Ignet

Gene Information

Gene symbol: CPB2

Gene name: carboxypeptidase B2 (plasma)

HGNC ID: 2300

Synonyms: CPU, PCPB, TAFI

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	ALB	1 hits
3	C20orf181	1 hits
4	CD40	1 hits
5	CD40LG	1 hits
6	COL9A3	1 hits
7	F2	1 hits
8	HBB	1 hits
9	IL6	1 hits
10	INS	1 hits
11	MMP1	1 hits
12	PI3	1 hits
13	PIK3CG	1 hits
14	PLAT	1 hits
15	PLG	1 hits
16	SERPINC1	1 hits
17	SERPINE1	1 hits
18	TFPI	1 hits
19	THBD	1 hits
20	TNNT2	1 hits
21	VEGFA	1 hits
22	VWF	1 hits
23	ZDHHC23	1 hits

Related Sentences

#	PMID	Sentence
1	2140181	Urinary (CPU) and plasma C peptide values at baseline (CP0) and under stimulation with glucagon were determined in healthy subjects (n = 17) and in insulin-dependent (IDD, n = 45) and non insulin-dependent (NIDD, n = 32) diabetics.
2	2140181	SD) was found on the one hand between the IDD group (CPU = 5.58 +/- 5.58 nmol/24 h; CP = 0.14 +/- 0.08 nmol/l; maximum C peptide value after stimulation (CPmax) = 0.33 +/- 0.31 nmol/l; C peptide delta (delta CP) = 0.14 +/- 0.14 nmol/l; area under the curve (A) = 5.00 +/- 4.84) and the NIDD group (CPU = 15.47 +/- 8.22 nmol/24 h; CP = 0.64 +/- 0.28 nmol/l; CPmax = 1.14 +/- 0.44 nmol/l; delta CP = 0.50 +/- 0.31 nmol/l; A = 17.5 +/- 5.86) and on the other hand between the IDD group and the control group (CPU = 18.20 +/- 8.40 nmol/24 h; CP = 0.41 +/- 0.11 nmol/l; CPmax = 1.00 +/- 0.31 nmol/l; delta CP = 0.69 +/- 0.20 nmol/l; A = 17.10 +/- 4.45).
3	2140181	Urinary (CPU) and plasma C peptide values at baseline (CP0) and under stimulation with glucagon were determined in healthy subjects (n = 17) and in insulin-dependent (IDD, n = 45) and non insulin-dependent (NIDD, n = 32) diabetics.
4	2140181	SD) was found on the one hand between the IDD group (CPU = 5.58 +/- 5.58 nmol/24 h; CP = 0.14 +/- 0.08 nmol/l; maximum C peptide value after stimulation (CPmax) = 0.33 +/- 0.31 nmol/l; C peptide delta (delta CP) = 0.14 +/- 0.14 nmol/l; area under the curve (A) = 5.00 +/- 4.84) and the NIDD group (CPU = 15.47 +/- 8.22 nmol/24 h; CP = 0.64 +/- 0.28 nmol/l; CPmax = 1.14 +/- 0.44 nmol/l; delta CP = 0.50 +/- 0.31 nmol/l; A = 17.5 +/- 5.86) and on the other hand between the IDD group and the control group (CPU = 18.20 +/- 8.40 nmol/24 h; CP = 0.41 +/- 0.11 nmol/l; CPmax = 1.00 +/- 0.31 nmol/l; delta CP = 0.69 +/- 0.20 nmol/l; A = 17.10 +/- 4.45).
5	10758916	Comparison of cardiac troponin T versus creatine kinase-MB for risk stratification in a chest pain evaluation unit.
6	10758916	We evaluated cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB) for risk stratification of chest pain unit (CPU) patients.
7	10758916	Routine use of cTnT in CPUs could facilitate risk stratification and management.
8	11836301	Insulin resistance is associated with increased circulating level of thrombin-activatable fibrinolysis inhibitor in type 2 diabetic patients.
9	11836301	Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI) has been isolated and characterized from human plasma.
10	11836301	The plasma levels of TAFI were independently and significantly correlated with glucose intolerance (HbA(1c)), with obesity (BMI, visceral fat area), and with an indicator of insulin resistance (glucose infusion rate).
11	11836301	This study showed that increased circulating level of TAFI may be an important causative factor of hypofibrinolysis in patients with type 2 diabetes, obesity and insulin resistance.
12	11836301	Insulin resistance is associated with increased circulating level of thrombin-activatable fibrinolysis inhibitor in type 2 diabetic patients.
13	11836301	Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI) has been isolated and characterized from human plasma.
14	11836301	The plasma levels of TAFI were independently and significantly correlated with glucose intolerance (HbA(1c)), with obesity (BMI, visceral fat area), and with an indicator of insulin resistance (glucose infusion rate).
15	11836301	This study showed that increased circulating level of TAFI may be an important causative factor of hypofibrinolysis in patients with type 2 diabetes, obesity and insulin resistance.
16	11836301	Insulin resistance is associated with increased circulating level of thrombin-activatable fibrinolysis inhibitor in type 2 diabetic patients.
17	11836301	Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI) has been isolated and characterized from human plasma.
18	11836301	The plasma levels of TAFI were independently and significantly correlated with glucose intolerance (HbA(1c)), with obesity (BMI, visceral fat area), and with an indicator of insulin resistance (glucose infusion rate).
19	11836301	This study showed that increased circulating level of TAFI may be an important causative factor of hypofibrinolysis in patients with type 2 diabetes, obesity and insulin resistance.
20	11836301	Insulin resistance is associated with increased circulating level of thrombin-activatable fibrinolysis inhibitor in type 2 diabetic patients.
21	11836301	Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI) has been isolated and characterized from human plasma.
22	11836301	The plasma levels of TAFI were independently and significantly correlated with glucose intolerance (HbA(1c)), with obesity (BMI, visceral fat area), and with an indicator of insulin resistance (glucose infusion rate).
