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
13 Ekim 2012 Cumartesi
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
12 Ekim 2012 Cuma
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
How the tabby cat got its stripes
To contact us Click HERE
Kaelin CB, Xu X, Hong LZ, et al. Specifying and sustaining pigmentation patterns in domestic and wild cats. Science. 2012; 337: 1536-41.
Mackerel versus blotched is the heritable variation of tabby markings in domestic cats (Felis catus). There are two features to tabby markings:
1) A light background component in which individual hairs have extensive light bands.
2) A superimposed darker component in which hairs have little or no banding. The dark component is organized into narrow vertical stripes with a constant and regular spacing in mackerel cats.
In cats with the blotched pattern, the dark component is expanded into a less organized structure with wide whorls. The authors believe the similar range of patterns in domestic cats suggests a mechanism whose appearance can be altered by selection. They identified the gene responsible for the tabby pattern variation in domestic cats. The gene is labeled as transmembrane aminopeptidase Q (Taqpep) that encodes for a membrane-bound metalloprotease. It was located by association mapping in feral cats from Northern California where they initially genotyped 58 SNPs in 8 blotched and 9 mackerel cats.
By performing analysis in 31 other felid species, they also identified Taqpep as the cause of the rare king cheetah phenotype where spots coalesce into blotches and stripes. Additional studies found that paracrine expression of Endothelin3 (Edn3) coordinates localized color differences. Further studies of color pattern in domestic-wild cat hybrids may offer opportunities in understanding complex color markings and how felids acquire their color patterns. [VT]
See also: Eizirik E, David VA, Buckley-Beason V, et al. Defining and mapping mammalian coat pattern genes: multiple genomic regions implicated in domestic cat stripes and spots. Genetics. 2010; 184: 267-75. [free full text article]
More on cat health:
Winn Feline Foundation Library
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Join us on Google+
Mackerel versus blotched is the heritable variation of tabby markings in domestic cats (Felis catus). There are two features to tabby markings:
1) A light background component in which individual hairs have extensive light bands.
2) A superimposed darker component in which hairs have little or no banding. The dark component is organized into narrow vertical stripes with a constant and regular spacing in mackerel cats.
In cats with the blotched pattern, the dark component is expanded into a less organized structure with wide whorls. The authors believe the similar range of patterns in domestic cats suggests a mechanism whose appearance can be altered by selection. They identified the gene responsible for the tabby pattern variation in domestic cats. The gene is labeled as transmembrane aminopeptidase Q (Taqpep) that encodes for a membrane-bound metalloprotease. It was located by association mapping in feral cats from Northern California where they initially genotyped 58 SNPs in 8 blotched and 9 mackerel cats. By performing analysis in 31 other felid species, they also identified Taqpep as the cause of the rare king cheetah phenotype where spots coalesce into blotches and stripes. Additional studies found that paracrine expression of Endothelin3 (Edn3) coordinates localized color differences. Further studies of color pattern in domestic-wild cat hybrids may offer opportunities in understanding complex color markings and how felids acquire their color patterns. [VT]
See also: Eizirik E, David VA, Buckley-Beason V, et al. Defining and mapping mammalian coat pattern genes: multiple genomic regions implicated in domestic cat stripes and spots. Genetics. 2010; 184: 267-75. [free full text article]
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
11 Ekim 2012 Perşembe
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
10 Ekim 2012 Çarşamba
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
9 Ekim 2012 Salı
Injection-site sarcomas in cats
To contact us Click HERE
Srivastav A, Kass PH, McGill LD, Farver TB and Kent MS. Comparative vaccine-specific and other injectable-specific risks of injection-site sarcomas in cats. J Am Vet Med Assoc. 2012; 241: 595-602.
