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Dive into the research topics where Diana Whitaker is active.

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Featured researches published by Diana Whitaker.


Journal of Cutaneous Pathology | 1991

Cytotoxic folliculitis in GvHD : evidence of follicular stem cell injury and recovery

George F. Murphy; Robert M. Lavker; Diana Whitaker; Robert Korngold

Recent observations indicate that stem cells of the murine hair follicle exist exclusively as a subpopulation of relatively undiffer‐entiated outer root sheath cells located in the bulge region at the mid‐portion of the follicle. Because it has been hypothesized that stem cells of interfollicular epidermis may represent targets of cytotoxic responses in acute graft‐versus‐host disease (AGVHD), we studied murine AGVHD and observed sequential skin biopsies for the presence and evolutionary pattern of follicular injury. Highly purified subsets of donor T cells were used to produce AGVHD to multiple minor histocompatibility (H) antigens in two strain combinations of mice matched for the major histocompatibility complex (MHC). In the C3H.SW‐>B6 strain combination, only CD8+ effector cells produced histologic evidence in skin of AGVHD, which peaked three weeks post‐transplant. In the B10.D2‐>DBA/2 strain combination, CD4+ effector cells, and to a lesser extent, GD8+ cells, mediated disease, which peaked during the fourth week posttransplant. Analysis of skin from both strain/effector cell combinations revealed follicular infiltrates preferentially involving follicular stem cell (FSC) regions (bulge) of anagen follicles between the second and third weeks post‐transplant. These infiltrates often preceded infiltration of adjacent interfollicular epidermis and were associated with follicular involution to telogen (resting) phase. By the fourth week post‐transplant, > 50% of follicles were in telogen phase and residual inflammation was minimal. This provided a unique opportunity to observe follicular recovery from telogen. This involved formation of buds of premordial hair matrix derived from FSC populations of the bulge regions, and subsequent descent of these buds, initially tethered by elongate columns of putative stem cell progeny, along the course of fibrous tracts corresponding to follicular sheaths. These findings suggest that stem cells of hair follicles, as well as epidermis, represent potential targets of cytotoxicity in AGVHD. Moreover, they provide in vivo demonstration that the newly‐described FSC population of the follicular bulge give rise to germinative matrix epithelium upon pathological stimulation.


Journal of Cutaneous Pathology | 1993

Expression of platelet-endothelial cell adhesion molecule-1 (PECAM-1) during melanoma-induced angiogenesis in vivo.

Randy Berger; Steven M. Albelda; David Berd; Michael D. Ioffreda; Diana Whitaker; George F. Murphy

Recent ultrastructural data indicate that tumor‐induced angiogenesis involves polarized outgrowth of endothelial cells from established vessels into tumor parenchyma and interstitium. Efforts to define the cytoarchitecture of the angiogenic response and to ascertain molecular determinants of polarized endothelial migration have been impeded by lack of sensitive and specific immunologic markers for endothelium and vessel wall components. In this study, we utilized monoclonal antibody to platelet‐endothelial cell adhesion molecule‐1 (PECAM‐1), a cell‐cell adhesion molecule belonging to the immunoglobulin superfamily, to determine extent and patterns of angiogenesis in metastatic melanomas before (N = 7) and after (N = 3) induction of tumor‐infiltrating lymphocyte responses provoked by administration of experimental melanoma vaccine. PECAM‐1 proved to be a more reliable marker for angiogenesis than antibodies to von Willebrand Factor. Although both normal and tumor vessels exhibited prominent staining for PECAM‐1, different patterns of endothelial reactivity were observed. Formation of new vessels was associated with i) PECAM‐1 redistribution from a constitutive circumferential membrane pattern to a pattern restricted to cell‐cell junctions; ii) formation of endothelial cords formed by cell‐cell interactions; and iii) eventual development of open lumens. Vessels within inflamed (vaccine‐treated) and non‐inflamed melanomas did not differ with regard to patterns of PECAM‐1 expression. Forming vessels of inflamed melanomas failed to express the cytokine‐inducible activation marker, E‐selectin. Although normal microvessels and reactive vessels of healing wounds demonstrated prominent staining for α6; laminin receptor, vessels within melanomas showed apparently diminished expression. These data establish PECAM‐1 as a sensitive and specific marker for experimental angiogenesis, and further support the possibility that cell‐cell adhesion mediated by PECAM‐1 may contribute to directed endothelial migration typical of tumor‐induced formation of new vessels.


Cambridge Symposium-Fiber/LASE '86 | 1987

Pulse Width Dependence Of Pigment Cell Damage At 694 nm In Guinea Pig Skin

Jeffrey S. Dover; Luigi L. Polla; Randall J. Margolis; Diana Whitaker; Schinichi Watanabe; George F. Murphy; John A. Parrish; R. Rox Anderson; Stephen N. Joffe

351 nm, 20-nsec XeF excimer laser irradiation has previously been shown to selectively target and damage melanosomes in human skin. In the following studies selective targeting with melanosomal photodisruption has been demonstrated in pigmented guinea pig skin with a Q-switched 40-nsec ruby laser, and a 750-nsec pulsed dye laser but not with a 400-usec pulsed dye laser. The pulse width dependence of melanosomal disruption, occurring only at pulsewidths shorter than the thermal relaxation time of the melanosome (0.5 - 1.0 usec), is in accordance with the theory of selective photothermolysis. Possible mechanisms of melanosomal photodisruption include development of sudden thermal gradients leading to cavitation or shock wave production.


