui Wang. "Effect of hydrogen peroxide on ROMK channels in the cortical collecting duct." American Journal of Physiology-Renal Physiology 292, no. 4 (April 2007): F1151—F1156. http://dx.doi.org/10.1152/ajprenal.00389.2006.

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We used the patch-clamp technique to study the effect of H2O2 on the apical ROMK-like small-conductance K (SK) channel in the cortical collecting duct (CCD). The addition of H2O2 decreased the activity of the SK channels and the inhibitory effect of H2O2 was larger in the CCD from rats on a K-deficient diet than that from rats on a normal-K or a high-K diet. However, application of H2O2 did not inhibit the SK channels in inside-out patches. This suggests that the H2O2-mediated inhibition of SK channels was not due to direct oxidation of the SK channel protein. Because a previous study showed that H2O2 stimulated the expression of Src family protein tyrosine kinase (PTK) which inhibited SK channels ( 3 ), we explored the role of PTK in mediating the effect of H2O2 on SK channels. The application of H2O2 stimulated the activity of endogenous PTK in M-1 cells and increased tyrosine phosphorylation of ROMK in HEK293 cells transfected with GFP-ROMK1 and c-Src. However, blockade of PTK only attenuated but did not completely abolish the inhibitory effect of H2O2 on SK channels. Since H2O2 has also been demonstrated to activate mitogen-activated protein kinase, P38, and ERK ( 3 ), we examined the role of P38 and ERK in mediating the effect of H2O2 on SK channels. Similar to blockade of PTK, suppression of P38 and ERK did not completely abolish the H2O2-induced inhibition of SK channels. However, combined use of ERK, P38, and PTK inhibitors completely abolished the effect of H2O2 on SK channels. Also, treatment of the CCDs with concanavalin A, an agent which has been shown to inhibit endocytosis ( 19 ), abolished the inhibitory effect of H2O2. We conclude that addition of H2O2 inhibited SK channels by stimulating PTK activity, P38, and ERK in the CCD and that H2O2 enhances the internalization of the SK channels.

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Schwalm, Stephanie, Tankica Maneva Timcheva, Iuliia Filipenko, Mahsa Ebadi, Lotte P. Hofmann, Uwe Zangemeister-Wittke, Josef Pfeilschifter, and Andrea Huwiler. "Sphingosine kinase 2 deficiency increases proliferation and migration of renal mouse mesangial cells and fibroblasts." Biological Chemistry 396, no. 6-7 (June 1, 2015): 813–25. http://dx.doi.org/10.1515/hsz-2014-0289.

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Abstract Both of the sphingosine kinase (SK) subtypes SK-1 and SK-2 catalyze the production of the bioactive lipid molecule sphingosine 1-phosphate (S1P). However, the subtype-specific cellular functions are largely unknown. In this study, we investigated the cellular function of SK-2 in primary mouse renal mesangial cells (mMC) and embryonic fibroblasts (MEF) from wild-type C57BL/6 or SK-2 knockout (SK2ko) mice. We found that SK2ko cells displayed a significantly higher proliferative and migratory activity when compared to wild-type cells, with concomitant increased cellular activities of the classical extracellular signal regulated kinase (ERK) and PI3K/Akt cascades, and of the small G protein RhoA. Furthermore, we detected an upregulation of SK-1 protein and S1P3 receptor mRNA expression in SK-2ko cells. The MEK inhibitor U0126 and the S1P1/3 receptor antagonist VPC23019 blocked the increased migration of SK-2ko cells. Additionally, S1P3ko mesangial cells showed a reduced proliferative behavior and reduced migration rate upon S1P stimulation, suggesting a crucial involvement of the S1P3 receptor. In summary, our data demonstrate that SK-2 exerts suppressive effects on cell growth and migration in renal mesangial cells and fibroblasts, and that therapeutic targeting of SKs for treating proliferative diseases requires subtype-selective inhibitors.

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Jia, Yanqiu, Zhe Li, Tianjun Wang, Mingyue Fan, Jiaxi Song, Peiyuan Lv, and Wei Jin. "Shikonin Attenuates Chronic Cerebral Hypoperfusion-Induced Cognitive Impairment by Inhibiting Apoptosis via PTEN/Akt/CREB/BDNF Signaling." Evidence-Based Complementary and Alternative Medicine 2021 (June 7, 2021): 1–9. http://dx.doi.org/10.1155/2021/5564246.