23	11836301	This study showed that increased circulating level of TAFI may be an important causative factor of hypofibrinolysis in patients with type 2 diabetes, obesity and insulin resistance.
24	12087030	Association between plasma thrombin-activatable fibrinolysis inhibitor levels and activated protein C in normotensive type 2 diabetic patients.
25	12574207	Increased plasma thrombin-activatable fibrinolysis inhibitor levels in normotensive type 2 diabetic patients with microalbuminuria.
26	12574207	Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI), has been isolated from human plasma.
27	12574207	In the present study, we investigated the plasma levels of TAFI and its relation to urinary albumin excretion in normotensive diabetic patients with normo- and microalbuminuria.
28	12574207	The plasma level of thrombin-antithrombin complex was significantly increased (22.1 +/- 2.6 vs. 8.3 +/- 1.0 nmol/liter; P < 0.05), whereas the D-dimer/thrombin-antithrombin complex ratio was significantly decreased (15.7 +/- 1.4 vs. 26.5 +/- 2.2; P < 0.05), showing the occurrence of hypercoagulability and hypofibrinolysis in diabetic patients.
29	12574207	Univariate analysis showed that the plasma TAFI levels are significantly and proportionally correlated with urinary albumin excretion rate (r = 0.58; P < 0.005) and with plasma soluble thrombomodulin level, a marker of endothelial cell damage, in all diabetic patients (r = 0.42; P < 0.01).
30	12574207	Increased plasma thrombin-activatable fibrinolysis inhibitor levels in normotensive type 2 diabetic patients with microalbuminuria.
31	12574207	Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI), has been isolated from human plasma.
32	12574207	In the present study, we investigated the plasma levels of TAFI and its relation to urinary albumin excretion in normotensive diabetic patients with normo- and microalbuminuria.
33	12574207	The plasma level of thrombin-antithrombin complex was significantly increased (22.1 +/- 2.6 vs. 8.3 +/- 1.0 nmol/liter; P < 0.05), whereas the D-dimer/thrombin-antithrombin complex ratio was significantly decreased (15.7 +/- 1.4 vs. 26.5 +/- 2.2; P < 0.05), showing the occurrence of hypercoagulability and hypofibrinolysis in diabetic patients.
34	12574207	Univariate analysis showed that the plasma TAFI levels are significantly and proportionally correlated with urinary albumin excretion rate (r = 0.58; P < 0.005) and with plasma soluble thrombomodulin level, a marker of endothelial cell damage, in all diabetic patients (r = 0.42; P < 0.01).
35	12574207	Increased plasma thrombin-activatable fibrinolysis inhibitor levels in normotensive type 2 diabetic patients with microalbuminuria.
36	12574207	Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI), has been isolated from human plasma.
37	12574207	In the present study, we investigated the plasma levels of TAFI and its relation to urinary albumin excretion in normotensive diabetic patients with normo- and microalbuminuria.
38	12574207	The plasma level of thrombin-antithrombin complex was significantly increased (22.1 +/- 2.6 vs. 8.3 +/- 1.0 nmol/liter; P < 0.05), whereas the D-dimer/thrombin-antithrombin complex ratio was significantly decreased (15.7 +/- 1.4 vs. 26.5 +/- 2.2; P < 0.05), showing the occurrence of hypercoagulability and hypofibrinolysis in diabetic patients.
39	12574207	Univariate analysis showed that the plasma TAFI levels are significantly and proportionally correlated with urinary albumin excretion rate (r = 0.58; P < 0.005) and with plasma soluble thrombomodulin level, a marker of endothelial cell damage, in all diabetic patients (r = 0.42; P < 0.01).
40	12574207	Increased plasma thrombin-activatable fibrinolysis inhibitor levels in normotensive type 2 diabetic patients with microalbuminuria.
41	12574207	Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI), has been isolated from human plasma.
42	12574207	In the present study, we investigated the plasma levels of TAFI and its relation to urinary albumin excretion in normotensive diabetic patients with normo- and microalbuminuria.
43	12574207	The plasma level of thrombin-antithrombin complex was significantly increased (22.1 +/- 2.6 vs. 8.3 +/- 1.0 nmol/liter; P < 0.05), whereas the D-dimer/thrombin-antithrombin complex ratio was significantly decreased (15.7 +/- 1.4 vs. 26.5 +/- 2.2; P < 0.05), showing the occurrence of hypercoagulability and hypofibrinolysis in diabetic patients.
44	12574207	Univariate analysis showed that the plasma TAFI levels are significantly and proportionally correlated with urinary albumin excretion rate (r = 0.58; P < 0.005) and with plasma soluble thrombomodulin level, a marker of endothelial cell damage, in all diabetic patients (r = 0.42; P < 0.01).
45	12960608	Thrombin activatable fibrinolysis inhibitor and hemostatic changes in patients with type I diabetes mellitus with and without microvascular complications.
46	12960608	We investigated thrombin activatable fibrinolysis inhibitor (TAFI) and its influence on fibrinolysis by measuring pro-TAFI activity and total TAFI antigen in 38 patients with type I diabetes mellitus (18 with and 20 without microvascular complications), as well as in 20 healthy controls.
47	12960608	Thrombin activatable fibrinolysis inhibitor and hemostatic changes in patients with type I diabetes mellitus with and without microvascular complications.
48	12960608	We investigated thrombin activatable fibrinolysis inhibitor (TAFI) and its influence on fibrinolysis by measuring pro-TAFI activity and total TAFI antigen in 38 patients with type I diabetes mellitus (18 with and 20 without microvascular complications), as well as in 20 healthy controls.
49	14682222	It has been postulated that TAFI-Thrombin Activatable Fibrinolysis Inhibitor, newly described glycoprotein, couples two opposite systems: coagulation and fibrinolysis.
