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Fletcher B Taylor - One of the best experts on this subject based on the ideXlab platform.
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active site inhibited factor viia degr viia attenuates the coagulant and interleukin 6 and 8 but not tumor necrosis factor responses of the baboon to LD100 escherichia coli
Blood, 1998Co-Authors: Fletcher B Taylor, A C K Chang, G Peer, A Li, M Ezban, U HednerAbstract:Antitissue factor antibody attenuated the coagulopathic and lethal responses to LD100 Escherichia coli , whereas active site inhibited factor Xa inhibited only the coagulopathic response. In this study, we wished to determine: (1) whether active site inhibited factor VIIa blocks the coagulopathic and/or attenuates the lethal effects of LD100 E coli and (2) whether these effects are accompanied by attenuation of the inflammatory cytokine response to LD100 E coli . Eight baboons infused for 2 hours with LD100 E coli also were given five bolus infusions of DEGR VIIa of 280 μg/kg at T = −10 minutes, +2, 4, 6, and 8 hours and observed for changes in vital signs, and the concentrations of hemostatic components (fibrinogen, platelets, fibrin degradation products) and inflammatory mediators (tumor necrosis factor [TNF], interleukin-6 [IL-6], IL-8) at T = 0, 1, 2, 4, 6, and 8 hours. Eight control baboons were also infused with LD100 E coli alone and followed as described above. Four of the eight baboons treated with DEGR VIIa were permanent 7-day survivors versus none in the control group. The mean survival times for the treated and control groups were 116 ± 22 and 26 ± 8 hours, respectively. These values differed significantly from each other, ( P = .0008). The decrease in platelet and fibrinogen concentrations and the increase in fibrin degradation products observed in the control group were significantly attenuated in the treated group, as was thrombosis of renal glomerular capillaries. Treatment with DEGR VIIa showed no effect on the peak TNF response to LD100 E coli at T = 2 hours (170 ± 32 v 120 ± 35 ng/mL). DEGR VIIa, however, did attenuate the IL-6 and IL-8 responses at T = 8 hours (ie, the IL-6 concentrations were 81 ± 10 for treated and 1,256 ± 236 for the control groups and the IL-8 concentrations were 28 ± 3.9 for the treated and 60 ± 8.2 for the control group). These values for IL-6 and IL-8 differed significantly from each other between the treated and control groups ( P = .0001 and .0074, respectively). It should be noted that the initial responses of IL-6 and IL-8 up to T = 4 hours were not attenuated. We concluded that DEGR VIIa treatment attenuates inflammatory, as well as hemostatic system responses to LD100 E coli . We hypothesize that this occurs through interference with the assembly and/or interactions of tissue factor/VIIa complexes.
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Sequential renal alterations in septic shock in the primate.
Circulatory shock, 1991Co-Authors: B. L. Voss, Lerner B. Hinshaw, L. E. De Bault, K. E. Blick, Alvin C. K. Chang, D. L. Stiers, Fletcher B TaylorAbstract:: This is a descriptive sequential study of the response of the baboon to LD100 Escherichia coli. The response was found to consist of three stages based on electron microscopic, physiologic, and clinical laboratory data. This study associates the inflammatory, coagulant, and cell injury (stage 1-3) responses with markers of activation of inflammatory cells (tumor necrosis factor) and of the vascular endothelium (tissue plasminogen activator). This work also shows that in contrast to the underlying parenchymal cells of the organ, the vascular endothelium remains intact throughout the response to LD100 E. coli. The possible role of the vascular endothelium in mediation of events at both its luminal (blood) and antiluminal (parenchymal) surfaces is discussed.
U Hedner - One of the best experts on this subject based on the ideXlab platform.
