The Experts below are selected from a list of 216 Experts worldwide ranked by ideXlab platform

Smriti Kundu-raychaudhuri - One of the best experts on this subject based on the ideXlab platform.

  • FR255734, a Humanized, Fc-Silent, Anti-CD28 Antibody, Improves Psoriasis in the SCID Mouse-Psoriasis Xenograft Model
    Journal of Investigative Dermatology, 2008
    Co-Authors: Siba P. Raychaudhuri, Smriti Kundu-raychaudhuri, Kouichi Tamura, Taro Masunaga, Kaori Kubo, Kaori Hanaoka, Wen Yue Jiang, Leonore A. Herzenberg
    Abstract:

    In psoriasis, CD28/B7 costimulatory molecules are well characterized. Here, using the severe combined immunodeficient (SCID) mouse-psoriasis xenograft model, we report therapeutic efficacy of a humanized anti-CD28 monoclonal antibody (FR255734; Astellas Pharmaceuticals Inc., Tokyo, Japan). Transplanted psoriasis plaques on the SCID mouse were treated weekly for 4 weeks with intraperitoneal injections of FR255734 at 10, 3, and 1-mg kg−1 doses. Groups treated with doses of 10 and 3 mg kg−1had significant thinning of the epidermis and reduced HLA-DR-positive lymphocytic infiltrates. The length of the Rete Pegs changed from 415.2±59.6 to 231.4±40.4 μm (P

  • K252a, a high-affinity nerve growth factor receptor blocker, improves psoriasis: An in vivo study using the severe combined immunodeficient mouse-human skin model
    Journal of Investigative Dermatology, 2004
    Co-Authors: Siba P. Raychaudhuri, Helena Weltman, Mrinmoy Sanyal, Smriti Kundu-raychaudhuri
    Abstract:

    The peripheral nervous system, in addition to its sensory and motor functions, can induce a local inflammatory response known as neurogenic inflammation. This phenomenon plays a critical role in several inflammatory diseases, e.g., asthma, atopy, rheumatoid arthritis, psoriasis, and ulcerative colitis. Neurogenic inflammation and the role of nerve growth factor (NGF) have been extensively studied in psoriasis. There are increased levels of NGF in the keratinocytes and upregulation of NGF receptor (NGF-R) in the cutaneous nerves of psoriatic plaques. NGF can influence all the salient pathologic events noticed in psoriasis such as proliferation of keratinocytes, angiogenesis, T cell activation, expression of adhesion molecules, proliferation of cutaneous nerves, and upregulation of neuropeptides. In this double-blinded, placebo-controlled study, we addressed the role of NGF/NGF-R in psoriasis in an in vivo system using the severe combined immunodeficient (SCID) mouse–human skin model of psoriasis. The transplanted psoriatic plaques on the SCID mice (n=12) were treated with K252a, a high-affinity NGF receptor blocker. Psoriasis significantly improved following 2 wk of therapy. The length of the Rete Pegs changed from 308.57±98.72 to 164.64±46.78 μm (p t test). A similar improvement of psoriasis was observed by directly inhibiting NGF with NGF-neutralizing antibody. NGF-neutralizing antibody in normal saline at 10 ng (n=4) and 20 ng (n=4) per kilogram of body weight doses were used. Both doses of NGF-neutralizing antibody reduced Rete peg lengths significantly, e.g., from 298.5±42.69 to 150.52±32.93 μm (p t test). This study provides evidence for the role of NGF and its high-affinity receptor in the pathogenesis of psoriasis and insights to develop novel therapeutic modalities.

  • K252a, a high-affinity nerve growth factor receptor blocker, improves psoriasis: An in vivo study using the severe combined immunodeficient mouse-human skin model
    Journal of Investigative Dermatology, 2004
    Co-Authors: Siba P. Raychaudhuri, Helena Weltman, Mrinmoy Sanyal, Smriti Kundu-raychaudhuri
    Abstract:

    The peripheral nervous system, in addition to its sensory and motor functions, can induce a local inflammatory response known as neurogenic inflammation. This phenomenon plays a critical role in several inflammatory diseases, e.g., asthma, atopy, rheumatoid arthritis, psoriasis, and ulcerative colitis. Neurogenic inflammation and the role of nerve growth factor (NGF) have been extensively studied in psoriasis. There are increased levels of NGF in the keratinocytes and upregulation of NGF receptor (NGF-R) in the cutaneous nerves of psoriatic plaques. NGF can influence all the salient pathologic events noticed in psoriasis such as proliferation of keratinocytes, angiogenesis, T cell activation, expression of adhesion molecules, proliferation of cutaneous nerves, and upregulation of neuropeptides. In this double-blinded, placebo-controlled study, we addressed the role of NGF/NGF-R in psoriasis in an in vivo system using the severe combined immunodeficient (SCID) mouse-human skin model of psoriasis. The transplanted psoriatic plaques on the SCID mice (n=12) were treated with K252a, a high-affinity NGF receptor blocker. Psoriasis significantly improved following 2 wk of therapy. The length of the Rete Pegs changed from 308.57+/-98.72 to 164.64+/-46.78 microm (p

Siba P. Raychaudhuri - One of the best experts on this subject based on the ideXlab platform.

  • FR255734, a Humanized, Fc-Silent, Anti-CD28 Antibody, Improves Psoriasis in the SCID Mouse-Psoriasis Xenograft Model
    Journal of Investigative Dermatology, 2008
    Co-Authors: Siba P. Raychaudhuri, Smriti Kundu-raychaudhuri, Kouichi Tamura, Taro Masunaga, Kaori Kubo, Kaori Hanaoka, Wen Yue Jiang, Leonore A. Herzenberg
    Abstract:

    In psoriasis, CD28/B7 costimulatory molecules are well characterized. Here, using the severe combined immunodeficient (SCID) mouse-psoriasis xenograft model, we report therapeutic efficacy of a humanized anti-CD28 monoclonal antibody (FR255734; Astellas Pharmaceuticals Inc., Tokyo, Japan). Transplanted psoriasis plaques on the SCID mouse were treated weekly for 4 weeks with intraperitoneal injections of FR255734 at 10, 3, and 1-mg kg−1 doses. Groups treated with doses of 10 and 3 mg kg−1had significant thinning of the epidermis and reduced HLA-DR-positive lymphocytic infiltrates. The length of the Rete Pegs changed from 415.2±59.6 to 231.4±40.4 μm (P

  • K252a, a high-affinity nerve growth factor receptor blocker, improves psoriasis: An in vivo study using the severe combined immunodeficient mouse-human skin model
    Journal of Investigative Dermatology, 2004
    Co-Authors: Siba P. Raychaudhuri, Helena Weltman, Mrinmoy Sanyal, Smriti Kundu-raychaudhuri
    Abstract:

    The peripheral nervous system, in addition to its sensory and motor functions, can induce a local inflammatory response known as neurogenic inflammation. This phenomenon plays a critical role in several inflammatory diseases, e.g., asthma, atopy, rheumatoid arthritis, psoriasis, and ulcerative colitis. Neurogenic inflammation and the role of nerve growth factor (NGF) have been extensively studied in psoriasis. There are increased levels of NGF in the keratinocytes and upregulation of NGF receptor (NGF-R) in the cutaneous nerves of psoriatic plaques. NGF can influence all the salient pathologic events noticed in psoriasis such as proliferation of keratinocytes, angiogenesis, T cell activation, expression of adhesion molecules, proliferation of cutaneous nerves, and upregulation of neuropeptides. In this double-blinded, placebo-controlled study, we addressed the role of NGF/NGF-R in psoriasis in an in vivo system using the severe combined immunodeficient (SCID) mouse–human skin model of psoriasis. The transplanted psoriatic plaques on the SCID mice (n=12) were treated with K252a, a high-affinity NGF receptor blocker. Psoriasis significantly improved following 2 wk of therapy. The length of the Rete Pegs changed from 308.57±98.72 to 164.64±46.78 μm (p t test). A similar improvement of psoriasis was observed by directly inhibiting NGF with NGF-neutralizing antibody. NGF-neutralizing antibody in normal saline at 10 ng (n=4) and 20 ng (n=4) per kilogram of body weight doses were used. Both doses of NGF-neutralizing antibody reduced Rete peg lengths significantly, e.g., from 298.5±42.69 to 150.52±32.93 μm (p t test). This study provides evidence for the role of NGF and its high-affinity receptor in the pathogenesis of psoriasis and insights to develop novel therapeutic modalities.

