5 resultados para Zinc and wound healing

em Digital Commons at Florida International University


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According to the American Podiatric Medical Association, about 15 percent of the patients with diabetes would develop a diabetic foot ulcer. Furthermore, foot ulcerations leads to 85 percent of the diabetes-related amputations. Foot ulcers are caused due to a combination of factors, such as lack of feeling in the foot, poor circulation, foot deformities and the duration of the diabetes. To date, the wounds are inspected visually to monitor the wound healing, without any objective imaging approach to look before the wound’s surface. Herein, a non-contact, portable handheld optical device was developed at the Optical Imaging Laboratory as an objective approach to monitor wound healing in foot ulcer. This near-infrared optical technology is non-radiative, safe and fast in imaging large wounds on patients. The FIU IRB-approved study will involve subjects that have been diagnosed with diabetes by a physician and who have developed foot ulcers. Currently, in-vivo imaging studies are carried out every week on diabetic patients with foot ulcers at two clinical sites in Miami. Near-infrared images of the wound are captured on subjects every week and the data is processed using customdeveloped Matlab-based image processing tools. The optical contrast of the wound to its peripheries and the wound size are analyzed and compared from the NIR and white light images during the weekly systematic imaging of wound healing.

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The elderly are at the highest risk of developing pressure ulcers that result in prolonged hospitalization, high health care costs, increased mortality, and decreased quality of life. The burden of pressure ulcers will intensify because of a rapidly increasing elderly population in the United States (US). Poor nutrition is a major predictor of pressure ulcer formation. The purpose of this study was to examine the effects of a comprehensive, interdisciplinary nutritional protocol on: (1) pressure ulcer wound healing (2) length of hospital stays, and (3) charges for pressure ulcer management. Using a pre-intervention/post intervention quasi-experimental design the study sample was composed of 100 patients 60 years or older, admitted with or acquiring a pressure ulcer. A pre-intervention group (n= 50) received routine pressure ulcer care (standard diet, dressing changes, and equipment). A post-intervention group received routine care plus an interdisciplinary nutrition intervention (physical therapy, speech therapy, occupational therapy, added protein and calories to the diet). Research questions were analyzed using descriptive statistics, frequencies, Chi-Square Tests, and T-tests. Findings indicated that the comprehensive, interdisciplinary nutritional protocol had a significant effect on the rate of wound healing in Week3 and Week4, total hospital length of stay (pre-intervention M= 43.2 days, SD=31.70 versus M=31.77, SID-12.02 post-intervention), and pressure ulcer length of stay (pre-intervention 25.28 days, SD5.60 versus 18.40 days, SD 5.27 post-intervention). Although there was no significant difference in total charges for the pre-intervention group ($727,245.00) compared to the post-intervention group ($702,065.00), charges for speech (m=$5885.12, SD=$332.55), pre albumin (m=$808.52,SD= $332.55), and albumin($278 .88, SD=55.00) were higher in the pre-intervention group and charges for PT ($5721.26, SD$3655.24) and OT($2544 .64, SD=1712.863) were higher in the post-intervention group. Study findings indicate that this comprehensive nutritional intervention was effective in improving pressure ulcer wound healing, decreasing both hospital length of stay for treatment of pressure ulcer and total hospital length of stay while showing no significant additional charges for treatment of pressure ulcers.

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The elderly are at the highest risk of developing pressure ulcers that result in prolonged hospitalization, high health care costs, increased mortality, and decreased quality of life. The burden of pressure ulcers will intensify because of a rapidly increasing elderly population in the United States (US). Poor nutrition is a major predictor of pressure ulcer formation. The purpose of this study was to examine the effects of a comprehensive, interdisciplinary nutritional protocol on: 1) pressure ulcer wound healing 2) length of hospital stays, and 3) charges for pressure ulcer management. Using a pre-intervention/post intervention quasi-experimental design the study sample was composed of 100 patients 60 years or older, admitted with or acquiring a pressure ulcer. A pre-intervention group (n= 50) received routine pressure ulcer care (standard diet, dressing changes, and equipment). A post-intervention group received routine care plus an interdisciplinary nutrition intervention (physical therapy, speech therapy, occupational therapy, added protein and calories to the diet). Research questions were analyzed using descriptive statistics, frequencies, Chi-Square Tests, and T-tests. Findings indicated that the comprehensive, interdisciplinary nutritional protocol had a significant effect on the rate of wound healing in Week3 and Week4, total hospital length of stay (pre-intervention M= 43.2 days, SD=31.70 versus M=31.77, SD=12.02 post-intervention), and pressure ulcer length of stay (pre-intervention 25.28 days, SD5.60 versus 18.40 days, SD 5.27 post-intervention). Although there was no significant difference in total charges for the pre-intervention group ($727,245.00) compared to the post-intervention group ($702,065.00), charges for speech (m=$5885.12, SD=$332.55), pre albumin (m=$808.52,SD= $332.55), and albumin($278 .88, SD=55.00) were higher in the pre-intervention group and charges for PT ($5721.26, SD$3655.24) and OT($2544 .64, SD=1712.863) were higher in the post-intervention group. Study findings indicate that this comprehensive nutritional intervention was effective in improving pressure ulcer wound healing, decreasing both hospital length of stay for treatment of pressure ulcer and total hospital length of stay while showing no significant additional charges for treatment of pressure ulcers.