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Shikonin (SK) exerts neuroprotective effects; however, to date, its protective effect against chronic cerebral hypoperfusion- (CCH-) induced vascular dementia (VaD) has not been investigated. Therefore, the current study investigated whether SK could mitigate the cognitive deficits caused by CCH. The effects of SK treatment on the PTEN/Akt/CREB/BDNF signaling pathway and apoptosis in hippocampal neurons were examined in a rat model of VaD established via bilateral common carotid artery occlusion (BCCAO). Fifty-two rats were randomly divided into 4 groups: sham, vehicle, SK-L (10 mg/kg SK per day), and SK-H (25 mg/kg SK per day). SK was regularly administered by gavage for 2 weeks. The results of the water maze test revealed that the escape latency in the vehicle group was significantly longer than that in the sham group, and rats in the vehicle group spent a smaller proportion of time in the target quadrant than those in the sham group. SK treatment reduced the escape latencies and increased the proportion of time spent in the target quadrant. Nissl staining showed morphological damage in the CA1 areas of the hippocampus in the vehicle group. SK treatment alleviated the injuries to hippocampal neurons. Western blot analysis showed higher p-PTEN and lower p-Akt, p-CREB, and BDNF expression in the vehicle group than in the sham group. SK administration reversed the upregulation of p-PTEN and the downregulation of p-Akt, p-CREB, and BDNF. The number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling- (TUNEL-) positive cells in the hippocampal CA1 region of the vehicle group was significantly increased. Treatment with SK decreased the number of positive cells. Furthermore, as marker proteins of apoptosis, bcl-2 expression was decreased and bax expression was increased; thus, the ratio of bcl-2/bax was decreased in the vehicle group. SK treatment upregulated the expression of bcl-2 and downregulated the expression of bax, thereby elevating the bcl-2/bax ratio. Moreover, the aforementioned effects of SK were dose-dependent. The effect of 25 mg/kg per day was more obvious than that of 10 mg/kg per day. In conclusion, SK inhibited hippocampal neuronal apoptosis to protect against CCH-induced injury by regulating the PTEN/Akt/CREB/BDNF signaling pathway, consequently improving cognitive impairment.

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Salas, Arelis, Suriyan Ponnusamy, Can E. Senkal, Marisa Meyers-Needham, Shanmugam Panneer Selvam, Sahar A. Saddoughi, Elif Apohan, et al. "Sphingosine kinase-1 and sphingosine 1-phosphate receptor 2 mediate Bcr-Abl1 stability and drug resistance by modulation of protein phosphatase 2A." Blood 117, no. 22 (June 2, 2011): 5941–52. http://dx.doi.org/10.1182/blood-2010-08-300772.

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Abstract The mechanisms by which sphingosine kinase-1 (SK-1)/sphingosine 1-phosphate (S1P) activation contributes to imatinib resistance in chronic myeloid leukemia (CML) are unknown. We show herein that increased SK-1/S1P enhances Bcr-Abl1 protein stability, through inhibition of its proteasomal degradation in imatinib-resistant K562/IMA-3 and LAMA-4/IMA human CML cells. In fact, Bcr-Abl1 stability was enhanced by ectopic SK-1 expression. Conversely, siRNA-mediated SK-1 knockdown in K562/IMA-3 cells, or its genetic loss in SK-1−/− MEFs, significantly reduced Bcr-Abl1 stability. Regulation of Bcr-Abl1 by SK-1/S1P was dependent on S1P receptor 2 (S1P2) signaling, which prevented Bcr-Abl1 dephosphorylation, and degradation via inhibition of PP2A. Molecular or pharmacologic interference with SK-1/S1P2 restored PP2A-dependent Bcr-Abl1 dephosphorylation, and enhanced imatinib- or nilotinib-induced growth inhibition in primary CD34+ mononuclear cells obtained from chronic phase and blast crisis CML patients, K562/IMA-3 or LAMA4/IMA cells, and 32Dcl3 murine progenitor cells, expressing the wild-type or mutant (Y253H or T315I) Bcr-Abl1 in situ. Accordingly, impaired SK-1/S1P2 signaling enhanced the growth-inhibitory effects of nilotinib against 32D/T315I-Bcr-Abl1–derived mouse allografts. Since SK-1/S1P/S1P2 signaling regulates Bcr-Abl1 stability via modulation of PP2A, inhibition of SK-1/S1P2 axis represents a novel approach to target wild-type- or mutant-Bcr–Abl1 thereby overcoming drug resistance.

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Meyer, Merle E., and Jonathan M. Shults. "Dopamine D1 receptor family agonists, SK&F38393, SK&F77434, and SK&F82958, Differentially affect locomotor activities in rats." Pharmacology Biochemistry and Behavior 46, no. 2 (October 1993): 269–74. http://dx.doi.org/10.1016/0091-3057(93)90352-t.