  • K252a, a high-affinity nerve growth factor receptor blocker, improves psoriasis: An in vivo study using the severe combined immunodeficient mouse-human skin model
    Journal of Investigative Dermatology, 2004
    Co-Authors: Siba P. Raychaudhuri, Helena Weltman, Mrinmoy Sanyal, Smriti Kundu-raychaudhuri
    Abstract:

    The peripheral nervous system, in addition to its sensory and motor functions, can induce a local inflammatory response known as neurogenic inflammation. This phenomenon plays a critical role in several inflammatory diseases, e.g., asthma, atopy, rheumatoid arthritis, psoriasis, and ulcerative colitis. Neurogenic inflammation and the role of nerve growth factor (NGF) have been extensively studied in psoriasis. There are increased levels of NGF in the keratinocytes and upregulation of NGF receptor (NGF-R) in the cutaneous nerves of psoriatic plaques. NGF can influence all the salient pathologic events noticed in psoriasis such as proliferation of keratinocytes, angiogenesis, T cell activation, expression of adhesion molecules, proliferation of cutaneous nerves, and upregulation of neuropeptides. In this double-blinded, placebo-controlled study, we addressed the role of NGF/NGF-R in psoriasis in an in vivo system using the severe combined immunodeficient (SCID) mouse-human skin model of psoriasis. The transplanted psoriatic plaques on the SCID mice (n=12) were treated with K252a, a high-affinity NGF receptor blocker. Psoriasis significantly improved following 2 wk of therapy. The length of the Rete Pegs changed from 308.57+/-98.72 to 164.64+/-46.78 microm (p

Helena Weltman - One of the best experts on this subject based on the ideXlab platform.

  • K252a, a high-affinity nerve growth factor receptor blocker, improves psoriasis: An in vivo study using the severe combined immunodeficient mouse-human skin model
    Journal of Investigative Dermatology, 2004
    Co-Authors: Siba P. Raychaudhuri, Helena Weltman, Mrinmoy Sanyal, Smriti Kundu-raychaudhuri
    Abstract:

    The peripheral nervous system, in addition to its sensory and motor functions, can induce a local inflammatory response known as neurogenic inflammation. This phenomenon plays a critical role in several inflammatory diseases, e.g., asthma, atopy, rheumatoid arthritis, psoriasis, and ulcerative colitis. Neurogenic inflammation and the role of nerve growth factor (NGF) have been extensively studied in psoriasis. There are increased levels of NGF in the keratinocytes and upregulation of NGF receptor (NGF-R) in the cutaneous nerves of psoriatic plaques. NGF can influence all the salient pathologic events noticed in psoriasis such as proliferation of keratinocytes, angiogenesis, T cell activation, expression of adhesion molecules, proliferation of cutaneous nerves, and upregulation of neuropeptides. In this double-blinded, placebo-controlled study, we addressed the role of NGF/NGF-R in psoriasis in an in vivo system using the severe combined immunodeficient (SCID) mouse–human skin model of psoriasis. The transplanted psoriatic plaques on the SCID mice (n=12) were treated with K252a, a high-affinity NGF receptor blocker. Psoriasis significantly improved following 2 wk of therapy. The length of the Rete Pegs changed from 308.57±98.72 to 164.64±46.78 μm (p t test). A similar improvement of psoriasis was observed by directly inhibiting NGF with NGF-neutralizing antibody. NGF-neutralizing antibody in normal saline at 10 ng (n=4) and 20 ng (n=4) per kilogram of body weight doses were used. Both doses of NGF-neutralizing antibody reduced Rete peg lengths significantly, e.g., from 298.5±42.69 to 150.52±32.93 μm (p t test). This study provides evidence for the role of NGF and its high-affinity receptor in the pathogenesis of psoriasis and insights to develop novel therapeutic modalities.

