Western Blot:Article Title: Morinda citrifolia mitigates rotenone-induced striatal neuronal loss in male Sprague-Dawley rats by preventing mitochondrial pathway of intrinsic apoptosis
Article Snippet: .. Both MCE and LD treatment reduces the cytochrome c levels in the cytosol by 12% (as the levels of mitochondrial cytochrome c levels were increased on treatment with MCE/LD by 28%) when compared with rotenone alone infused Group III rats. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Immunoblot analysis of cytosolic (a) and mitochondrial (b) cytochrome c in the striatum of experimental animals followed by densitometric analysis of respective protein levels (c). (d) depicts the ratio of cytosolic and mitochondrial cytochrome c. Values are expressed as mean ± SEM for three experiments in each group. .. Values are statistically significant at the level of P < 0.05 where ‘a’ represents Control, Sham Vs other groups, ‘b’ represents Rot Ind vs LD, MCE. mRNA and protein expression of pro-apoptotic and anti-apoptotic proteins and show the levels of mRNA and protein of pro-apoptotic Bax, caspase-3 and caspase-9 and anti-apoptotic Bcl-2 in the striatum of stereotaxically rotenone-infused Parkinsonian rats treated with or without MCE/LD.
Staining:Article Title: LetB structure reveals a tunnel for lipid transport across the bacterial envelope
Article Snippet: .. Thus, naturally occurring MCE proteins have evolved to form barrels with a range of lengths, perhaps in part to adapt to differences in the mean periplasmic width in different species and to accommodate larger or smaller interacting complexes in the IM or OM. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 3. caption a7 caption a8 MCE domains are modular building blocks that determine the length of MCE protein assemblies. (A) Cartoon representations of E. coli MCE proteins MlaD (PDB ID: 5UW2), PqiB (PDB ID: 5UVN) and LetB, which contain one, three and seven MCE domains, respectively, and form architectures with the corresponding number of rings. (B) Negative stain EM 2D class averages of naturally occurring proteins encoding four ( Desulfocapsa sulfexigens ), five ( Nitrincola nitratireducens ), six ( Pseudomonas aeruginosa ), seven ( E. coli , LetB), and eight ( Denitrovibrio acetiphilus ) MCE domains ( Figure S6 ). .. Schematics to the left of 2D class averages indicate number of MCE domains present in the gene (rectangles) and expected number of rings based on modularity of MCE domains (ovals). (C) Truncated constructs designed to modulate number of MCE rings in LetB and their expected length in the context of the periplasm.
other:Article Title: Analysis of Cloud-Resolving Model Simulations for Scale Dependence of Convective Momentum Transport
Article Snippet: MC3E-0520 squall line shows similar results to MCE-0523 (Figures not shown), indicating that both updraft and downdraft mass fluxes have strong scale dependency. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 4. caption a7 Time-height cross sections of ensemble mean mass flux (kg m −2 s −1 ) in (a) convective updrafts and (b) downdrafts for dx = 8 km and dx = 128 km from MC3E-0523.
Ex Vivo:Article Title: Platelet protein S limits venous but not arterial thrombosis propensity by controlling coagulation in the thrombus
Article Snippet: .. In addition, the clot elasticity attributable to platelets (MCE plt ) 39 was comparable in Pros1 lox/lox Pf4-Cre − mice and Pros1 lox/lox Pf4-Cre + mice (211 ± 10 vs 209 ± 62, respectively; P > .05). fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 3. caption a7 Lack of PS in platelets affects global hemostasis assessment ex vivo and in vivo. (A-B) Whole blood activation of coagulation and clot polymerization determined by ROTEM analysis rotational (thromboelastography). (A) Extrinsic‐activated rotational thromboelastometry (EXTEM) assay, (B) extrinsically activated thromboelastometric test with cytochalasin D (FIBTEM). .. CT, coagulation time; CFT, clot formation time; α, α-angle; CFR, clot formation rate, MCF, maximum clot firmness; MCE, maximum clot elasticity. (C-D) Total thrombus-formation analysis on whole blood on collagen and TF-coated chip (AR-chip) at low (240 s −1 , C) and high (600 s −1 , D) shear rate. (E-F) Bleeding time (E) and blood loss (F) were measured after 2-mm tail transection in Pros1 lox/lox Pf4-Cre − (n = 7), Pros1 lox/lox Pf4-Cre + (n = 7), and Pros1 lox/− (n = 5) mice.