50	14682222	We assessed: TAFI concentration, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2 (markers of TAFI activation), a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes, a marker of TAFI cataliser to TAFIa-thrombomodulin using commercially available kits.
51	14682222	All four groups studied did not differ in regard to fibrinogen, thrombomodulin, plasmin-antiplasmin complexes, and TAFI concentration.
52	14682222	It has been postulated that TAFI-Thrombin Activatable Fibrinolysis Inhibitor, newly described glycoprotein, couples two opposite systems: coagulation and fibrinolysis.
53	14682222	We assessed: TAFI concentration, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2 (markers of TAFI activation), a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes, a marker of TAFI cataliser to TAFIa-thrombomodulin using commercially available kits.
54	14682222	All four groups studied did not differ in regard to fibrinogen, thrombomodulin, plasmin-antiplasmin complexes, and TAFI concentration.
55	14682222	It has been postulated that TAFI-Thrombin Activatable Fibrinolysis Inhibitor, newly described glycoprotein, couples two opposite systems: coagulation and fibrinolysis.
56	14682222	We assessed: TAFI concentration, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2 (markers of TAFI activation), a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes, a marker of TAFI cataliser to TAFIa-thrombomodulin using commercially available kits.
57	14682222	All four groups studied did not differ in regard to fibrinogen, thrombomodulin, plasmin-antiplasmin complexes, and TAFI concentration.
58	14983223	Thrombin activatable fibrinolysis inhibitor (TAFI) and markers of endothelial cell injury in dialyzed patients with diabetic nephropathy.
59	14983223	It has been postulated that TAFI-thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients.
60	14983223	We assessed: TAFI and TAFIa, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1+2, a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes in diabetic and non-diabetic patients on hemodialyses-HD, peritoneal dialyses-CAPD, patients with chronic renal failure with and without diabetic nephropathy on conservative treatment.
61	14983223	Linear regression analysis showed that TAFI concentration was directly related to albumin in HD and CAPD patients without diabetic nephropathy, whereas TAFIa correlated with triglycerides, fibrinogen and leukocytes count in this group.
62	14983223	Thrombin activatable fibrinolysis inhibitor (TAFI) and markers of endothelial cell injury in dialyzed patients with diabetic nephropathy.
63	14983223	It has been postulated that TAFI-thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients.
64	14983223	We assessed: TAFI and TAFIa, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1+2, a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes in diabetic and non-diabetic patients on hemodialyses-HD, peritoneal dialyses-CAPD, patients with chronic renal failure with and without diabetic nephropathy on conservative treatment.
65	14983223	Linear regression analysis showed that TAFI concentration was directly related to albumin in HD and CAPD patients without diabetic nephropathy, whereas TAFIa correlated with triglycerides, fibrinogen and leukocytes count in this group.
66	14983223	Thrombin activatable fibrinolysis inhibitor (TAFI) and markers of endothelial cell injury in dialyzed patients with diabetic nephropathy.
67	14983223	It has been postulated that TAFI-thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients.
68	14983223	We assessed: TAFI and TAFIa, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1+2, a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes in diabetic and non-diabetic patients on hemodialyses-HD, peritoneal dialyses-CAPD, patients with chronic renal failure with and without diabetic nephropathy on conservative treatment.
69	14983223	Linear regression analysis showed that TAFI concentration was directly related to albumin in HD and CAPD patients without diabetic nephropathy, whereas TAFIa correlated with triglycerides, fibrinogen and leukocytes count in this group.
70	14983223	Thrombin activatable fibrinolysis inhibitor (TAFI) and markers of endothelial cell injury in dialyzed patients with diabetic nephropathy.
71	14983223	It has been postulated that TAFI-thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients.
72	14983223	We assessed: TAFI and TAFIa, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1+2, a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes in diabetic and non-diabetic patients on hemodialyses-HD, peritoneal dialyses-CAPD, patients with chronic renal failure with and without diabetic nephropathy on conservative treatment.
73	14983223	Linear regression analysis showed that TAFI concentration was directly related to albumin in HD and CAPD patients without diabetic nephropathy, whereas TAFIa correlated with triglycerides, fibrinogen and leukocytes count in this group.
74	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
75	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
76	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
77	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
78	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
79	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
80	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
81	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
82	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
83	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
84	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
85	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
86	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
87	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
88	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
89	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
90	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
91	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
92	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
93	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
94	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
95	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
96	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
97	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
98	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
99	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
100	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
101	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
102	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
103	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
104	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
105	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
106	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
107	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
108	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
109	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
110	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
111	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
112	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
113	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
114	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
115	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
116	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
117	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
118	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
119	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
120	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
121	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
122	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
123	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
124	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
125	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
126	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
127	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
128	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
129	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
130	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
131	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
132	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
133	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
134	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
135	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
136	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
137	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
138	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
139	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
140	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
141	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
142	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
143	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
144	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
145	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
146	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
147	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
148	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
149	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
150	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
151	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
152	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
153	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
154	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
155	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
156	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
157	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
158	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
159	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
160	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
161	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
162	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
163	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
164	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
165	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
166	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
167	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
168	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
169	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
170	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
171	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
172	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
173	15647842	Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway.
174	15647842	Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis.
175	15647842	We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes.
176	15647842	Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI.
177	15647842	To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes.
178	15647842	TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes.
179	15647842	PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects.
180	15647842	These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway.
181	15647842	Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt.
182	15647842	In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes.
183	15647842	It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance.
184	15668188	Thrombin activatable fibrinolysis inhibitor in Behçet's disease.
185	16114812	Von Willebrand factor (VWF), thrombin activatable fibrinolysis inhibitor, activated protein C (APC) ratio, factor V, and prothrombin time had heritabilities greater than 0.50.
186	16114812	Significant (p < or = 0.05) positive genetic correlations (0.37-0.51) occurred with factors II and VIII, VWF, total protein S (tPS), and tissue factor pathway inhibitor.