Injection site sarcomas are malignant tumors that have been associated with vaccination sites. However, the factors associated with injection site tumors remain largely unknown or controversial at best. This study examined the associations between vaccine types and other injectable drugs with the subsequent development of injection site sarcomas in cats. For this study, pathologic samples from 181 cats with soft tissue sarcomas (STS) at injection sites were compared with 96 cats with tumors at non-injection sites and 159 cats with other tumor types. By examining both anatomic and temporal associations, it was found that association of STS with injections of long-acting steroids was higher in cats with tumors at injection sites (interscapular) than cats without tumors at these sites. It was also found that recombinant vaccines were less likely to have been used at injection site sarcomas than inactivated vaccines. Overall, the propensity for tumors to arise at injection sites was small. [MK]
See also: Wilcock B, Wilcock A and Bottoms K. Feline postvaccinal sarcoma: 20 years later. Can Vet J. 2012; 53: 430-4. [free full text article]
More on cat health:
Winn Feline Foundation Library
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Injection site sarcomas are malignant tumors that have been associated with vaccination sites. However, the factors associated with injection site tumors remain largely unknown or controversial at best. This study examined the associations between vaccine types and other injectable drugs with the subsequent development of injection site sarcomas in cats. For this study, pathologic samples from 181 cats with soft tissue sarcomas (STS) at injection sites were compared with 96 cats with tumors at non-injection sites and 159 cats with other tumor types. By examining both anatomic and temporal associations, it was found that association of STS with injections of long-acting steroids was higher in cats with tumors at injection sites (interscapular) than cats without tumors at these sites. It was also found that recombinant vaccines were less likely to have been used at injection site sarcomas than inactivated vaccines. Overall, the propensity for tumors to arise at injection sites was small. [MK]
See also: Wilcock B, Wilcock A and Bottoms K. Feline postvaccinal sarcoma: 20 years later. Can Vet J. 2012; 53: 430-4. [free full text article]
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
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
8 Ekim 2012 Pazartesi
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
7 Ekim 2012 Pazar
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
6 Ekim 2012 Cumartesi
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
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
5 Ekim 2012 Cuma
Did the ancient Egyptians domesticate the cat?
To contact us Click HERE
Kurushima JD, Ikram S, Knudsen J, Bleiberg E, Grahn RA and Lyons LA. Cats of the pharaohs: Genetic comparison of Egyptian cat mummies to their feline Contemporaries. Journal of Archaeological Science. 2012; 39: 3217-23.
Ancient Egyptian culture is well known for its reverence and mummification of cats based on art and skeletal remains dating back to about 4000 BC. From this historical association between man and cat, many scholars concluded that the ancient Egyptians likely domesticated our present day feline companions. However, an archeological finding in Cyprus of a potential wildcat buried with a human dates to approximately 7500 BC, before the Predynastic Egyptian period. Additionally, recent genetic studies have suggested that the origins of cat domestication occurred in the adjacent Near Eastern sites including the Fertile Crescent regions. The origin of cats in Egypt may have arisen via trade through the Near East as already domesticated animals.
Mummification of cats (and other animals) was a long-standing tradition in ancient Egypt, reaching its zenith during the Late Period (664-332 BC). Cat mummies can be divided into four categories: pets, revered gods (e.g., Bastet the cat goddess and protectress), food offerings, and votive (i.e. vow) offerings. The majority of offerings found in Egypt and museums are of the votive type. Genetic analyses in this study included two long bones (dated from about 664 BC to 250 AD) and a mandible (dated from about 400 BC to 200 AD) from three mummified cats of the votive type. After identifying a portion of mitochondrial DNA with sufficient variability to distinguish among various modern wild cats and domestic cat mitotypes, overcoming the antagonism of the votive mummification process to PCR chemistry, and in spite of the environmental insult to the mummy remains through antiquity, these authors were able to successfully amplify DNA from Egyptian cat mummies for the first time. Their research supports the view that cats, revered by the ancient Egyptians, were likely Felis silvestris catus (domestic cats) implying cats were domesticated prior to extensive votive mummification. [GO]
See also: Gnudi G, Volta A, Manfredi S, Ferri F and Conversi R. Radiological investigation of an over 2000-year-old Egyptian mummy of a cat. J Feline Med Surg. 2012; 14: 292-4.
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Ancient Egyptian culture is well known for its reverence and mummification of cats based on art and skeletal remains dating back to about 4000 BC. From this historical association between man and cat, many scholars concluded that the ancient Egyptians likely domesticated our present day feline companions. However, an archeological finding in Cyprus of a potential wildcat buried with a human dates to approximately 7500 BC, before the Predynastic Egyptian period. Additionally, recent genetic studies have suggested that the origins of cat domestication occurred in the adjacent Near Eastern sites including the Fertile Crescent regions. The origin of cats in Egypt may have arisen via trade through the Near East as already domesticated animals.