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active site inhibited factor viia degr viia attenuates the coagulant and interleukin 6 and 8 but not tumor necrosis factor responses of the baboon to LD100 escherichia coli
Blood, 1998Co-Authors: Fletcher B Taylor, A C K Chang, G Peer, A Li, M Ezban, U HednerAbstract:Antitissue factor antibody attenuated the coagulopathic and lethal responses to LD100 Escherichia coli , whereas active site inhibited factor Xa inhibited only the coagulopathic response. In this study, we wished to determine: (1) whether active site inhibited factor VIIa blocks the coagulopathic and/or attenuates the lethal effects of LD100 E coli and (2) whether these effects are accompanied by attenuation of the inflammatory cytokine response to LD100 E coli . Eight baboons infused for 2 hours with LD100 E coli also were given five bolus infusions of DEGR VIIa of 280 μg/kg at T = −10 minutes, +2, 4, 6, and 8 hours and observed for changes in vital signs, and the concentrations of hemostatic components (fibrinogen, platelets, fibrin degradation products) and inflammatory mediators (tumor necrosis factor [TNF], interleukin-6 [IL-6], IL-8) at T = 0, 1, 2, 4, 6, and 8 hours. Eight control baboons were also infused with LD100 E coli alone and followed as described above. Four of the eight baboons treated with DEGR VIIa were permanent 7-day survivors versus none in the control group. The mean survival times for the treated and control groups were 116 ± 22 and 26 ± 8 hours, respectively. These values differed significantly from each other, ( P = .0008). The decrease in platelet and fibrinogen concentrations and the increase in fibrin degradation products observed in the control group were significantly attenuated in the treated group, as was thrombosis of renal glomerular capillaries. Treatment with DEGR VIIa showed no effect on the peak TNF response to LD100 E coli at T = 2 hours (170 ± 32 v 120 ± 35 ng/mL). DEGR VIIa, however, did attenuate the IL-6 and IL-8 responses at T = 8 hours (ie, the IL-6 concentrations were 81 ± 10 for treated and 1,256 ± 236 for the control groups and the IL-8 concentrations were 28 ± 3.9 for the treated and 60 ± 8.2 for the control group). These values for IL-6 and IL-8 differed significantly from each other between the treated and control groups ( P = .0001 and .0074, respectively). It should be noted that the initial responses of IL-6 and IL-8 up to T = 4 hours were not attenuated. We concluded that DEGR VIIa treatment attenuates inflammatory, as well as hemostatic system responses to LD100 E coli . We hypothesize that this occurs through interference with the assembly and/or interactions of tissue factor/VIIa complexes.
Sigit Kirana Lintang Bhima - One of the best experts on this subject based on the ideXlab platform.
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perbandingan pemberian brodifakum ld50 dan LD100 terhadap perubahan gambaran histopatologi usus halus tikus wistar
DIPONEGORO MEDICAL JOURNAL ( JURNAL KEDOKTERAN DIPONEGORO ), 2016Co-Authors: Alfian Salahudin Al Ayoubi, Tuntas Dhanardhono, Sigit Kirana Lintang BhimaAbstract:Background : Brodifacoum is an anticoagulant substance which usually used as pest control, but this substance has a poisoning effect the body. Brodifacoum is absorbed through gastrointestinal tract which can cause the disorder of blod clotting by slowing down the process of epoxide reductase of vitamin-K. Aim : To know the comparison of Histopathology Rattus norvegicus Intestine against brodifacoum administration LD50 and LD100. Methods : This study was an experimental study with post test only group design. The sample of this study are 27 Rattus norvegicus which given per oral administration of brodifacoum. Barthel Manja scores were used to assess changes in intestine Histopatology. Normal and desquamation are a minor damage, while erosion and ulcers are major damage. Non-parametric test of Mann-Whitney to the results are revealed significant if p <0.05. Results : On LD50, 2 rats died on days 3, 5 on day 5, and 2 rats terminated on day 7. In LD100 2 rats died on day 3, 2 on day 5, and 5 rats terminated on day 7. On LD50 groups there are 66,67% minor damage and 33,33% major damage, while in LD100 groups there are 55,56% minor damage and 44,44% major damage. Test non parametric Mann-Whitney in the control group with LD50 was found p = 0.269, in control group with LD100 was found p = 0106, then group with the LD50 and LD100 found p = 0.159. Conclusion : There are not significant differentiation of histopatology picture between LD50 and LD100 dose ( p = 0.159 )
