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At least 397 records · Page 22Linked to original sources
PubMed1979

The effect of topical crude coal tar treatment on unstimulated hairless hamster skin.

Topical treatment of hairless hamster skin with crude coal tar has been shown to induce epidermal thickening, an increased labelling index in the basal cell layer, an elevation in NADP-dependent glucose-6-phosphate dehydrogenase activity throughout the epidermis, an increased squame count, comedo formation, and atrophy of the sebaceous glands. Ultraviolet light fluorescence microscopy of sections of treated skin suggests that the hair follicle is an important route for skin penetration by coal tar.

Acne Vulgaris↗
PubMed1970

Mode of action of vibriocin.

The mechanism of action of vibriocin, a bacteriocin produced by Vibrio comma, was investigated. Its lethal action (as defined by the loss in colony-forming ability) was reversed by tryptic digestion within 7 to 10 min after adsorption. The bacteriocin had a pronounced inhibitory effect on deoxyribonucleic acid (DNA) synthesis, whereas ribonucleic acid (RNA) and protein synthesis continued, although at a reduced rate. Chloramphenicol protected sensitive bacteria from the lethal action. Degradation of bacterial DNA prelabeled with (3)H-thymidine, as measured by changes in acid-precipitable radioactivity, occurred 10 min after treatment with vibriocin. The bacteriocin per se had no detectable deoxyribonuclease activity. Observation of vibriocin-treated cells by phase-contrast microscopy, measurement of ultraviolet light-absorbing capacity of extracellular fluid, and (42)K-efflux studies indicated a damaged bacterial membrane. This impairment of membrane function occurred in the presence of chloramphenicol and thus, unlike the lethal effect of vibriocin, was independent of protein synthesis.

Adsorption↗
PubMed2006

Effect of ganciclovir on the hydrolytic degradation of poly(lactide-co-glycolide) microspheres.

Ganciclovir (GCV)-loaded poly(lactide-co-glycolide) (PLGA) microspheres, 125 +/- 11 mum in diameter, are produced using the emulsification/solvent evaporation technique. The release rate of the drug is studied for 20 weeks in a phosphate-buffered solution of pH 7 at 37 degrees C. The release of the drug shows a triphasic release pattern, i.e., an initial burst, a diffusive phase, and a second burst. The initial burst occurs within the first 2 days of immersion. After the burst, the release is by diffusion for up to 13 weeks, followed by another burst release, which signals the onset of bulk degradation of the PLGA polymer. The presence of GCV molecules decreases the hydrolytic rate of PLGA degradation. Gel permeation chromatography (GPC), differential scanning calorimetry (DSC), field emission scanning electron microscopy (FESEM), and ultraviolet (UV) spectroscopy are used to assess the hydrolytic degradation and drug release rate of the microspheres.

Absorbable Implants↗
PubMed2005

Depth profiling of the optical absorption coefficient in ultraviolet-degraded poly(vinylchloride) films by dual beam light profile microscopy.

Dual beam laser light profile microscopy (LPM) was applied in this work to the depth mapping of the optical absorption coefficient in photo-degraded poly(vinyl chloride) films. Depth profiles followed the absorption coefficient of a conjugated polyene photoproduct at visible wavelengths in photolyzed films of approximately 200 mum thickness. Both continuous and layered (separable laminate) films were studied. The absorption coefficient profiles reconstructed from photo-degraded thin films showed the classic concentration profiles seen in the literature for PVC degraded in the presence of oxygen and nitrogen atmospheres. In the case of single thin layers with continuous properties, the depth profiles were smooth and regular with minimum spatial noise. In the LPM of laminate structures, more optical anomalies were present because of the multiply interfacial structures that appeared in both the images and the reconstructed depth profiles. Notwithstanding, it was possible to profile the optical absorption coefficient at a level of error comparable to standard microtome methods. The latter was determined by comparing the LPM results to a destructive layer-by-layer analysis performed in parallel on the imaged materials. The dual beam LPM method should be generally useful for establishing polyene concentration profiles in industrial materials produced by photochemical, thermal, and chemical degradation mechanisms.

Absorption↗
PubMed1997

Neutrophil superoxide release is required for spontaneous and FMLP-mediated but not for TNF alpha-mediated apoptosis.

