Treatment of cutaneous ulcers with benzoyl peroxide.
Benzoyl peroxide, a powerful organic oxidizing agent, was applied topically according to a carefully developed technique to cutaneous ulcers of different types. The healing time was shortened greatly by the rapid development of healthy granulation tissue and the quick ingrowth of epithelium. Exceptionally large pressure ulcers with deep cavities, undercut edges and sinus tracts were sucessfully treated, as were stasis ulcers of long duration resistant to all other therapy. There were only 13 treatment failures among the 133 cases. The slow, sustained release of oxygen by benzoyl peroxide was though to be responsible for the success. The only complications were contact irritant dermatitis in 3% and contact allergic dermatitis in 2% of patients treated. (+info)
Analysis of Chinese herbal creams prescribed for dermatological conditions.
OBJECTIVE: To determine whether Chinese herbal creams used for the treatment of dermatological conditions contain steroids. DESIGN: 11 herbal creams obtained from patients attending general and paediatric dermatology outpatient clinics were analysed with high resolution gas chromatography and mass spectrometry. SETTING: Departments of dermatology and clinical biochemistry. MAIN OUTCOME MEASURE: Presence of steroid. RESULTS: Eight creams contained dexamethasone at a mean concentration of 456 micrograms/g (range 64 to 1500 micrograms/g). All were applied to areas of sensitive skin such as face and flexures. CONCLUSION: Greater regulation needs to be imposed on Chinese herbalists to prevent illegal and inappropriate prescribing of potent steroids. (+info)
Bacteriologic cure of experimental Pseudomonas keratitis.
Two long-term therapy trials with high concentrations of antibiotic were carried out to determine the duration of therapy required to achieve bacteriologic cure of experimental Pseudomonas keratitis in guinea pigs. In the first study, corneas still contained Pseudomonas after 4 days of continual topical therapy with either tobramycin 400 mg/ml, amikacin 250 mg/ml, ticarcillin 400 mg/ml, or carbenicillin 400 mg/ml. In an 11-day trial of topical therapy with tobramycin 20 mg/ml, 34 of 36 corneas grew no Pseudomonas after 6 or more days of therapy. The bacteriologic response to therapy in this model occurred in two phases. About 99.9% or more of the organisms in the cornea were killed in the first 24 hr of therapy. The numbers of bacteria remaining in the cornea declined gradually over the next several days until the corneas were sterile. Optimal antibiotic therapy may include two stages: initial intensive therapy with high concentrations of antibiotic applied frequently to achieve a large rapid decrease in numbers of organisms in the cornea, followed by prolonged, less intensive therapy to eradicate organisms and prevent relapse. (+info)
Effect of leukocytes on corneal cellular proliferation and wound healing.
PURPOSE: To establish whether fucoidin, by blocking the adhesion of leukocytes on the limbal vascular endothelium, prevents extravasation of the cells from the blood stream into the limbal stroma and the wounded area after corneal injury. Successful leukocyte blocking enabled investigation of the influence of leukocytes on corneal cellular proliferation after corneal wounding. METHODS: Thirty-two New Zealand White rabbits were used. Photorefractive keratectomy (PRK) and a standardized alkali corneal wound were used as models in two sets of experiments. In half of the injured rabbits fucoidin was used to prevent leukocytes from leaving the local vessels. The efficiency of the blocking technique was evaluated by counting the number of leukocytes in the limbal and wounded corneal areas. Proliferating cell nuclear antigen (PCNA) was used as a marker for proliferative activity. RESULTS: The infiltration of leukocytes into the limbus and the cornea after PRK and alkali injuries can be blocked by fucoidin. The healing rate of corneal epithelium after alkali burn was retarded in the absence of leukocytes. PCNA expression was enhanced in the presence of leukocytes. Fucoidin per se had no influence on corneal cell proliferation and wound healing. CONCLUSIONS: Polymorphonuclear leukocytes (PMNs) can be prevented from entering the cornea in vivo by fucoidin after PRK and after alkali burn. The corneal epithelial healing rate is delayed in the absence of PMNs in vivo, and PCNA expression increases in the presence of leukocytes. (+info)
Riluzole improves functional recovery after ischemia in the rat retina.