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perbandingan pemberian brodifakum dosis ld50 dan LD100 terhadap residu brodifakum pada hepar tikus wistar
DIPONEGORO MEDICAL JOURNAL ( JURNAL KEDOKTERAN DIPONEGORO ), 2016Co-Authors: Nugraha Adiyasa, Tuntas Dhanardhono, Sigit Kirana Lintang BhimaAbstract:Latar Belakang : Brodifakum adalah senyawa yang umumnya digunakan sebagai racun tikus. Namun, sering disalah gunakan pada kasus kriminal. Brodifakum akan di metabolisme tubuh melalui organ ekskresi diantaranya hepar. Paparan brodifakum dalam dosis yang berbeda akan menghasilkan kadar residu yang berbeda pula. Tujuan: Mengetahui perbandingan pemberian brodifakum dosis LD50 dan LD100 terhadap jumlah residu brodifakum pada hepar tikus wistar. Metode: Penelitian ini merupakan penelitian eksperimental dengan menggunakan pendekatan post test only control group design. 27 sampel tikus wistar diberikan perlakuan pemberian brodifakum secara per oral. Residu brodifakum dideteksi menggunakan High Performance Liquid Chromatography. Dilakukan analisa deskriptif, uji non parametrik Mann-Whitney terhadap data. Hasil analisis dinyatakan bermakna bila nilai p<0,05. Hasil: Konsentrasi brodifakum pada hepar hewan coba meningkat berdasarkan jumlah brodifakum yang dimakan. Tikus mati pada hari ke-3 sebanyak 4, pada hari ke-5 sebanyak 7 dan pada hari terminasi sebanyak 16 tikus diterminasi. Kadar residu terendah didapatkan pada angka 0,00002 mg/kg dan tertinggi pada angka 0,00100 mg/kg. Uji Mann-Whitney didapatkan hasil perbandingan residu brodifakum pada hepar tikus pada dosis kontrol dan LD50 (p=0,001) dan pada kontrol dan LD100 (p=0,000). Antara jumlah residu brodifakum pada hepar tikus pada dosis LD50 dan LD100 (p=0,539). Simpulan: Tidak ada perbedaan bermakna antara jumlah residu brodifakum pada hepar tikus pada dosis LD50 dan LD100 (p=0,539).
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perbandingan pemberian brodifakum ld50 dan LD100 terhadap perubahan gambaran patologi anatomi gaster tikus wistar
Jurnal Kedokteran Diponegoro, 2015Co-Authors: Ricky P Renardi, Tuntas Dhanardhono, Sigit Kirana Lintang BhimaAbstract:Background : Brodifakum is a substance that often used as rat poison and disrupt the process of blood coagulation.As a result of this disorder can cause bleeding in vital organs of rat. This study was conducted to assess the gastric anatomic pathology due to Brodifakum. Aim : To know the comparison of Anatomical Pathology Rattus norvegicus Gastric againstbrodifacoum administration LD50 and LD100. Methods :This study was an experimental study with post test only group design. The sample of this study are 27 Rattus norvegicus which given per oral administration of brodifacoum. Barthel Manja scores were used to assess changes in gastric Anatomical Pathology.Normal and desquamation are a minor damage, while erosion and ulcers are major damage.Non-parametric test of Mann-Whitney to the results are revealed significant if p <0.05. Results :On LD50, 2 rats died on days 3, 5 on day 5, and 2 rats terminated on day 7. In LD100 2 rats died on day 3, 2 on day 5, and 5 rats terminated on day 7. On LD50 groups there are 44.44% minor damage and55.56% major damage,whilein LD100 discovered at 100% major damage. Test non parametric Mann-Whitney in the control group with LD50was found p = 0.106, in control group with LD100was found p = 0.001, then group with the LD50and LD100 found p = 0.028. Conclusion :There are significant differentiation of anatomic pathology picture between LD50 and LD100 dose ( p = 0.028 )
C Mittermayer - One of the best experts on this subject based on the ideXlab platform.