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Kurniawan, Fatwa Aji, and Ahmad Aftah Syukron. "Karakteristik Briket Bioarang dari Campuran Limbah Baglog Jamur Tiram (Pleurotus Ostreatus) dan Sekam Padi." INDONESIAN JOURNAL OF APPLIED PHYSICS 9, no. 02 (December 8, 2019): 76. http://dx.doi.org/10.13057/ijap.v9i2.34478.

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Kebijakan diversifikasi energi yang dikeluarkan Pemerintah Indonesia menuntut masyarakat untuk menemukan bahan bakar selain fosil. Penelitian ini bertujuan untuk menghasilkan briket dari campuran arang limbah baglog jamur tiram (JT) dan arang sekam padi (SK) yang berkualitas sehingga dapat digunakan sebagai bahan bakar alternatif. Penelitian ini secara garis besar dilakukan dalam tiga tahap yaitu pengarangan atau karbonisasi, pembriketan dan pengujian kualitas briket. Variabel yang digunakan dalam penelitian ini adalah komposisi campuran JT dan SK. Komposisi campuran yang digunakan yaitu 100% JT:0% SK untuk sampel A, 75% JT:25% SK untuk sampel B, 50% JT:50% SK untuk sampel C, 25% JT:75% SK untuk sampel D dan 0% JT:100% SK untuk sampel E. Dari hasil penelitian disimpulkan bahwa campuran yang paling optimal untuk mendapatkan briket berkualitas baik yaitu dengan komposisi 50% arang limbah baglog jamur tiram : 50% arang sekam padi dimana diperoleh nilai kalor sebesar 3541 kal/gr, kadar air 1.57% dan kadar abu 36.20%.

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Bonder, Claudine S., Wai Y. Sun, Tyson Matthews, Carlos Cassano, Xiaochun Li, Hayley S. Ramshaw, Stuart M. Pitson, et al. "Sphingosine kinase regulates the rate of endothelial progenitor cell differentiation." Blood 113, no. 9 (February 26, 2009): 2108–17. http://dx.doi.org/10.1182/blood-2008-07-166942.

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Circulating endothelial progenitor cells (EPCs) are incorporated into foci of neovascularization where they undergo differentiation to mature endothelial cells (ECs). We show here that the enzyme sphingosine kinase-1 (SK-1) regulates the rate and direction of EPC differentiation without effect on the hematopoietic compartment. EPCs have high levels of SK-1 activity, which diminishes with differentiation and is, at least partially, responsible for maintaining their EPC phenotype. EPCs from SK-1 knockout mice form more adherent EC units and acquire a mature EC phenotype more rapidly. Conversely, EPCs from mice overexpressing SK-1 in the EC compartment are retarded in their differentiation. Exogenous regulation of SK-1 levels in normal EPCs, by genetic and pharmacologic means, including the immunomodulating drug FTY720, recapitulates these effects on EC differentiation. SK-1 knockout mice have higher levels of circulating EPCs, an exaggerated response to erythropoietin-induced EPC mobilization, and, in a mouse model of kidney ischemia reperfusion injury, exhibit a recovery similar to that of ischemic mice administered exogenous EPCs. Thus, SK-1 is a critical player in EPC differentiation into EC pointing to the potential utility of SK-1 modifying agents in the specific manipulation of endothelial development and repair.

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Lee, Jeong Min, Chae Young Kim, Sung-Hoon Chung, Yong-Sung Choi, and Chong-Woo Bae. "Comparison of Maternal and Child Health Statistics between South and North Korea." Journal of The Korean Society of Maternal and Child Health 24, no. 3 (July 31, 2020): 170–80. http://dx.doi.org/10.21896/jksmch.2020.24.3.170.

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Purpose: This study aimed to investigate the extent of the difference in health status between South Korea (SK) and North Korea (NK) by comparing indicators relevant to maternal and child health.Methods: The maternal and child health status of SK and NK considering population, birth, and mortality was reviewed using 2 Korean statistics, United Nations Children’s Fund, and United Nations databases from 1950 to 2017.Results: The annual number of total live births in SK had decreased from 1,006,600 in 1970 to 326,900 in 2018, and that in NK had declined from 530,000 in 1970 to 360,000 in 2015. The percentage of children among the total population was higher in NK than in SK, and the decrease in the percentage of children in SK is remarkable, which is related to a low fertility rate in the last few decades. However, the mortality rates related to children were higher in NK than in SK. In 2017, neonatal mortality rates (per 1,000 live births) in SK and NK were 1.5 and 9.0, respectively. The fertile female population of SK and NK in 2015 was 50.2% and 52.0%, respectively, and SK and NK’s aging index (%) in 2017 was 107.3 and 46.1, respectively.Conclusion: This study shows the different population distributions and maternal and child health statuses between SK and NK, which may have a negative impact on social integration after reunification. Therefore, it is important to understand the indicators of maternal and child health to become the powerbase of efficient healthcare system integration by minimizing the impact at the beginning of the reunification.