Mummification of cats (and other animals) was a long-standing tradition in ancient Egypt, reaching its zenith during the Late Period (664-332 BC). Cat mummies can be divided into four categories: pets, revered gods (e.g., Bastet the cat goddess and protectress), food offerings, and votive (i.e. vow) offerings. The majority of offerings found in Egypt and museums are of the votive type. Genetic analyses in this study included two long bones (dated from about 664 BC to 250 AD) and a mandible (dated from about 400 BC to 200 AD) from three mummified cats of the votive type. After identifying a portion of mitochondrial DNA with sufficient variability to distinguish among various modern wild cats and domestic cat mitotypes, overcoming the antagonism of the votive mummification process to PCR chemistry, and in spite of the environmental insult to the mummy remains through antiquity, these authors were able to successfully amplify DNA from Egyptian cat mummies for the first time. Their research supports the view that cats, revered by the ancient Egyptians, were likely Felis silvestris catus (domestic cats) implying cats were domesticated prior to extensive votive mummification. [GO]
See also: Gnudi G, Volta A, Manfredi S, Ferri F and Conversi R. Radiological investigation of an over 2000-year-old Egyptian mummy of a cat. J Feline Med Surg. 2012; 14: 292-4.
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
4 Ekim 2012 Perşembe
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
Dental Did You Know: Research Impacts of Dental Journals
To contact us Click HERE
The research impacts and influences of the three most prestigious medical journals are approximately 10 times greater than those of the three most frequently cited dental publications. (New England Journal of Medicine, Lancet, Journal of the American Medical Associations vs. Journal of Clinical Periodontology, Journal of Dental Research, Oral Oncology)
Source: Hardie J, Why Research Findings are Usually Wrong, Oral Health, Vol 102, No 9, September 2012, pg 40-51.
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: Hardie J, Why Research Findings are Usually Wrong, Oral Health, Vol 102, No 9, September 2012, pg 40-51.
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
3 Ekim 2012 Çarşamba
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
2 Ekim 2012 Salı
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
Intestinal pathogens in shelter cats
To contact us Click HERE
Sabshin SJ, Levy JK, Tupler T, Tucker SJ, Greiner EC and Leutenegger CM. Enteropathogens identified in cats entering a Florida animal shelter with normal feces or diarrhea. J Am Vet Med Assoc. 2012; 241: 331-7.
Some pathogens of the intestines of cats are transmissible to people. Some pathogens may be more common in shelter-housed cats than pet cats likely due to lack of preventive health care. Often times infected cats are completely asymptomatic. These investigators examined the feces of cats entering a shelter for various enteric pathogens. They tested 100 cats from a municipal shelter, 50 with diarrhea and 50 without, for a variety of enteric pathogens. Twelve different agents were identified. Interestingly, cats with diarrhea were no more likely to be infected with more than one pathogen than cats without any symptoms. Only feline coronavirus was more likely to be found in cats with diarrhea than cats with normal stools.
Among the 12 agents identified in the cats tested, several were zoonotic agents, transmissible to people. These included various parasites as well as Salmonella. It is not possible to test all shelter cats for these pathogens, thus it is imperative that appropriate management and biosecurity measures be used by personnel at shelters for their protection. [MK]
See also: Queen EV, Marks SL and Farver TB. Prevalence of selected bacterial and parasitic agents in feces from diarrheic and healthy control Cats from Northern California. J Vet Intern Med. 2012; 26: 54-60.
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Some pathogens of the intestines of cats are transmissible to people. Some pathogens may be more common in shelter-housed cats than pet cats likely due to lack of preventive health care. Often times infected cats are completely asymptomatic. These investigators examined the feces of cats entering a shelter for various enteric pathogens. They tested 100 cats from a municipal shelter, 50 with diarrhea and 50 without, for a variety of enteric pathogens. Twelve different agents were identified. Interestingly, cats with diarrhea were no more likely to be infected with more than one pathogen than cats without any symptoms. Only feline coronavirus was more likely to be found in cats with diarrhea than cats with normal stools.