In Vivo:Article Title: Platelet protein S limits venous but not arterial thrombosis propensity by controlling coagulation in the thrombus
Article Snippet: .. In addition, the clot elasticity attributable to platelets (MCE plt ) 39 was comparable in Pros1 lox/lox Pf4-Cre − mice and Pros1 lox/lox Pf4-Cre + mice (211 ± 10 vs 209 ± 62, respectively; P > .05). fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 3. caption a7 Lack of PS in platelets affects global hemostasis assessment ex vivo and in vivo. (A-B) Whole blood activation of coagulation and clot polymerization determined by ROTEM analysis rotational (thromboelastography). (A) Extrinsic‐activated rotational thromboelastometry (EXTEM) assay, (B) extrinsically activated thromboelastometric test with cytochalasin D (FIBTEM). .. CT, coagulation time; CFT, clot formation time; α, α-angle; CFR, clot formation rate, MCF, maximum clot firmness; MCE, maximum clot elasticity. (C-D) Total thrombus-formation analysis on whole blood on collagen and TF-coated chip (AR-chip) at low (240 s −1 , C) and high (600 s −1 , D) shear rate. (E-F) Bleeding time (E) and blood loss (F) were measured after 2-mm tail transection in Pros1 lox/lox Pf4-Cre − (n = 7), Pros1 lox/lox Pf4-Cre + (n = 7), and Pros1 lox/− (n = 5) mice.
Activation Assay:Article Title: Platelet protein S limits venous but not arterial thrombosis propensity by controlling coagulation in the thrombus
Article Snippet: .. In addition, the clot elasticity attributable to platelets (MCE plt ) 39 was comparable in Pros1 lox/lox Pf4-Cre − mice and Pros1 lox/lox Pf4-Cre + mice (211 ± 10 vs 209 ± 62, respectively; P > .05). fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 3. caption a7 Lack of PS in platelets affects global hemostasis assessment ex vivo and in vivo. (A-B) Whole blood activation of coagulation and clot polymerization determined by ROTEM analysis rotational (thromboelastography). (A) Extrinsic‐activated rotational thromboelastometry (EXTEM) assay, (B) extrinsically activated thromboelastometric test with cytochalasin D (FIBTEM). .. CT, coagulation time; CFT, clot formation time; α, α-angle; CFR, clot formation rate, MCF, maximum clot firmness; MCE, maximum clot elasticity. (C-D) Total thrombus-formation analysis on whole blood on collagen and TF-coated chip (AR-chip) at low (240 s −1 , C) and high (600 s −1 , D) shear rate. (E-F) Bleeding time (E) and blood loss (F) were measured after 2-mm tail transection in Pros1 lox/lox Pf4-Cre − (n = 7), Pros1 lox/lox Pf4-Cre + (n = 7), and Pros1 lox/− (n = 5) mice.
Coagulation:Article Title: Platelet protein S limits venous but not arterial thrombosis propensity by controlling coagulation in the thrombus
Article Snippet: .. In addition, the clot elasticity attributable to platelets (MCE plt ) 39 was comparable in Pros1 lox/lox Pf4-Cre − mice and Pros1 lox/lox Pf4-Cre + mice (211 ± 10 vs 209 ± 62, respectively; P > .05). fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 3. caption a7 Lack of PS in platelets affects global hemostasis assessment ex vivo and in vivo. (A-B) Whole blood activation of coagulation and clot polymerization determined by ROTEM analysis rotational (thromboelastography). (A) Extrinsic‐activated rotational thromboelastometry (EXTEM) assay, (B) extrinsically activated thromboelastometric test with cytochalasin D (FIBTEM). .. CT, coagulation time; CFT, clot formation time; α, α-angle; CFR, clot formation rate, MCF, maximum clot firmness; MCE, maximum clot elasticity. (C-D) Total thrombus-formation analysis on whole blood on collagen and TF-coated chip (AR-chip) at low (240 s −1 , C) and high (600 s −1 , D) shear rate. (E-F) Bleeding time (E) and blood loss (F) were measured after 2-mm tail transection in Pros1 lox/lox Pf4-Cre − (n = 7), Pros1 lox/lox Pf4-Cre + (n = 7), and Pros1 lox/− (n = 5) mice.
FIBTEM Assay:Article Title: Platelet protein S limits venous but not arterial thrombosis propensity by controlling coagulation in the thrombus
Article Snippet: .. In addition, the clot elasticity attributable to platelets (MCE plt ) 39 was comparable in Pros1 lox/lox Pf4-Cre − mice and Pros1 lox/lox Pf4-Cre + mice (211 ± 10 vs 209 ± 62, respectively; P > .05). fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 3. caption a7 Lack of PS in platelets affects global hemostasis assessment ex vivo and in vivo. (A-B) Whole blood activation of coagulation and clot polymerization determined by ROTEM analysis rotational (thromboelastography). (A) Extrinsic‐activated rotational thromboelastometry (EXTEM) assay, (B) extrinsically activated thromboelastometric test with cytochalasin D (FIBTEM). .. CT, coagulation time; CFT, clot formation time; α, α-angle; CFR, clot formation rate, MCF, maximum clot firmness; MCE, maximum clot elasticity. (C-D) Total thrombus-formation analysis on whole blood on collagen and TF-coated chip (AR-chip) at low (240 s −1 , C) and high (600 s −1 , D) shear rate. (E-F) Bleeding time (E) and blood loss (F) were measured after 2-mm tail transection in Pros1 lox/lox Pf4-Cre − (n = 7), Pros1 lox/lox Pf4-Cre + (n = 7), and Pros1 lox/− (n = 5) mice.
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