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Coral reefs are in decline worldwide and coral disease is a significant contributing factor. However, etiologies of coral diseases are still not well understood. In contrast with the Caribbean, extremely little is known about coral diseases in the Philippines. In 2005, off Southeast Negros Island, Philippines, I investigated relationships between environmental parameters and prevalence of the two most common coral diseases, ulcerative white spot (UWS) and massive Porites growth anomalies (MPGAs). Samples were collected along a disease prevalence gradient 40.5 km long. Principal component analyses showed prevalence of MPGAs was positively correlated with water column nitrogen, organic carbon of surface sediments, and colony density. UWS was positively correlated with water column phosphorus. This is the first quantitative evidence linking anthropogenically-impacted water and sediment to a higher prevalence of these diseases. Histological and cytological alterations were investigated by comparing tissues from two distinct types of MPGA lesions (types 1 and 2) and healthy coral using light and electron microscopy. Skeletal abnormalities and sloughing, swelling, thinning, and loss of tissues in MPGAs resembled tissues exposed to bacterial or fungal toxins. Both lesion types had decreases in symbiotic zooxanthellae, which supply nutrients to corals. Notable alterations included migrations of chromophore cells (amoebocytes) (1) nocturnally to outer epithelia to perform wound-healing, including plugging gaps and secreting melanin in degraded tissues, and (2) diurnally to the interior of the tissue possibly to prevent shading zooxanthellae in order to maximize photosynthate production. Depletion of melanin (active in wound healing) in type 2 lesions suggested type 2 tissues were overtaxed and less stable. MPGAs contained an abundance of endolithic fungi and virus-like particles, which may result from higher nutrient levels and play roles in disease development. Swollen cells and mucus frequently blocked gastrovascular canals (GVCs) in MPGAs. Type 1 lesions appeared to compensate for impeded flow of wastes and nutrients through these canals with proliferation of new GVCs, which were responsible for the observed thickened tissues. In contrast, type 2 tissues were thin and more degraded. Dysplasia and putative neoplasia were also observed in MPGAs which may result from the tissue regeneration capacity being overwhelmed.

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Coral reefs are in decline worldwide and coral disease is a significant contributing factor. However, etiologies of coral diseases are still not well understood. In contrast with the Caribbean, extremely little is known about coral diseases in the Philippines. In 2005, off Southeast Negros Island, Philippines, I investigated relationships between environmental parameters and prevalence of the two most common coral diseases, ulcerative white spot (UWS) and massive Porites growth anomalies (MPGAs). Samples were collected along a disease prevalence gradient 40.5 km long. Principal component analyses showed prevalence of MPGAs was positively correlated with water column nitrogen, organic carbon of surface sediments, and colony density. UWS was positively correlated with water column phosphorus. This is the first quantitative evidence linking anthropogenically-impacted water and sediment to a higher prevalence of these diseases. Histological and cytological alterations were investigated by comparing tissues from two distinct types of MPGA lesions (types 1 and 2) and healthy coral using light and electron microscopy. Skeletal abnormalities and sloughing, swelling, thinning, and loss of tissues in MPGAs resembled tissues exposed to bacterial or fungal toxins. Both lesion types had decreases in symbiotic zooxanthellae, which supply nutrients to corals. Notable alterations included migrations of chromophore cells (amoebocytes) (1) nocturnally to outer epithelia to perform wound-healing, including plugging gaps and secreting melanin in degraded tissues, and (2) diurnally to the interior of the tissue possibly to prevent shading zooxanthellae in order to maximize photosynthate production. Depletion of melanin (active in wound healing) in type 2 lesions suggested type 2 tissues were overtaxed and less stable. MPGAs contained an abundance of endolithic fungi and virus-like particles, which may result from higher nutrient levels and play roles in disease development. Swollen cells and mucus frequently blocked gastrovascular canals (GVCs) in MPGAs. Type 1 lesions appeared to compensate for impeded flow of wastes and nutrients through these canals with proliferation of new GVCs, which were responsible for the observed thickened tissues. In contrast, type 2 tissues were thin and more degraded. Dysplasia and putative neoplasia were also observed in MPGAs which may result from the tissue regeneration capacity being overwhelmed.