Among the 12 agents identified in the cats tested, several were zoonotic agents, transmissible to people. These included various parasites as well as Salmonella. It is not possible to test all shelter cats for these pathogens, thus it is imperative that appropriate management and biosecurity measures be used by personnel at shelters for their protection. [MK]
See also: Queen EV, Marks SL and Farver TB. Prevalence of selected bacterial and parasitic agents in feces from diarrheic and healthy control Cats from Northern California. J Vet Intern Med. 2012; 26: 54-60.
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
1 Ekim 2012 Pazartesi
Dental Did You Know: The Price of John Lennon's Tooth.
To contact us Click HERE
Apparently, John Lennon's molar was sold for about $31000 at the Omega Auction House on November 4th. It went for double its listed price and was originally given by him to his former housekeeper. It is also reported to be now in the possession of a Canadian dentist (not confirmed and not me :)
Source: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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: Rolling Stone Magazine (Online), November 6th, Read November 7th, http://www.rollingstone.com/music/news/john-lennons-tooth-sells-for-more-than-31-000-at-auction-20111106
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
2012 Winn feline health grants
To contact us Click HERE
Earlier this year, Winn announced the funding of 10 new feline health research projects for a total of over $174,000. Each year, the Winn Feline Foundation receives proposals from veterinary researchers around the world who are interested in improving feline health. To date, Winn’s cumulative total in feline health research funding exceeds $4 million.
Winn is seeking donations of $250 and up to sponsor specific projects. Sponsors will receive progress reports as they are available and copies of any publications that result from the project that are provided by the investigators. Your help in sponsoring these projects means Winn can fund even more research next year.
Available for 2012 sponsorship:
W12-026: Anti-immune evasive therapy for feline infectious peritonitis
An effective therapy for feline infectious peritonitis (FIP) is not currently available and most affected cats succumb to their disease. Previous research has shown that FIP virus can evade the host's immune system and that a specific drug can act as a blocking agent to inhibit this evasion mechanism. In a previous project funded by Winn, it was shown that this drug is well tolerated when given to healthy cats. In this project, the efficacy of the drug as a treatment for FIP in 10 naturally infected cats will be evaluated. If the results of the pilot study are promising, the project will be expanded into a full trial.
W12-027: Development of tools to assess chronic pain in cats
It is crucially important to identify pain fighting medications that are safe for cats, so we can treat conditions such as arthritis or cancer better. Once a treatment option has been identified, studies must be designed carefully to prove that the new treatment is effective. The greatest obstacle is the need for reliable ways to measure pain in cats. The goal of this project is to develop a tool called the "Feline Brief Pain Inventory." This will be an owner-completed questionnaire that will identify and report on how the cat behaves at home, focusing on behaviors that relate to pain. The project will also evaluate the use of an activity monitor that is worn on the cat's collar while at home to determine how many days the monitor must be worn to collect reliable data.
W12-034: Decontamination of textiles exposed to ringworm
Ringworm in cats is most commonly caused by the fungus Microsporum canis. While this skin disease is curable, treatment can be challenging because infected cats shed large amounts of infected hairs and spores into their environment. Effective cleaning is necessary to prevent contamination of the environment and prevent re-infection of cats. No evidence-based information is available for cleaning of household textiles such as fabric, carpeting, and clothing. This project will determine the efficacy of decontamination options for household textiles to identify safe and effective practices.
W12-039: Pimobendan for treatment of chronic kidney disease
Chronic kidney disease (CKD) is one of the most common reasons that senior cats are presented to veterinarians. These investigators have administered pimobendan to cats with combined kidney and heart disease after the patients developed congestive heart failure. In some of these patients, a greater improvement in kidney values and clinical response than is typically noted occurred when they were treated with pimobendan. Pimobendan is an effective drug for management of heart failure in dogs and may support kidney function through improved heart function and improved blood supply to the kidneys. This drug is also given to cats with heart disease. This pilot study will assess the effect of administering pimobendan to cats that only have CKD compared with standard treatment methods.