187	16123492	Metabolic syndrome accompanied by hypercholesterolemia is strongly associated with proinflammatory state and impairment of fibrinolysis in patients with type 2 diabetes: synergistic effects of plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor.
188	16389166	Thrombin-activatable fibrinolysis inhibitor activity and global fibrinolytic capacity in Type 1 diabetes: evidence for normal fibrinolytic state.
189	16389166	There is little information, however, regarding the status of fibrinolytic system in Type 1 diabetes, in particular as reflected by thrombin-activatable fibrinolysis inhibitor (TAFI) activity and global fibrinolytic capacity (GFC).
190	16389166	TAFI activity did not significantly correlate with age, albumin excretion, fasting plasma glucose, HbA(1c), D-dimer, and fibrinogen by Spearman rank correlation test.
191	16389166	Thrombin-activatable fibrinolysis inhibitor activity and global fibrinolytic capacity in Type 1 diabetes: evidence for normal fibrinolytic state.
192	16389166	There is little information, however, regarding the status of fibrinolytic system in Type 1 diabetes, in particular as reflected by thrombin-activatable fibrinolysis inhibitor (TAFI) activity and global fibrinolytic capacity (GFC).
193	16389166	TAFI activity did not significantly correlate with age, albumin excretion, fasting plasma glucose, HbA(1c), D-dimer, and fibrinogen by Spearman rank correlation test.
194	16389166	Thrombin-activatable fibrinolysis inhibitor activity and global fibrinolytic capacity in Type 1 diabetes: evidence for normal fibrinolytic state.
195	16389166	There is little information, however, regarding the status of fibrinolytic system in Type 1 diabetes, in particular as reflected by thrombin-activatable fibrinolysis inhibitor (TAFI) activity and global fibrinolytic capacity (GFC).
196	16389166	TAFI activity did not significantly correlate with age, albumin excretion, fasting plasma glucose, HbA(1c), D-dimer, and fibrinogen by Spearman rank correlation test.
197	16458385	Different metabolic correlations of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 in non-obese type 2 diabetic patients.
198	16458385	We investigated the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) and their relation with clinical and metabolic parameters in non-obese type 2 diabetic patients.
199	16458385	The plasma levels of TAFI and PAI-1 were evaluated in 47 non-obese type 2 diabetic patients and 31 normal subjects.
200	16458385	The plasma levels of TAFI (169.0+/-108.8% versus 103.7+/-52.3%; p<0.001, mean+/-S.D.) and PAI-1 (82.7+/-54.5ng/ml versus 52.9+/-51.7ng/ml; p<0.05) were significantly higher in non-obese type 2 diabetic patients than in normal subjects.
201	16458385	There was no significant correlation between plasma levels of TAFI and PAI-1 (r=0.04).
202	16458385	These results show that the plasma levels of TAFI and PAI-1 differently correlate with insulin resistance and visceral fat accumulation, suggesting that different factors are implicated in the plasma elevation of TAFI and PAI-1 in non-obese type 2 diabetes mellitus.
203	16458385	Different metabolic correlations of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 in non-obese type 2 diabetic patients.
204	16458385	We investigated the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) and their relation with clinical and metabolic parameters in non-obese type 2 diabetic patients.
205	16458385	The plasma levels of TAFI and PAI-1 were evaluated in 47 non-obese type 2 diabetic patients and 31 normal subjects.
206	16458385	The plasma levels of TAFI (169.0+/-108.8% versus 103.7+/-52.3%; p<0.001, mean+/-S.D.) and PAI-1 (82.7+/-54.5ng/ml versus 52.9+/-51.7ng/ml; p<0.05) were significantly higher in non-obese type 2 diabetic patients than in normal subjects.
207	16458385	There was no significant correlation between plasma levels of TAFI and PAI-1 (r=0.04).
208	16458385	These results show that the plasma levels of TAFI and PAI-1 differently correlate with insulin resistance and visceral fat accumulation, suggesting that different factors are implicated in the plasma elevation of TAFI and PAI-1 in non-obese type 2 diabetes mellitus.
209	16458385	Different metabolic correlations of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 in non-obese type 2 diabetic patients.
210	16458385	We investigated the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) and their relation with clinical and metabolic parameters in non-obese type 2 diabetic patients.
211	16458385	The plasma levels of TAFI and PAI-1 were evaluated in 47 non-obese type 2 diabetic patients and 31 normal subjects.
212	16458385	The plasma levels of TAFI (169.0+/-108.8% versus 103.7+/-52.3%; p<0.001, mean+/-S.D.) and PAI-1 (82.7+/-54.5ng/ml versus 52.9+/-51.7ng/ml; p<0.05) were significantly higher in non-obese type 2 diabetic patients than in normal subjects.
213	16458385	There was no significant correlation between plasma levels of TAFI and PAI-1 (r=0.04).
214	16458385	These results show that the plasma levels of TAFI and PAI-1 differently correlate with insulin resistance and visceral fat accumulation, suggesting that different factors are implicated in the plasma elevation of TAFI and PAI-1 in non-obese type 2 diabetes mellitus.
215	16458385	Different metabolic correlations of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 in non-obese type 2 diabetic patients.
216	16458385	We investigated the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) and their relation with clinical and metabolic parameters in non-obese type 2 diabetic patients.
217	16458385	The plasma levels of TAFI and PAI-1 were evaluated in 47 non-obese type 2 diabetic patients and 31 normal subjects.
218	16458385	The plasma levels of TAFI (169.0+/-108.8% versus 103.7+/-52.3%; p<0.001, mean+/-S.D.) and PAI-1 (82.7+/-54.5ng/ml versus 52.9+/-51.7ng/ml; p<0.05) were significantly higher in non-obese type 2 diabetic patients than in normal subjects.
219	16458385	There was no significant correlation between plasma levels of TAFI and PAI-1 (r=0.04).