PURPOSE: Retinal ischemia leads to neuronal death. The effects of riluzole, a drug that protects against the deleterious effect of cerebral ischemia by acting on several types of ion channels and blocking glutamatergic neurotransmission, were investigated in a rat model of retinal ischemic injury. METHODS: Retinal ischemia was induced by increasing intraocular pressure above systolic blood pressure for 30 minutes. Electroretinograms were recorded before ischemia and at different periods of reperfusion. Riluzole was injected or topically applied to the eye before or after ischemia and twice daily during the reperfusion period. Retinas were harvested for histopathology (toluidine blue and silver-impregnation stainings, Tdt-dUTP terminal nick-end labeling [TUNEL] method) and immunohistochemistry for cytoskeletal glial fibrillary acid protein and c-jun NH2-terminal kinase (p-JNK). RESULTS: Ischemia for 30 minutes caused a reduction of a- and b-waves of the electroretinogram. Systemic and topical treatments with riluzole significantly enhanced the recovery of the reduced a- and b-waves after defined reperfusion times. Riluzole also prevented or attenuated ischemia-induced retinal cell death (necrosis and apoptosis) and reduced the activation of p-JNK, c-jun phosphorylation, and the increase of cytoskeletal proteins induced by ischemic injury. CONCLUSIONS: Riluzole acted in vivo as a potent neuroprotective agent against pressure-induced ischemia. Therefore, riluzole may be a major drug for use in protection against retinal injury. (+info)
Topical psoriasis therapy.
Psoriasis is a common dermatosis, affecting from 1 to 3 percent of the population. Until recently, the mainstays of topical therapy have been corticosteroids, tars, anthralins and keratolytics. Recently, however, vitamin D analogs, a new anthralin preparation and topical retinoids have expanded physicians' therapeutic armamentarium. These new topical therapies offer increased hope and convenience to the large patient population with psoriasis. (+info)
Contact hypersensitivity: a simple model for the characterization of disease-site targeting by liposomes.
A murine model of delayed-type hypersensitivity (DTH) is characterized with respect to liposome accumulation at a site of inflammation. Mice were sensitized by painting the abdominal region with a solution of 2,4-dinitrofluorobenzene (DNFB) and inflammation was induced 5 days later by challenging the ear with a dilute solution of DNFB. The inflammatory response was readily monitored by measuring ear thickness (edema) and radiolabeled leukocyte infiltration. Maximum ear swelling and cellular infiltration occurred 24 h after the epicutaneous challenge with the ear returning to normal size after approximately 72 h. We demonstrate that large unilamellar vesicles (LUV) accumulate at the site of inflammation to a level more than 20-fold higher than that measured in the untreated ear. Vesicle delivery to the ear correlated with increased vascular leakage resulting from endothelium remodeling in response to DNFB challenge, and was not a consequence of increased local tissue blood volume. Extravasation occurred only during the first 24 h after ear challenge; after this time the permeability of the endothelium to vesicles returned to normal. We further showed that LUV with a diameter of 120 nm exhibit maximum levels of accumulation, that a polyethylene glycol surface coating does not increase delivery, and that the process can be inhibited by the application of topical corticosteroids at the time of induction. These data and the inflammation model are discussed with respect to developing lipid-based drug delivery vehicles designed to accumulate at inflammatory disease sites. (+info)
Topical gene delivery to murine skin.
We topically applied naked plasmid DNA containing the luciferase or chloramphenicol acetyltransferase cDNA directly to mouse skin. Gene expression was detected in skin samples as early as 4 h after DNA application, plateaued from 16 to 72 h post-application, and had decreased significantly by 7 d post-application. Reporter gene activity following topical DNA delivery was comparable with that produced by intradermal injection of DNA. Plasmid DNA at concentrations > or =0.25 microg per microl were required to achieve maximal expression levels. Reporter gene expression following topical administration was largely confined to the superficial layers of the epidermis and to hair follicles. Surprisingly, certain cationic liposomes inhibited the efficiency of cutaneous gene transfer. This technique provides a simple, clinically relevant approach to deliver genes to the skin, with potential application in treating a variety of cutaneous disorders. (+info)