To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
31 Aralık 2012 Pazartesi
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
27 Aralık 2012 Perşembe
Added a New Blog to my Reading List: JCDA's Question and Answer Blog
To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
Evaluating natriuretic peptides in hyperthyroid cats
To contact us Click HERE
Menaut P, Connolly DJ, Volk A, et al. Circulating natriuretic peptide concentrations in hyperthyroid cats. J Small Anim Pract. 2012; 53: 673-8.
Natriuretic peptides (NPs) are neurohormones stored in heart muscle cells (atrial cardiomyocytes) and released in response to atrial stretch. They possess potent natriuretic and vasorelaxant properties. They have been shown to be chronically up-regulated in cats with underlying heart disease and have thus been used as a biomarker to detect occult heart disease and differentiate cardiac from non-cardiac dyspnea in emergency situations. In particular, the non-biologically active N-terminal fragment from atrial natriuretic peptide, (NT-proANP), and from brain natriuretic peptide, NT-proBNP, have commonly been studied due to their stability in plasma.
Hyperthyroidism is the most common endocrine disease of cats. In humans with hyperthyroidism, a number of studies have shown NP concentrations to be elevated. Therefore, since NP measurement is increasingly being used to assess feline cardiac disease, determining the influence of elevated thyroid function on NP concentrations is essential.
In this study, 61 hyperthyroid cats were assessed before and after treatment for hyperthyroidism. Treatment included using methimazole or methimazole and subsequent surgical thyroidectomy. Cats with overt heart failure or systemic hypertension were excluded from the study due to previous reports showing these conditions to be associated with an increase in NT-proBNP. Assessment included full physical examination, systolic blood pressure (SBP), plasma biochemistries, total thyroid level (TT4), packed cell volume (PCV), and urinalysis, as well as measurement of NT-proBNP and NT-proANP concentrations. The length of time between pre- and post-treatment evaluation was 35 days and the length of time that the cats were on treatment before post-treatment sample was 28 days. Total T4, heart rate, SBP, and PCV all decreased and body weight and creatinine concentrations increased once euthyroidism was established. In addition, NT-proBNP significantly declined, but no change in NT-proANP concentrations was noted. In conclusion, hyperthyroidism has a modest but significant effect on elevating NT-proBNP with little effect on NT-proANP. Therefore, thyroid status should be taken into account when interpreting NT-proBNP results. [GO]
See also: Singletary GE, Rush JE, Fox PR, Stepien RL and Oyama MA. Effect of NT-pro-BNP assay on accuracy and confidence of general practitioners in diagnosing heart failure or respiratory disease in cats with respiratory signs. J Vet Intern Med. 2012; 26: 542-6.
Related blog articles:
Biochemical testing for feline heart disease (March 2009)
Cardiac biomarkers in feline heart disease (July 2011)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Natriuretic peptides (NPs) are neurohormones stored in heart muscle cells (atrial cardiomyocytes) and released in response to atrial stretch. They possess potent natriuretic and vasorelaxant properties. They have been shown to be chronically up-regulated in cats with underlying heart disease and have thus been used as a biomarker to detect occult heart disease and differentiate cardiac from non-cardiac dyspnea in emergency situations. In particular, the non-biologically active N-terminal fragment from atrial natriuretic peptide, (NT-proANP), and from brain natriuretic peptide, NT-proBNP, have commonly been studied due to their stability in plasma.
Hyperthyroidism is the most common endocrine disease of cats. In humans with hyperthyroidism, a number of studies have shown NP concentrations to be elevated. Therefore, since NP measurement is increasingly being used to assess feline cardiac disease, determining the influence of elevated thyroid function on NP concentrations is essential.In this study, 61 hyperthyroid cats were assessed before and after treatment for hyperthyroidism. Treatment included using methimazole or methimazole and subsequent surgical thyroidectomy. Cats with overt heart failure or systemic hypertension were excluded from the study due to previous reports showing these conditions to be associated with an increase in NT-proBNP. Assessment included full physical examination, systolic blood pressure (SBP), plasma biochemistries, total thyroid level (TT4), packed cell volume (PCV), and urinalysis, as well as measurement of NT-proBNP and NT-proANP concentrations. The length of time between pre- and post-treatment evaluation was 35 days and the length of time that the cats were on treatment before post-treatment sample was 28 days. Total T4, heart rate, SBP, and PCV all decreased and body weight and creatinine concentrations increased once euthyroidism was established. In addition, NT-proBNP significantly declined, but no change in NT-proANP concentrations was noted. In conclusion, hyperthyroidism has a modest but significant effect on elevating NT-proBNP with little effect on NT-proANP. Therefore, thyroid status should be taken into account when interpreting NT-proBNP results. [GO]
See also: Singletary GE, Rush JE, Fox PR, Stepien RL and Oyama MA. Effect of NT-pro-BNP assay on accuracy and confidence of general practitioners in diagnosing heart failure or respiratory disease in cats with respiratory signs. J Vet Intern Med. 2012; 26: 542-6.
Related blog articles:
Biochemical testing for feline heart disease (March 2009)
Cardiac biomarkers in feline heart disease (July 2011)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
20 Aralık 2012 Perşembe
Added a New Blog to my Reading List: JCDA's Question and Answer Blog
To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
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