220	16458385	These results show that the plasma levels of TAFI and PAI-1 differently correlate with insulin resistance and visceral fat accumulation, suggesting that different factors are implicated in the plasma elevation of TAFI and PAI-1 in non-obese type 2 diabetes mellitus.
221	16458385	Different metabolic correlations of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 in non-obese type 2 diabetic patients.
222	16458385	We investigated the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) and their relation with clinical and metabolic parameters in non-obese type 2 diabetic patients.
223	16458385	The plasma levels of TAFI and PAI-1 were evaluated in 47 non-obese type 2 diabetic patients and 31 normal subjects.
224	16458385	The plasma levels of TAFI (169.0+/-108.8% versus 103.7+/-52.3%; p<0.001, mean+/-S.D.) and PAI-1 (82.7+/-54.5ng/ml versus 52.9+/-51.7ng/ml; p<0.05) were significantly higher in non-obese type 2 diabetic patients than in normal subjects.
225	16458385	There was no significant correlation between plasma levels of TAFI and PAI-1 (r=0.04).
226	16458385	These results show that the plasma levels of TAFI and PAI-1 differently correlate with insulin resistance and visceral fat accumulation, suggesting that different factors are implicated in the plasma elevation of TAFI and PAI-1 in non-obese type 2 diabetes mellitus.
227	16458385	Different metabolic correlations of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 in non-obese type 2 diabetic patients.
228	16458385	We investigated the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) and their relation with clinical and metabolic parameters in non-obese type 2 diabetic patients.
229	16458385	The plasma levels of TAFI and PAI-1 were evaluated in 47 non-obese type 2 diabetic patients and 31 normal subjects.
230	16458385	The plasma levels of TAFI (169.0+/-108.8% versus 103.7+/-52.3%; p<0.001, mean+/-S.D.) and PAI-1 (82.7+/-54.5ng/ml versus 52.9+/-51.7ng/ml; p<0.05) were significantly higher in non-obese type 2 diabetic patients than in normal subjects.
231	16458385	There was no significant correlation between plasma levels of TAFI and PAI-1 (r=0.04).
232	16458385	These results show that the plasma levels of TAFI and PAI-1 differently correlate with insulin resistance and visceral fat accumulation, suggesting that different factors are implicated in the plasma elevation of TAFI and PAI-1 in non-obese type 2 diabetes mellitus.
233	16877877	The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade.
234	16877877	Thrombin induces thrombin activatable fibrinolysis inhibitor.
235	16877877	Thrombin activatable fibrinolysis inhibitor is a carboxypeptidase that cleaves the carboxylic lysine residues on fibrin, thereby abolishing the critical binding site for tPA-plasminogen decreasing plasmin formation.
236	16877877	The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade.
237	16877877	Thrombin induces thrombin activatable fibrinolysis inhibitor.
238	16877877	Thrombin activatable fibrinolysis inhibitor is a carboxypeptidase that cleaves the carboxylic lysine residues on fibrin, thereby abolishing the critical binding site for tPA-plasminogen decreasing plasmin formation.
239	17046544	Postprandial thrombin activatable fibrinolysis inhibitor and markers of endothelial dysfunction in type 2 diabetic patients.
240	17046544	The aim of this study was to assess postprandial changes in thrombin activatable fibrinolysis inhibitor (TAFI) antigen, a thrombin-dependent fibrinolysis inhibitor with anti-inflammatory properties, and soluble markers of endothelial dysfunction in normotriglyceridemic type 2 diabetic patients.
241	17046544	Fasting and postprandial TAFI antigen, thrombomodulin, tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor 1 were assessed in 12 normotriglyceridemic type 2 diabetic patients treated with diet (hemoglobin A1c, 6.80% +/- 0.67%) and 14 controls.
242	17046544	Fasting low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, free fatty acids and apolipoprotein B, and fasting and postprandial triglyceride, glucose, and insulin were also measured.
243	17046544	This decrement was correlated with fasting TAFI, glucose and hemoglobin A1c, and the area under the curve of glucose.
244	17046544	Thrombomodulin, TFPI, and plasminogen activator inhibitor 1 were similar in both groups, with thrombomodulin and TFPI showing a transient postprandial increase.
245	17046544	Postprandial thrombin activatable fibrinolysis inhibitor and markers of endothelial dysfunction in type 2 diabetic patients.
246	17046544	The aim of this study was to assess postprandial changes in thrombin activatable fibrinolysis inhibitor (TAFI) antigen, a thrombin-dependent fibrinolysis inhibitor with anti-inflammatory properties, and soluble markers of endothelial dysfunction in normotriglyceridemic type 2 diabetic patients.
247	17046544	Fasting and postprandial TAFI antigen, thrombomodulin, tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor 1 were assessed in 12 normotriglyceridemic type 2 diabetic patients treated with diet (hemoglobin A1c, 6.80% +/- 0.67%) and 14 controls.
248	17046544	Fasting low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, free fatty acids and apolipoprotein B, and fasting and postprandial triglyceride, glucose, and insulin were also measured.
249	17046544	This decrement was correlated with fasting TAFI, glucose and hemoglobin A1c, and the area under the curve of glucose.
250	17046544	Thrombomodulin, TFPI, and plasminogen activator inhibitor 1 were similar in both groups, with thrombomodulin and TFPI showing a transient postprandial increase.
251	17046544	Postprandial thrombin activatable fibrinolysis inhibitor and markers of endothelial dysfunction in type 2 diabetic patients.
252	17046544	The aim of this study was to assess postprandial changes in thrombin activatable fibrinolysis inhibitor (TAFI) antigen, a thrombin-dependent fibrinolysis inhibitor with anti-inflammatory properties, and soluble markers of endothelial dysfunction in normotriglyceridemic type 2 diabetic patients.
