The night before his fourth birthday, Rohan Giare of Rockville rolled off his bed and gashed the bridge of his nose. Rohan’s dad, not knowing whether he should focus on getting the bleeding to stop or go immediately to the emergency room, snapped pictures of the cut with his BlackBerry and sent them to his doctor friend, Neal Sikka.

“I just gave [Sikka] a ring,” Vishal Giare said, “and got initial input on how serious it might be.”

Sikka, an emergency physician at George Washington University, looked at the photos and recommended a trip to the hospital.

Sikka has gotten comfortable using his camera phone to make informal diagnoses for friends and family since he became a doctor in 1999. And as he embraced cellphone culture, Sikka said, he wondered if he could confidently and consistently make diagnoses if regular patients sent him injury snapshots.

In May, Sikka began a six-month study examining how accurately emergency doctors and physician assistants at GWU Hospital could diagnose wounds from patient-generated cellphone images. According to Sikka, it is the largest “mobile health” study looking at acute wound care.

“Mobile health” does not mean a clinic on wheels. It is an emerging field within telemedicine that comprises all aspects of care generated from or available on a portable mobile device such as a cellphone.

Doctors already use traditional forms of telemedicine — teleconferencing and videoconferencing — but Sikka said “mHealth” goes further, eliminating the need for scheduling conference rooms and reserving equipment.

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Washington Post Staff Writer
Tuesday, August 31, 2010

Keys To Effective Documentation That Can Help You In Court

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Recalcitrant lower extremity wounds of various etiologies stuck in the inflammatory stage of healing are frequently treated with antimicrobial dressings. Even without the clinical signs of infection, chronic wounds may have an increased bacterial burden that slows healing.¹ Over the past several years, different topical antimicrobial wound care products have emerged on the market. Although silver, a frequently utilized antimicrobial ingredient, has been found effective, it may cause stinging or burning in some patients.^1,2

Researchers have found a honey with plant-derived characteristics that make it ideal for use in wound care.^3,4 Active Leptospermum honey (ALH) used as a wound dressing has demonstrated antimicrobial properties that promote rapid healing and an anti-inflammatory action secondary to the presence of antioxidants.⁵ Free radicals produced during the inflammation process are absorbed by the antioxidant in the honey, promoting anti-inflammatory action that, in turn, reduces pain and swelling, the latter action fostering appropriate blood supply to the damaged areas to facilitate healing.⁶

As the main ingredient in MEDIHONEY dressings (Derma Sciences, Princeton, NJ), ALH provides a soothing alternative to silver-based dressings while also promoting debridement of necrotic tissue, decreasing edema, reducing inflammation, and decreasing odor.³ Honey also has antibacterial agents, including hydrogen peroxide, which is produced by the honey enzyme glucose oxidase when diluted by exudate.⁷ Although use of hydrogen peroxide in wounds is generally thought to cause cellular and protein damage, the hydrogen peroxide generated by the diluted ALH is approximately 1mmoL/L — 1,000 times less concentrated than the standard 3% hydrogen peroxide solution used as an antiseptic.³ Additionally, honey’s hydrogen peroxide stimulates new cell and blood vessel growth and is not harmful to tissues.^3,4,6

The following case study reports the change in pain level and wound healing progress with the use of ALH-impregnated calcium alginate. Along with its antimicrobial properties, this product has been shown to assist with debridement of slough and to remove nonviable tissue, as well as decrease wound pain

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author:

The care of wounds represents a significant portion of healthcare spending. In 2008, more than 89 million people in the US were treated for wound conditions that accounted for costs in excess of $25 billion.¹ Access to efficacious therapies for the treatment of one common wound type, diabetic foot ulcers, is essential to help contain healthcare spending and to ensure optimum outcomes for persons suffering with these wounds. However, access to effective treatments can be restricted depending on where the patient lives, where and by whom care is provided, or by the payer’s coverage criteria.^2-5
The financial burden of diabetic foot ulcers is considerable. An uncomplicated diabetic foot ulcer is estimated to cost $8,000 to treat. An infected ulcer can cost $17,000 and the cost of amputation can reach $45,000.^6,7 In 2007, more than 100,000 people with diabetes in the US had a foot amputation.8
Use of Total Contact Casting (TCC) results in a greater percent of diabetic ulcers healing in a shorter time. Many clinical studies, most randomized, controlled comparative studies, have demonstrated improved healing rates and cost savings when compared to standard methods of care for diabetic foot ulcers without TCC.^9-20 Reducing the time a diabetic wound is open can help reduce the risks of complications such as infection or amputation. These dramatically increase the cost of care and can negatively impact a person’s life. Many clinical Guidelines and treatment protocols ^21,22 recommend the use of TCC for the management of diabetic foot ulcerations.