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
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Read the Cat Health News Weekly
Join us on Google+
 |
| 2012 Winn grant review panel meeting |
Winn is seeking donations of $250 and up to sponsor specific projects. Sponsors will receive progress reports as they are available and copies of any publications that result from the project that are provided by the investigators. Your help in sponsoring these projects means Winn can fund even more research next year.
Available for 2012 sponsorship:
W12-026: Anti-immune evasive therapy for feline infectious peritonitis
An effective therapy for feline infectious peritonitis (FIP) is not currently available and most affected cats succumb to their disease. Previous research has shown that FIP virus can evade the host's immune system and that a specific drug can act as a blocking agent to inhibit this evasion mechanism. In a previous project funded by Winn, it was shown that this drug is well tolerated when given to healthy cats. In this project, the efficacy of the drug as a treatment for FIP in 10 naturally infected cats will be evaluated. If the results of the pilot study are promising, the project will be expanded into a full trial.
W12-027: Development of tools to assess chronic pain in cats
 |
| Feline health symposium, Austin TX, 2007 |
W12-034: Decontamination of textiles exposed to ringworm
Ringworm in cats is most commonly caused by the fungus Microsporum canis. While this skin disease is curable, treatment can be challenging because infected cats shed large amounts of infected hairs and spores into their environment. Effective cleaning is necessary to prevent contamination of the environment and prevent re-infection of cats. No evidence-based information is available for cleaning of household textiles such as fabric, carpeting, and clothing. This project will determine the efficacy of decontamination options for household textiles to identify safe and effective practices.
W12-039: Pimobendan for treatment of chronic kidney disease
Chronic kidney disease (CKD) is one of the most common reasons that senior cats are presented to veterinarians. These investigators have administered pimobendan to cats with combined kidney and heart disease after the patients developed congestive heart failure. In some of these patients, a greater improvement in kidney values and clinical response than is typically noted occurred when they were treated with pimobendan. Pimobendan is an effective drug for management of heart failure in dogs and may support kidney function through improved heart function and improved blood supply to the kidneys. This drug is also given to cats with heart disease. This pilot study will assess the effect of administering pimobendan to cats that only have CKD compared with standard treatment methods.
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Read the Cat Health News Weekly
Join us on Google+
Cats and canine parvovirus
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Clegg SR, Coyne KP, Dawson S, et al. Canine parvovirus in asymptomatic feline carriers. Vet Microbiol 2012;157:78-85.
Parvoviruses are important pathogens of dogs and cats, and have a high mutation rate. The canine strains that have emerged in recent years have the ability to infect and cause disease in cats as well as dogs. These investigators looked at the numbers of healthy cats in rescue shelters that harbor canine parvovirus in their feces. In fact, CPV was found in one-third of cats in a cat-only rescue shelter and a mixed rescue shelter. Interestingly, no feline parvovirus was found in these cats. Also interesting was the fact that none of the cats were clinically ill. This indicates that normal cats could potentially be shedding canine parvovirus and may be a potential source for dogs in the same environment. [MK]
See also: Battilani M, Balboni A, Ustulin M, et al. Genetic complexity and multiple infections with more Parvovirus species in naturally infected cats. Vet Res 2011;42:43. [free, full text article]
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Read the Cat Health News Weekly
Join us on Google+
Parvoviruses are important pathogens of dogs and cats, and have a high mutation rate. The canine strains that have emerged in recent years have the ability to infect and cause disease in cats as well as dogs. These investigators looked at the numbers of healthy cats in rescue shelters that harbor canine parvovirus in their feces. In fact, CPV was found in one-third of cats in a cat-only rescue shelter and a mixed rescue shelter. Interestingly, no feline parvovirus was found in these cats. Also interesting was the fact that none of the cats were clinically ill. This indicates that normal cats could potentially be shedding canine parvovirus and may be a potential source for dogs in the same environment. [MK]
See also: Battilani M, Balboni A, Ustulin M, et al. Genetic complexity and multiple infections with more Parvovirus species in naturally infected cats. Vet Res 2011;42:43. [free, full text article]
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Read the Cat Health News Weekly
Join us on Google+
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