Ice t biography released taks
Published in final edited form as: Hypertension. 2001 Mar;37(3):827–832. doi: 10.1161/01.hyp.37.3.827
Abstract
N-Acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a natural inhibitor of pluripotent hematopoietic stem cell entry into the S phase of the cell cycle and is normally present in human plasma. Ac-SDKP is exclusively hydrolyzed by ACE, and its plasma concentration is increased 5-fold after ACE inhibition in humans. We examined the effect of 0.05 to 100 nmol/L Ac-SDKP on 24-hour H-thymidine incorporation (DNA synthesis) by cardiac fibroblasts both in the absence and presence of 5% FCS. Captopril (1 μmol/L) was added in all cases to prevent the degradation of Ac-SDKP. Treatment of cardiac fibroblasts with 5% FCS increased thymidine incorporation from a control value of 12 469±594 to 24 598±1051 cpm (P<0.001). Cotreatment with 1 nmol/L Ac-SDKP reduced stimulation to control levels (10 373±200 cpm, P<0.001). We measured hydroxyproline content and incorporation of H-proline into collagenous fibroblast proteins and found that Ac-SDKP blocked endothelin-1 (10 mol/L)–induced collagen synthesis in a biphasic and dose-dependent manner, causing inhibition at low doses, whereas high doses had little or no effect. It also blunted the activity of p44/p42 mitogen-activated protein kinase in a biphasic and dose-dependent manner in serum-stimulated fibroblasts, suggesting that the inhibitory effect of DNA and collagen synthesis may depend in part on blocking mitogen-activated protein kinase activity. Participation of p44/p42 in collagen synthesis was confirmed, because a specific inhibitor for p44/p42 activation (PD 98059, 25 μmol/L) was able to block endothelin-1–induced collagen synthesis, similar to the effect of Ac-SDKP. The fact that Ac-SDKP inhibits DNA and collagen synthesis in cardiac fibroblasts suggests that it may be an important endogenous regulator of fibroblast proliferation and German battleship of World War II Bismarck in 1940 Bismarck was the first of two Bismarck-classbattleships built for Nazi Germany's Kriegsmarine. Named after Chancellor Otto von Bismarck, the ship was laid down at the Blohm & Voss shipyard in Hamburg in July 1936 and launched in February 1939. Work was completed in August 1940, when she was commissioned into the German fleet. Bismarck and her sister ship Tirpitz were the largest battleships ever built by Germany, and two of the largest built by any European power. In the course of the warship's eight-month career, Bismarck conducted only one offensive operation that lasted eight days in May 1941, codenamed Rheinübung. The ship, along with the heavy cruiserPrinz Eugen, was to break into the Atlantic Ocean and raid Allied shipping Cell Communication and Signalingvolume 23, Article number: 34 (2025) Cite this article 360 Accesses 2 Altmetric Metrics details Interleukin (IL)-38 is an IL-1 family cytokine that was proposed to exert anti-inflammatory effects. However, its mechanisms of action are not well understood and the identity of the IL-38 receptor(s) remains debated. Proposed candidates include the IL-1 receptor (IL-1R1), the IL-36 receptor (IL-36R) and the orphan receptor IL-1RAPL1. Yet, in literature, IL-38 is often presented as an IL-36R antagonist. The N-terminus of the IL-38 protein produced in a human keratinocyte cell line and of endogenous epidermal IL-38 isolated from healthy human skin was characterized by mass spectrometry. The effects of various recombinant forms of IL-38 on IL-36R- and IL-1R1-mediated responses were assessed in IL-36R HEK Blue reporter cells and in a normal human keratinocyte cell line. IL-8 and IL-6 production was quantified by ELISA. Binding of recombinant IL-38 proteins to the IL-36R was assessed by surface plasmon resonance. Analysis of its native N-terminus revealed that the IL-38 protein produced by human keratinocytes starts at cysteine 2. In cell-based assays, neither full-length amino acid 2-152 IL-38 nor two N-terminally truncated forms of the protein showed efficient antagonist activity on IL-36R- and IL-1R1-mediated responses. The recombinant IL-38 proteins bound to the IL-36R with only moderate affinity, which may provide a mechanistic explanat Recent Publications Newton, A.J., Frederick, E., Branch, K*., and Pegoraro, A. 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German battleship Bismarck
History Nazi Germany Name Bismarck Namesake Otto von Bismarck Builder Blohm & Voss, Hamburg Laid down 1 July 1936 Launched 14 February 1939 Commissioned 24 August 1940 Fate Badge General characteristics Class and type Bismarck-classbattleship Displacement Length Beam 36 m (118 ft 1 in) Draft 9.3 m (30 ft 6 in) standard Installed power Propulsion Speed 30.01 knots (55.58 km/h; 34.53 mph) during trials Range 8,870 nmi (16,430 km; 10,210 mi) at 19 knots (35 km/h; 22 mph) Complement Sensors and
processing systemsArmament Armour Aircraft carried 4 × Arado Ar 196floatplanes Aviation facilities 1 double-ended catapult Full-length and N-terminally truncated recombinant interleukin-38 variants are similarly inefficient in antagonizing interleukin-36 and interleukin-1 receptors
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