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Author(s):

Abstract

Endogenous electric currents generated instantly at skin wounds direct migration of epithelial cells and are likely to be important in wound healing. Migration of fibroblasts is critical in wound healing. It remains unclear how wound electric fields guide migration of dermal fibroblasts. We report here that mouse skin wounds generated endogenous electric currents for many hours. Human dermal fibroblasts of both primary and cell-line cultures migrated directionally but slowly toward the anode in an electric field of 50–100 mV mm⁻¹. This is different from keratinocytes, which migrate quickly to the cathode. It took more than 1 hour for dermal fibroblasts to manifest detectable directional migration. Larger field strength (400 mV mm⁻¹) was required to induce directional migration within 1 hour after onset of the field. Phosphatidylinositol-3-OH kinase (PI3 kinase) mediates cathode-directed migration of keratinocytes. We tested the role of PI3 kinase in anode-directed migration of fibroblasts. An applied electric field activated PI3 kinase/Akt in dermal fibroblasts. Dermal fibroblasts from p110γ (a PI3 kinase catalytic subunit) null mice showed significantly decreased directional migration. These results suggest that physiological electric fields may regulate motility of dermal fibroblasts and keratinocytes differently, albeit using similar PI3 kinase-dependent mechanisms.

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Aihua Guo^1,2, Bing Song^1,3, Brian Reid^1,3, Yu Gu^1,3, John V Forrester¹, Colin A B Jahoda² and Min Zhao^1,3,4

Abstract

CC chemokine receptor 3 (CCR3), the sole receptor for eotaxins, is expressed on eosinophils and T helper type 2 (Th2) cells. In Hodgkin’s disease, eotaxin-1 secreted by fibroblasts collects Th2 cells and eosinophils within the tissue. Similarly, many Th2 cells infiltrate the lesional skin of cutaneous T-cell lymphoma (CTCL). In this study, we investigated the role of eotaxins in the development of the Th2 environment of CTCL. We revealed that fibroblasts from lesional skin of CTCL expressed higher amounts of eotaxin-3 messenger RNA (mRNA) compared with those from normal skin. Lesional skin of CTCL at advanced stages contained significantly higher levels of eotaxin-3 and CCR3 mRNA, compared with early stages of CTCL. IL-4 mRNA was expressed in some cases at advanced stages. Immunohistochemistry revealed that keratinocytes, endothelial cells, and dermal fibroblasts in lesional skin of CTCL showed a stronger expression of eotaxin-3 than did normal skin. CCR3⁺ lymphocytes and IL-4 expression were observed in some cases of advanced CTCL. Furthermore, both serum eotaxin-3 and eotaxin-1 levels of CTCL patients at advanced stages were significantly higher than those of healthy individuals. The concentrations of these chemokines correlated with serum soluble IL-2 receptor levels. These results suggest that interaction of eotaxins and CCR3 regulates the Th2-dominant tumor environment, which is closely related to the development of CTCL.

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Tomomitsu Miyagaki¹, Makoto Sugaya¹, Hideki Fujita¹, Hanako Ohmatsu¹, Takashi Kakinuma¹, Takafumi Kadono¹, Kunihiko Tamaki¹ and Shinichi Sato¹

Abstract

Production of antimicrobial peptides by epithelia is an essential defense against infectious pathogens. In this study we evaluated whether the commensal microorganism Staphylococcus epidermidis may enhance production of antimicrobial peptides by keratinocytes and thus augment skin defense against infection. Exposure of cultured undifferentiated human keratinocytes to a sterile nontoxic small molecule of <10 kDa from S. epidermidis conditioned culture medium (SECM), but not similar preparations from other bacteria, enhanced human β-defensin 2 (hBD2) and hBD3 mRNA expression and increased the capacity of cell lysates to inhibit the growth of group A Streptococcus (GAS) and S. aureus. Partial gene silencing of hBD3 inhibited this antimicrobial action. This effect was relevant in vivo as administration of SECM to mice decreased susceptibility to infection by GAS. Toll-like receptor 2 (TLR2) was important to this process as a TLR2-neutralizing antibody blocked induction of hBDs 2 and 3, and Tlr2-deficient mice did not show induction of mBD4. Taken together, these findings reveal a potential use for normal commensal bacterium S. epidermidis to activate TLR2 signaling and induce antimicrobial peptide expression, thus enabling the skin to mount an enhanced response to pathogens.

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Yuping Lai^1,2, Anna L Cogen¹, Katherine A Radek¹, Hyun Jeong Park^1,3, Daniel T MacLeod¹, Anke Leichtle⁴, Allen F Ryan⁴, Anna Di Nardo¹ and Richard L Gallo¹