253	17046544	Fasting and postprandial TAFI antigen, thrombomodulin, tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor 1 were assessed in 12 normotriglyceridemic type 2 diabetic patients treated with diet (hemoglobin A1c, 6.80% +/- 0.67%) and 14 controls.
254	17046544	Fasting low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, free fatty acids and apolipoprotein B, and fasting and postprandial triglyceride, glucose, and insulin were also measured.
255	17046544	This decrement was correlated with fasting TAFI, glucose and hemoglobin A1c, and the area under the curve of glucose.
256	17046544	Thrombomodulin, TFPI, and plasminogen activator inhibitor 1 were similar in both groups, with thrombomodulin and TFPI showing a transient postprandial increase.
257	17046544	Postprandial thrombin activatable fibrinolysis inhibitor and markers of endothelial dysfunction in type 2 diabetic patients.
258	17046544	The aim of this study was to assess postprandial changes in thrombin activatable fibrinolysis inhibitor (TAFI) antigen, a thrombin-dependent fibrinolysis inhibitor with anti-inflammatory properties, and soluble markers of endothelial dysfunction in normotriglyceridemic type 2 diabetic patients.
259	17046544	Fasting and postprandial TAFI antigen, thrombomodulin, tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor 1 were assessed in 12 normotriglyceridemic type 2 diabetic patients treated with diet (hemoglobin A1c, 6.80% +/- 0.67%) and 14 controls.
260	17046544	Fasting low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, free fatty acids and apolipoprotein B, and fasting and postprandial triglyceride, glucose, and insulin were also measured.
261	17046544	This decrement was correlated with fasting TAFI, glucose and hemoglobin A1c, and the area under the curve of glucose.
262	17046544	Thrombomodulin, TFPI, and plasminogen activator inhibitor 1 were similar in both groups, with thrombomodulin and TFPI showing a transient postprandial increase.
263	17184758	Thrombin activatable fibrinolysis inhibitor (TAFI): a role in pre-eclampsia?
264	17184758	Pro-thrombin activatable fibrinolysis inhibitor (pro-TAFI) is a relatively recently described glycoprotein that can be converted into its active form (TAFIa) by thrombin, thrombin-thrombomodulin and plasmin.
265	17184758	Thrombin activatable fibrinolysis inhibitor (TAFI): a role in pre-eclampsia?
266	17184758	Pro-thrombin activatable fibrinolysis inhibitor (pro-TAFI) is a relatively recently described glycoprotein that can be converted into its active form (TAFIa) by thrombin, thrombin-thrombomodulin and plasmin.
267	18075282	Plasminogen activator inhibitor-1 and thrombin activatable fibrinolysis inhibitor levels in non-alcoholic steatohepatitis.
268	18350479	Thrombin-activatable fibrinolysis inhibitor and cardiovascular risk factors in polycystic ovary syndrome.
269	18406001	Gestational diabetes has no additional effect on plasma thrombin-activatable fibrinolysis inhibitor antigen levels beyond pregnancy.
270	18406001	The aim of the present study is to investigate the effect of gestational diabetes on plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels.
271	18406001	Plasma TAFI and PAI-1 antigen levels were measured in 26 pregnant women with gestational diabetes, 25 pregnant women with normal glucose tolerance, and age-matched 24 non-pregnant women with no history of gestational diabetes.
272	18406001	Despite increased PAI-1 antigen levels associated with gestational diabetes, the effect of gestational diabetes on TAFI antigen levels is lacking.
273	18406001	Gestational diabetes has no additional effect on plasma thrombin-activatable fibrinolysis inhibitor antigen levels beyond pregnancy.
274	18406001	The aim of the present study is to investigate the effect of gestational diabetes on plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels.
275	18406001	Plasma TAFI and PAI-1 antigen levels were measured in 26 pregnant women with gestational diabetes, 25 pregnant women with normal glucose tolerance, and age-matched 24 non-pregnant women with no history of gestational diabetes.
276	18406001	Despite increased PAI-1 antigen levels associated with gestational diabetes, the effect of gestational diabetes on TAFI antigen levels is lacking.
277	18406001	Gestational diabetes has no additional effect on plasma thrombin-activatable fibrinolysis inhibitor antigen levels beyond pregnancy.
278	18406001	The aim of the present study is to investigate the effect of gestational diabetes on plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels.
279	18406001	Plasma TAFI and PAI-1 antigen levels were measured in 26 pregnant women with gestational diabetes, 25 pregnant women with normal glucose tolerance, and age-matched 24 non-pregnant women with no history of gestational diabetes.
280	18406001	Despite increased PAI-1 antigen levels associated with gestational diabetes, the effect of gestational diabetes on TAFI antigen levels is lacking.
281	18406001	Gestational diabetes has no additional effect on plasma thrombin-activatable fibrinolysis inhibitor antigen levels beyond pregnancy.
282	18406001	The aim of the present study is to investigate the effect of gestational diabetes on plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels.
283	18406001	Plasma TAFI and PAI-1 antigen levels were measured in 26 pregnant women with gestational diabetes, 25 pregnant women with normal glucose tolerance, and age-matched 24 non-pregnant women with no history of gestational diabetes.
284	18406001	Despite increased PAI-1 antigen levels associated with gestational diabetes, the effect of gestational diabetes on TAFI antigen levels is lacking.
285	19436948	Serum VEGF and plasma von Willebrand factor, soluble thrombomodulin, plasminogen activator inhibitor 1, thrombin-activatable fibrinolysis inhibitor (TAFI) and tissue plasminogen activator (t-PA) were measured using enzyme-linked immunosorbent assay in all subjects.
286	19436948	Only TAFI correlated with VEGF in MAU.
287	19436948	Serum VEGF and plasma von Willebrand factor, soluble thrombomodulin, plasminogen activator inhibitor 1, thrombin-activatable fibrinolysis inhibitor (TAFI) and tissue plasminogen activator (t-PA) were measured using enzyme-linked immunosorbent assay in all subjects.