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Lebrazi, Jamal, Gérard Helft, Mustapha Abdelouahed, Ismaïl Elalamy, Massoud Mirshahi, Michel Meyer Samama, and Thomas Lecompte. "Human Anti-Streptokinase Antibodies Induce Platelet Aggregation in an Fc Receptor (CD32) Dependent Manner." Thrombosis and Haemostasis 74, no. 03 (1995): 938–42. http://dx.doi.org/10.1055/s-0038-1649851.

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SummaryExposure to streptokinase (SK) elicits anti-SK antibodies (Abs), which inhibit fibrinolysis and induce platelet aggregation. The mechanism of the latter is not fully understood, although it seems to involve platelet binding by a plasminogen streptokinase and anti-SK ternary complex. Anti-SK Abs were purified by affinity chromatography from serum of patients having received SK for acute myocardial infarction (AMI), and were shown to be of the IgG type. Their effects were studied with (i) human platelets in citrated plasma in the presence of SK or acetylated plasminogen-SK activator complex (APSAC), and (ii) in washed platelets, resuspended in Tyrode buffer after lowering the ionic strength, in the presence of APSAC (which provides both SK and plasminogen). An antibody concentration-response curve was obtained, showing a plateau in the presence of 0.1 mg/ml IgG. By increasing the concentration of APSAC, we obtained a unimodal response curve, the optimal concentration of APSAC being 0.05 U/ml. Aggregation was suppressed by chelating calcium with EDTA, blocking fibrinogen binding by the synthetic peptide Arg-Gly-Asp-Ser (RGDS), and raising intraplatelet cAMP with Iloprost (a prostacyclin analogue). Aggregation required the interaction of the anti-SK Ab Fc domain with the platelet Fc-gamma receptor type II, also known as CD32, since: (i) it was blocked by the monoclonal antibody IV-3 directed against CD32, (ii) it did not occur with F(ab)’2 fragments, which block the response to the intact IgG. The clinical relevance of these platelet-activating anti-SK antibodies remains to be determined. Two factors might influence clinical outcome: (i) the amount and type of pre-existing anti-SK Abs; (ii) the known interindividual variability of the platelet response to binding and activation by IgG involving the CD32 molecule.

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Li, Weiyan, David B. Halling, Amelia W. Hall, and Richard W. Aldrich. "EF hands at the N-lobe of calmodulin are required for both SK channel gating and stable SK–calmodulin interaction." Journal of General Physiology 134, no. 4 (September 14, 2009): 281–93. http://dx.doi.org/10.1085/jgp.200910295.

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Abstract:

Small conductance calcium-activated potassium (SK) channels respond to intracellular Ca2+ via constitutively associated calmodulin (CaM). Previous studies have proposed a modular design for the interaction between CaM and SK channels. The C-lobe and the linker of CaM are thought to regulate the constitutive binding, whereas the N-lobe binds Ca2+ and gates SK channels. However, we found that coexpression of mutant CaM (E/Q) where the N-lobe has only one functional EF hand leads to rapid rundown of SK channel activity, which can be recovered with exogenously applied wild-type (WT), but not mutant, CaM. Our results suggest that the mutation at the N-lobe EF hand disrupts the stable interaction between CaM and SK channel subunits, such that mutant CaM dissociates from the channel complex when the inside of the membrane is exposed to CaM-free solution. The disruption of the stable interaction does not directly result from the loss of Ca2+-binding capacity because SK channels and WT CaM can stably interact in the absence of Ca2+. These findings question a previous conclusion that CaM where the N-lobe has only one functional EF hand can stably support the gating of SK channels. They cannot be explained by the current model of modular interaction between CaM and SK channels, and they imply a role for N-lobe EF hand residues in binding to the channel subunits. Additionally, we found that a potent enhancer for SK channels, 3-oxime-6,7-dichloro-1H-indole-2,3-dione (NS309), enables the recovery of channel activity with CaM (E/Q), suggesting that NS309 stabilizes the interaction between CaM and SK channels. CaM (E/Q) can regulate Ca2+-dependent gating of SK channels in the presence of NS309, but with a lower apparent Ca2+ affinity than WT CaM.

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