Cellular Immunology | 1991

Induction of local inflammation by recombinant human platelet factor 4 in the mouse

Richard J. Sharpe; George F. Murphy; Diana Whitaker; Stephen J. Galli; Theodore E. Maione

Platelet factor 4 (PF-4) has been shown to be chemotactic for neutrophils and monocytes in vitro. To assess whether these observations have in vivo relevance, we tested the ability of recombinant human PF-4 (rPF-4) to induce acute and chronic dermal inflammation in the mouse. When injected as a single dose intradermally, rPF-4 induced an acute inflammatory response that peaked at 6 to 12 hr and which resolved by 36 hr. Injection of an equivalent amount of cytochrome c, buffer alone, or an amino-terminal PF-4 peptide failed to elicit a significant inflammatory response; however, the carboxy-terminal PF-4 peptide retained proinflammatory properties. The inflammatory infiltrate induced by a single injection of either rPF-4 or the 41 amino acid carboxy-terminal peptide was composed of neutrophils and smaller numbers of mononuclear cells. Repeated injection of rPF-4 resulted in nearly equal numbers of neutrophils and mononuclear cells. Moreover, marked dermal fibrosis developed after only 5 days of daily injection of rPF-4. Although relatively high concentrations of rPF-4 were required to elicit an inflammatory response, these concentrations may be locally attainable during platelet aggregation. Our findings thus support the hypothesis that PF-4 may contribute to the development of inflammatory responses at sites of platelet aggregation.


Proceedings of Laser-Tissue Interaction | 1990

Structural and functional alterations in rhodamine-123- and doxycycline-photosensitized cells

Christopher R. Shea; Diana Whitaker; George F. Murphy; Norah Chen; Joanne Wimberly; Manfred Scholz; Margaret E. Sherwood; Thomas J. Flotte; Tayyaba Hasan

In order to elucidate the mechanisms of photosensitized injury to mitochondria, two photosensitizers have been compared. Both doxycycline (DOTC) and rhodamine-l23 (R123) localize preferentially within the mitochondria of MGH-IJ1 bladder carcinoma cells j1 vitro, and both sensitize phototoxic injury that is selective for mitochondria. Mitochondria of cells pretreated with DOTC and irradiated with UVA (1 J/cm2, 320-400 rim) undergo massive swelling that begins by 10 mm after irradiation, is maximal by 1 h, and is partially repaired by 4 h; damage caused by exposure to a higher UVA dose (6 J/cm2), however, is not repaired. In contrast, cells pretreated with R123 and irradiated with an argon-ion laser (10 J/cm2, 514.5 rim) undergo a different type of mitochondrial injury, characterized by the delayed (4 h) onset of moderate mitochondrial swelling and striking mitochondrial distortion and fragmentation, which is not repaired by 48 h after irradiation. These differences indicate that the reactions underlying cellular phototoxicity can be distinguished even on an ultrastructural level. Probably both the primary photochemistry and the submitochondrial targets of these reactions differ with the two photosensitizers.


Proceedings of the National Academy of Sciences of the United States of America | 1991

Human dermal mast cells contain and release tumor necrosis factor alpha, which induces endothelial leukocyte adhesion molecule 1.

Laurence J. Walsh; G Trinchieri; H. A. Waldorf; Diana Whitaker; George F. Murphy


Journal of Investigative Dermatology | 1987

Melanosomes are a primary target of Q-switched ruby laser irradiation in guinea pig skin

Luigi L. Polla; Randall J. Margolis; Jeffrey S. Dover; Diana Whitaker; George F. Murphy; Steven L. Jacques; R. Rox Anderson


Journal of Investigative Dermatology | 1989

Intercellular adhesion molecule expression in the evolving human cutaneous delayed hypersensitivity reaction.

Rachel E. Lewis; Marion E. Buchsbaum; Diana Whitaker; George F. Murphy


Journal of Investigative Dermatology | 1989

The Systemic Administration of Gamma Interferon Inhibits Collagen Synthesis and Acute Inflammation in a Murine Skin Wounding Model

Richard D. Granstein; Mary Rose Deak; Steven L. Jacques; Randall J. Margolis; Thomas J. Flotte; Diana Whitaker; Frederick H. Long; Edward P. Amento


Laboratory Investigation | 1993

Novel interactions between dermal dendrocytes and mast cells in human skin. Implications for hemostasis and matrix repair.

Hirohiko Sueki; Diana Whitaker; Marion E. Buchsbaum; George F. Murphy

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George F. Murphy

Brigham and Women's Hospital

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Robert Korngold

Hackensack University Medical Center

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Hirohiko Sueki

University of Pennsylvania

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Michael D. Ioffreda

Penn State Milton S. Hershey Medical Center

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