288	19436948	Only TAFI correlated with VEGF in MAU.
289	19718465	The effects of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor.
290	19718465	The aim of this study was to determine the effect of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor (TAFI).
291	19718465	Glycated TAFI showed decreased activity after activation by thrombin-thrombomodulin in a glyceraldehyde-dose-dependent manner and a reduced anti-fibrinolytic potential.
292	19718465	This is in contrast to fibrinolytic factors as plasminogen-activator inhibitor I and tissue-type plasminogen activator, which are affected.
293	19718465	The effects of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor.
294	19718465	The aim of this study was to determine the effect of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor (TAFI).
295	19718465	Glycated TAFI showed decreased activity after activation by thrombin-thrombomodulin in a glyceraldehyde-dose-dependent manner and a reduced anti-fibrinolytic potential.
296	19718465	This is in contrast to fibrinolytic factors as plasminogen-activator inhibitor I and tissue-type plasminogen activator, which are affected.
297	19718465	The effects of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor.
298	19718465	The aim of this study was to determine the effect of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor (TAFI).
299	19718465	Glycated TAFI showed decreased activity after activation by thrombin-thrombomodulin in a glyceraldehyde-dose-dependent manner and a reduced anti-fibrinolytic potential.
300	19718465	This is in contrast to fibrinolytic factors as plasminogen-activator inhibitor I and tissue-type plasminogen activator, which are affected.
301	20216989	Association between the Thr325Ile polymorphism of the thrombin-activatable fibrinolysis inhibitor and stroke in the Ludwigshafen Risk and Cardiovascular Health Study.
302	20216989	The thrombin-activatable fibrinolysis inhibitor (TAFI) is a key mediator in the regulation of endogenous fibrinolysis, down-regulating clot lysis by degrading the C-terminal lysine residues from fibrin, which are important for binding and activating plasminogen.
303	20216989	Association between the Thr325Ile polymorphism of the thrombin-activatable fibrinolysis inhibitor and stroke in the Ludwigshafen Risk and Cardiovascular Health Study.
304	20216989	The thrombin-activatable fibrinolysis inhibitor (TAFI) is a key mediator in the regulation of endogenous fibrinolysis, down-regulating clot lysis by degrading the C-terminal lysine residues from fibrin, which are important for binding and activating plasminogen.
305	20828799	The role of thrombin-activatable fibrinolysis inhibitor in diabetic wound healing.
306	21406417	Plasma thrombin-activatable fibrinolysis inhibitor levels are not associated with glucose intolerance and subclinical atherosclerosis in women with previous gestational diabetes.
307	21406417	We aimed to determine plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in women with previous gestational diabetes mellitus (GDM) and to evaluate the possible association of plasma TAFI with glucose intolerance and markers of subclinical atherosclerosis.
308	21406417	Circulating lipids, interleukin-6, matrix metalloproteinase-1, fibrinogen, plasminogen activator inhibitor-1, and TAFI antigen levels were assayed.
309	21406417	Thrombin-activatable fibrinolysis inhibitor was not associated with the indices of insulin resistance, glucose intolerance, markers of atherosclerosis, and carotid IMT.
310	21406417	Plasma thrombin-activatable fibrinolysis inhibitor levels are not associated with glucose intolerance and subclinical atherosclerosis in women with previous gestational diabetes.
311	21406417	We aimed to determine plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in women with previous gestational diabetes mellitus (GDM) and to evaluate the possible association of plasma TAFI with glucose intolerance and markers of subclinical atherosclerosis.
312	21406417	Circulating lipids, interleukin-6, matrix metalloproteinase-1, fibrinogen, plasminogen activator inhibitor-1, and TAFI antigen levels were assayed.
313	21406417	Thrombin-activatable fibrinolysis inhibitor was not associated with the indices of insulin resistance, glucose intolerance, markers of atherosclerosis, and carotid IMT.
314	21406417	Plasma thrombin-activatable fibrinolysis inhibitor levels are not associated with glucose intolerance and subclinical atherosclerosis in women with previous gestational diabetes.
315	21406417	We aimed to determine plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in women with previous gestational diabetes mellitus (GDM) and to evaluate the possible association of plasma TAFI with glucose intolerance and markers of subclinical atherosclerosis.
316	21406417	Circulating lipids, interleukin-6, matrix metalloproteinase-1, fibrinogen, plasminogen activator inhibitor-1, and TAFI antigen levels were assayed.
317	21406417	Thrombin-activatable fibrinolysis inhibitor was not associated with the indices of insulin resistance, glucose intolerance, markers of atherosclerosis, and carotid IMT.
318	21406417	Plasma thrombin-activatable fibrinolysis inhibitor levels are not associated with glucose intolerance and subclinical atherosclerosis in women with previous gestational diabetes.
319	21406417	We aimed to determine plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in women with previous gestational diabetes mellitus (GDM) and to evaluate the possible association of plasma TAFI with glucose intolerance and markers of subclinical atherosclerosis.
320	21406417	Circulating lipids, interleukin-6, matrix metalloproteinase-1, fibrinogen, plasminogen activator inhibitor-1, and TAFI antigen levels were assayed.
321	21406417	Thrombin-activatable fibrinolysis inhibitor was not associated with the indices of insulin resistance, glucose intolerance, markers of atherosclerosis, and carotid IMT.
322	21519232	The relationship among TAFI, t-PA, PAI-1 and F1 + 2 in type 2 diabetic patients with normoalbuminuria and microalbuminuria.
323	21519232	The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria.
324	21519232	TAFI, PAI-1, t-PA and F1+2 were assessed by enzyme-linked immunosorbent assay (ELISA) in all patients.
325	21519232	TAFI was significantly increased in the MAU group, PAI-1 and F1+2 were increased in both groups and t-PA was not elevated in either group compared to controls.