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induction of heat shock protein 70 by zinc bis dlhydrogenaspartate reduces cytokine liberation apoptosis and mortality rate in a rat model of LD100 endotoxemia
Shock, 1997Co-Authors: B Klosterhalfen, S Hauptmann, Felixalbert Offner, B K Amotakyi, Christian Tons, G Winkeltau, Mamdouh Affify, Werner Kupper, Charlesjames Kirkpatrick, C MittermayerAbstract:: A prospective, randomized model of LD100/24 h endotoxemia was performed in male Wistar rats (n = 26; 250-300 g). The animals were divided into four groups: Group I (n = 5; saline treatment only), Group II (n = 5; Zn2+ treatment only), Group III (n = 8; saline pretreatment, lipopolysaccharide (LPS) treatment), and Group IV (n = 8; Zn2+ pretreatment, LPS treatment). Zn2+ pretreatment was carried out by intraperitoneal injection of 50 mg/kg zinc-bis-(DL-hydrogenaspartate) (10 mg/kg Zn2+). LD100/24 h endotoxemia was induced by intraperitoneal administration of 20 mg/kg LPS of the Escherichia coli strain WO111:B4. Tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 were detected by enzyme-linked immunosorbent assay (ELISA). HSP70 expression in the lungs, the liver, and the kidneys was determined by immunohistochemistry, Western blotting, and an HSP70 ELISA. Apoptosis was also detected by an in situ apoptosis detection kit (TUNEL) and a cell death detection ELISA, respectively. This rat model of endotoxemia proves the close relationship between HSP70 expression, cytokine liberation, and development of apoptosis. The data demonstrate that: 1) Zn2+ is a potent inducer of HSP70 expression; 2) the application of Zn2+ leads to slightly increased cytokine plasma levels; and 3) the manipulation of the heat shock response by Zn2+ significantly increases the survival rate after LD100 endotoxemia. Enhanced survival rate in animals pretreated with Zn2+ may be explained by increased tissue levels of HSP70, a subsequent significantly decreased liberation of the proinflammatory cytokines after LPS challenge, and a significantly decreased rate of apoptosis.
B Klosterhalfen - One of the best experts on this subject based on the ideXlab platform.
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induction of heat shock protein 70 by zinc bis dlhydrogenaspartate reduces cytokine liberation apoptosis and mortality rate in a rat model of LD100 endotoxemia
Shock, 1997Co-Authors: B Klosterhalfen, S Hauptmann, Felixalbert Offner, B K Amotakyi, Christian Tons, G Winkeltau, Mamdouh Affify, Werner Kupper, Charlesjames Kirkpatrick, C MittermayerAbstract:: A prospective, randomized model of LD100/24 h endotoxemia was performed in male Wistar rats (n = 26; 250-300 g). The animals were divided into four groups: Group I (n = 5; saline treatment only), Group II (n = 5; Zn2+ treatment only), Group III (n = 8; saline pretreatment, lipopolysaccharide (LPS) treatment), and Group IV (n = 8; Zn2+ pretreatment, LPS treatment). Zn2+ pretreatment was carried out by intraperitoneal injection of 50 mg/kg zinc-bis-(DL-hydrogenaspartate) (10 mg/kg Zn2+). LD100/24 h endotoxemia was induced by intraperitoneal administration of 20 mg/kg LPS of the Escherichia coli strain WO111:B4. Tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 were detected by enzyme-linked immunosorbent assay (ELISA). HSP70 expression in the lungs, the liver, and the kidneys was determined by immunohistochemistry, Western blotting, and an HSP70 ELISA. Apoptosis was also detected by an in situ apoptosis detection kit (TUNEL) and a cell death detection ELISA, respectively. This rat model of endotoxemia proves the close relationship between HSP70 expression, cytokine liberation, and development of apoptosis. The data demonstrate that: 1) Zn2+ is a potent inducer of HSP70 expression; 2) the application of Zn2+ leads to slightly increased cytokine plasma levels; and 3) the manipulation of the heat shock response by Zn2+ significantly increases the survival rate after LD100 endotoxemia. Enhanced survival rate in animals pretreated with Zn2+ may be explained by increased tissue levels of HSP70, a subsequent significantly decreased liberation of the proinflammatory cytokines after LPS challenge, and a significantly decreased rate of apoptosis.