  • K252a, a high-affinity nerve growth factor receptor blocker, improves psoriasis: An in vivo study using the severe combined immunodeficient mouse-human skin model
    Journal of Investigative Dermatology, 2004
    Co-Authors: Siba P. Raychaudhuri, Helena Weltman, Mrinmoy Sanyal, Smriti Kundu-raychaudhuri
    Abstract:

    The peripheral nervous system, in addition to its sensory and motor functions, can induce a local inflammatory response known as neurogenic inflammation. This phenomenon plays a critical role in several inflammatory diseases, e.g., asthma, atopy, rheumatoid arthritis, psoriasis, and ulcerative colitis. Neurogenic inflammation and the role of nerve growth factor (NGF) have been extensively studied in psoriasis. There are increased levels of NGF in the keratinocytes and upregulation of NGF receptor (NGF-R) in the cutaneous nerves of psoriatic plaques. NGF can influence all the salient pathologic events noticed in psoriasis such as proliferation of keratinocytes, angiogenesis, T cell activation, expression of adhesion molecules, proliferation of cutaneous nerves, and upregulation of neuropeptides. In this double-blinded, placebo-controlled study, we addressed the role of NGF/NGF-R in psoriasis in an in vivo system using the severe combined immunodeficient (SCID) mouse-human skin model of psoriasis. The transplanted psoriatic plaques on the SCID mice (n=12) were treated with K252a, a high-affinity NGF receptor blocker. Psoriasis significantly improved following 2 wk of therapy. The length of the Rete Pegs changed from 308.57+/-98.72 to 164.64+/-46.78 microm (p

Mrinmoy Sanyal - One of the best experts on this subject based on the ideXlab platform.

  • K252a, a high-affinity nerve growth factor receptor blocker, improves psoriasis: An in vivo study using the severe combined immunodeficient mouse-human skin model
    Journal of Investigative Dermatology, 2004
    Co-Authors: Siba P. Raychaudhuri, Helena Weltman, Mrinmoy Sanyal, Smriti Kundu-raychaudhuri
    Abstract:

    The peripheral nervous system, in addition to its sensory and motor functions, can induce a local inflammatory response known as neurogenic inflammation. This phenomenon plays a critical role in several inflammatory diseases, e.g., asthma, atopy, rheumatoid arthritis, psoriasis, and ulcerative colitis. Neurogenic inflammation and the role of nerve growth factor (NGF) have been extensively studied in psoriasis. There are increased levels of NGF in the keratinocytes and upregulation of NGF receptor (NGF-R) in the cutaneous nerves of psoriatic plaques. NGF can influence all the salient pathologic events noticed in psoriasis such as proliferation of keratinocytes, angiogenesis, T cell activation, expression of adhesion molecules, proliferation of cutaneous nerves, and upregulation of neuropeptides. In this double-blinded, placebo-controlled study, we addressed the role of NGF/NGF-R in psoriasis in an in vivo system using the severe combined immunodeficient (SCID) mouse–human skin model of psoriasis. The transplanted psoriatic plaques on the SCID mice (n=12) were treated with K252a, a high-affinity NGF receptor blocker. Psoriasis significantly improved following 2 wk of therapy. The length of the Rete Pegs changed from 308.57±98.72 to 164.64±46.78 μm (p t test). A similar improvement of psoriasis was observed by directly inhibiting NGF with NGF-neutralizing antibody. NGF-neutralizing antibody in normal saline at 10 ng (n=4) and 20 ng (n=4) per kilogram of body weight doses were used. Both doses of NGF-neutralizing antibody reduced Rete peg lengths significantly, e.g., from 298.5±42.69 to 150.52±32.93 μm (p t test). This study provides evidence for the role of NGF and its high-affinity receptor in the pathogenesis of psoriasis and insights to develop novel therapeutic modalities.

  • K252a, a high-affinity nerve growth factor receptor blocker, improves psoriasis: An in vivo study using the severe combined immunodeficient mouse-human skin model
    Journal of Investigative Dermatology, 2004
    Co-Authors: Siba P. Raychaudhuri, Helena Weltman, Mrinmoy Sanyal, Smriti Kundu-raychaudhuri
    Abstract:

    The peripheral nervous system, in addition to its sensory and motor functions, can induce a local inflammatory response known as neurogenic inflammation. This phenomenon plays a critical role in several inflammatory diseases, e.g., asthma, atopy, rheumatoid arthritis, psoriasis, and ulcerative colitis. Neurogenic inflammation and the role of nerve growth factor (NGF) have been extensively studied in psoriasis. There are increased levels of NGF in the keratinocytes and upregulation of NGF receptor (NGF-R) in the cutaneous nerves of psoriatic plaques. NGF can influence all the salient pathologic events noticed in psoriasis such as proliferation of keratinocytes, angiogenesis, T cell activation, expression of adhesion molecules, proliferation of cutaneous nerves, and upregulation of neuropeptides. In this double-blinded, placebo-controlled study, we addressed the role of NGF/NGF-R in psoriasis in an in vivo system using the severe combined immunodeficient (SCID) mouse-human skin model of psoriasis. The transplanted psoriatic plaques on the SCID mice (n=12) were treated with K252a, a high-affinity NGF receptor blocker. Psoriasis significantly improved following 2 wk of therapy. The length of the Rete Pegs changed from 308.57+/-98.72 to 164.64+/-46.78 microm (p

Braham Shroot - One of the best experts on this subject based on the ideXlab platform.

  • 080 The Effects of Papain‐Urea‐Copper Chlorophyllin Ointment on Healing of Wounds in an Acute Infected Full Thickness Porcine Model
    Wound Repair and Regeneration, 2008
    Co-Authors: D. Telgenhoff, Paul Attar, M. Cooper, K. Posadas, S. Ramsay, V. Vasquez, Braham Shroot
    Abstract:

    Removal of necrotic tissue is essential for wound-bed preparation for the treatment of chronic wounds. Enzymatic debridement appears to be most useful in the removal of eschar when surgical techniques cannot be utilized. The purpose of this study is to determine the efficacy of papain–urea chlorophyllin ointment compared to moist wound care using an infected, acute, porcine full thickness wound model. Twenty full thickness wounds were created on the dorsum of domestic pigs. Following hemostasis, the wounds were contaminated with wound-isolated bacteria then treated with test articles and dressed with moisture-Retentive dressing. All the wounds were evaluated 1, 4, 8, 11, 14,18, and 21 days postsurgery for epithelialization and biopsies were obtained for microscopic evaluation. The results showed no adverse effect in reepithelialization in acute wounds when using papain–urea chlorophyllin "ointment compared to moist wound care, TEWL measurements also showed no adverse affects from the treatment. Microscopic examination reveals an increase in the number of keratinocytes present in the epidermis of the treated pigs as well as an increase in the depth of Rete Pegs. New blood vessel formation was increased at all examined time points in the papain–urea chlorophyllin ointment treated pigs, which was verified with CD31 and von Willebrand Factor staining. VEGF was increased after 1 week in the wound fluid from treated wounds compared to moist control. While the reepithelialization rate does not appear to be inhibited by papain–urea-chlorophyllin combination in acute wounds, the healing appears to be more complete based on the number of keratinocytes present in the epidermis and the extensive Rete peg formation. The wounds also appear to have enhanced vascularization which is vital in supplying nutrients to the newly healed wound.

  • Influence of papain urea copper chlorophyllin on wound matrix remodeling.
    Wound Repair and Regeneration, 2007
    Co-Authors: D. Telgenhoff, Sarah Ramsay, Valerie Vasquez, Kristine Villareal, Paul Slusarewicz, Paul Attar, Braham Shroot
    Abstract:

    The purpose of this study was to examine the dermal and epidermal alterations associated with wound healing in wounds treated with papain urea copper chlorophyllin (PUC), papain-urea, copper chlorophyllin, or urea base ointment and compare these with moist wound care using a porcine full-thickness infected wound model. All the wounds were evaluated postsurgery for erythema, transepidermal water loss, microscopic morphology, and changes in protein expression. Examination of stained paraffin sections revealed an increase in the number of keratinocytes present in the epidermis of the PUC and papain-treated pigs, relative to moist control. This increase in keratinocyte number corresponded to an increase in the movement of the keratinocytes into the underlying dermis in the form of Rete Pegs. In the dermis, there appeared to be an increase in blood vessel formation, collagen I deposition, and mature collagen in the papain and PUC treated tissues. The quality of healing appears to be enhanced based on the number of keratinocytes present in the epidermis, the extensive Rete peg formation, the increase in vasculature, and the increase in collagen birefringence.