326	21519232	We found positive correlations in the NAU: TAFI and fibrinogen (r=0.65, P=0.02), PAI-1 and triglycerides (r=0.67, P=0.01), in the MAU: TAFI and F1+2 (r=0.48, P=0.02), TAFI and systolic blood pressure (r=0.53, P=0.01), PAI-1 and BMI (r=0.43, P<0.05).
327	21519232	TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1.
328	21519232	The relationship among TAFI, t-PA, PAI-1 and F1 + 2 in type 2 diabetic patients with normoalbuminuria and microalbuminuria.
329	21519232	The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria.
330	21519232	TAFI, PAI-1, t-PA and F1+2 were assessed by enzyme-linked immunosorbent assay (ELISA) in all patients.
331	21519232	TAFI was significantly increased in the MAU group, PAI-1 and F1+2 were increased in both groups and t-PA was not elevated in either group compared to controls.
332	21519232	We found positive correlations in the NAU: TAFI and fibrinogen (r=0.65, P=0.02), PAI-1 and triglycerides (r=0.67, P=0.01), in the MAU: TAFI and F1+2 (r=0.48, P=0.02), TAFI and systolic blood pressure (r=0.53, P=0.01), PAI-1 and BMI (r=0.43, P<0.05).
333	21519232	TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1.
334	21519232	The relationship among TAFI, t-PA, PAI-1 and F1 + 2 in type 2 diabetic patients with normoalbuminuria and microalbuminuria.
335	21519232	The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria.
336	21519232	TAFI, PAI-1, t-PA and F1+2 were assessed by enzyme-linked immunosorbent assay (ELISA) in all patients.
337	21519232	TAFI was significantly increased in the MAU group, PAI-1 and F1+2 were increased in both groups and t-PA was not elevated in either group compared to controls.
338	21519232	We found positive correlations in the NAU: TAFI and fibrinogen (r=0.65, P=0.02), PAI-1 and triglycerides (r=0.67, P=0.01), in the MAU: TAFI and F1+2 (r=0.48, P=0.02), TAFI and systolic blood pressure (r=0.53, P=0.01), PAI-1 and BMI (r=0.43, P<0.05).
339	21519232	TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1.
340	21519232	The relationship among TAFI, t-PA, PAI-1 and F1 + 2 in type 2 diabetic patients with normoalbuminuria and microalbuminuria.
341	21519232	The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria.
342	21519232	TAFI, PAI-1, t-PA and F1+2 were assessed by enzyme-linked immunosorbent assay (ELISA) in all patients.
343	21519232	TAFI was significantly increased in the MAU group, PAI-1 and F1+2 were increased in both groups and t-PA was not elevated in either group compared to controls.
344	21519232	We found positive correlations in the NAU: TAFI and fibrinogen (r=0.65, P=0.02), PAI-1 and triglycerides (r=0.67, P=0.01), in the MAU: TAFI and F1+2 (r=0.48, P=0.02), TAFI and systolic blood pressure (r=0.53, P=0.01), PAI-1 and BMI (r=0.43, P<0.05).
345	21519232	TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1.
346	21519232	The relationship among TAFI, t-PA, PAI-1 and F1 + 2 in type 2 diabetic patients with normoalbuminuria and microalbuminuria.
347	21519232	The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria.
348	21519232	TAFI, PAI-1, t-PA and F1+2 were assessed by enzyme-linked immunosorbent assay (ELISA) in all patients.
349	21519232	TAFI was significantly increased in the MAU group, PAI-1 and F1+2 were increased in both groups and t-PA was not elevated in either group compared to controls.
350	21519232	We found positive correlations in the NAU: TAFI and fibrinogen (r=0.65, P=0.02), PAI-1 and triglycerides (r=0.67, P=0.01), in the MAU: TAFI and F1+2 (r=0.48, P=0.02), TAFI and systolic blood pressure (r=0.53, P=0.01), PAI-1 and BMI (r=0.43, P<0.05).
351	21519232	TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1.
352	21519232	The relationship among TAFI, t-PA, PAI-1 and F1 + 2 in type 2 diabetic patients with normoalbuminuria and microalbuminuria.
353	21519232	The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria.
354	21519232	TAFI, PAI-1, t-PA and F1+2 were assessed by enzyme-linked immunosorbent assay (ELISA) in all patients.
355	21519232	TAFI was significantly increased in the MAU group, PAI-1 and F1+2 were increased in both groups and t-PA was not elevated in either group compared to controls.
356	21519232	We found positive correlations in the NAU: TAFI and fibrinogen (r=0.65, P=0.02), PAI-1 and triglycerides (r=0.67, P=0.01), in the MAU: TAFI and F1+2 (r=0.48, P=0.02), TAFI and systolic blood pressure (r=0.53, P=0.01), PAI-1 and BMI (r=0.43, P<0.05).
357	21519232	TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1.
358	23086579	Ex vivo plasma fibrin clot permeability (K(s)) and lysis time (t(50%)) induced by 1 μg/mL recombinant tissue plasminogen activator (tPA), along with plasma levels of plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), tPA, von Willebrand factor (vWF), P-selectin, soluble CD40 ligand (sCD40L), were measured.
359	23086579	Concomitant DM2 was associated with higher glucose (+24.3%, p < 0.001), fibrinogen (+9.0%, p = 0.037), PAI-1 (+58.7%, p < 0.001), tPA (+24.0%, p < 0.001) and P-selectin (+12.2%, p < 0.001).
360	23086579	Multiple regression analysis of the whole study group showed that vWF, PAI-1, fibrinogen and DM2 were the independent predictors of t(50%) (R(2) = 0.58, p < 0.001), while only vWF was an independent predictor of K(s) (R(2) = 0.22, p < 0.001).
361	23945058	Thrombin activatable fibrinolysis inhibitor (TAFI) is an important procoagulant factor.