Polymorphonuclear leukocyte (PMN) lifespan is characterized by both rapid production and apoptotic cell death. The mechanisms triggering apoptosis in PMN are not completely understood. In this study, the relationship of neutrophil activation and apoptosis as related to released superoxide was investigated. PMN apoptosis was detected by DNA fragmentation, and ultraviolet and light microscopy, and was quantified by flow cytometry; superoxide release was measured by superoxide dismutase-inhibitable reduction of ferricytochrome C. Incubation of PMN with 20 ng/ml tumor necrosis factor (TNF)alpha induced superoxide release (8.8 +/- 7.5 nmol O2-/30 min, n = 7) in normal PMN and also resulted in apoptosis within 2 h, whereas a subactivating dose of 2 ng/ml TNF alpha, which did not trigger superoxide release (3.1 +/- 1.7 nmol O2-, n = 10), did facilitate apoptosis, although to a lesser degree. PMN cultured under nonstimulating conditions underwent apoptotic cell death after 8 h. Exogenous superoxide dismutase did not inhibit apoptosis induced by 20 ng/ml TNF alpha. No upregulation of endogenous manganese superoxide dismutase mRNA expression was observed in response to TNF alpha as measured by reverse transcription PCR. Formyl-methionyl-leucyl-phenylalanine (FMLP) stimulation (10(-7) M) resulting in superoxide release of 31.7 +/- 6.1 nmol O2-/30 min (n = 10) also significantly increased the percentage of apoptosis, but at 24 h (P < 0.05). Exogenous superoxide dismutase did inhibit FMLP-induced apoptosis, as well as apoptosis due to aging in culture. In conclusion, aging and FMLP-stimulated PMN undergo apoptosis by a superoxide release-dependent pathway, whereas TNF alpha-facilitated apoptosis appears to be unrelated to respiratory burst oxidase activity.

Apoptosis↗
PubMed2005

Role of water in the transmission of cyclosporiarsis in Sharkia Governorate, Egypt.

Water samples were collected form five residential areas in El-Ekhewa Village where the human populations use this water for daily activity and for consumption. These water sources were Bahr El-Baker drain, low running irrigation canal, underground water at shallow depth (3-8 m), finished piped water and underground water >35 m deep. The samples were concentrated by flocculation method and the concentrated pellets were examined by ultraviolet (UV) epifluorescence microscopy for Cyclospora oocysts. The densities of water contamination by 8-10 microm oocysts/liter in the five sources were respectively: 2400, 1900, 700, 200 and zero. This indicated that finished water was sewage contaminated. Stool samples from 109 diarrheal patients and 231 non-diarrheal ones from these areas were examined by the acid fast-trichrome stain, Saline Haemo De single slide trichrome stain and by standard bacteriologic techniques. Those with Cyclospora as single pathogen were considered (5.6%) of diarrheal and (2.3%) of the non-diarrheal individuals. The correlation between the density of water contamination and the prevalence of cyclosporiasis among the individuals of each area was significant. No doubt, water was the main vehicle of transmission in the present community. Soil contact and poultry were significant risk factors.

Animals↗
PubMed2000

Topical treatment with liposomes containing T4 endonuclease V protects human skin in vivo from ultraviolet-induced upregulation of interleukin-10 and tumor necrosis factor-alpha.

Exposing human skin to ultraviolet radiation causes DNA damage, sunburn, immune alterations, and eventually, skin cancer. We wished to determine whether liposomes containing a DNA repair enzyme could prevent any of the acute effects of irradiation when applied after ultraviolet exposure. Fifteen human patients with a prior history of skin cancer were exposed to two minimal erythema doses of ultraviolet radiation on their buttock skin. Liposomes containing T4 endonuclease V or heat-inactivated enzyme were applied immediately and at 2, 4, and 5 h after ultraviolet irradiation. Transmission electron microscopy after anti-T4 endonuclease V-staining and immunogold labeling on biopsies taken at 6 h after ultraviolet exposure revealed that the enzyme was present within cells in the skin. Immunohistochemical DNA damage studies suggested a trend toward improved DNA repair at the active T4 endonuclease V liposome-treated test sites. Although the active T4 endonuclease V liposomes did not significantly affect the ultraviolet-induced erythema response and microscopic sunburn cell formation, they nearly completely prevented ultraviolet-induced upregulation of interleukin-10 and tumor necrosis factor-alpha RNA message and of interleukin-10 protein. These studies demonstrate that liposomes can be used for topical intracellular delivery of small proteins to human skin and suggest that liposomes containing DNA repair enzymes may provide a new avenue for photoprotection against some forms of ultraviolet-induced skin damage.

Administration, Topical↗
PubMed1993

Ultrastructural studies bearing on the mechanism of UVB-impaired induction of contact hypersensitivity to DNCB in man.

In both murine and human experimental systems, acute, low dose exposure of skin to ultraviolet B light (UVB) impairs the induction of allergic contact dermatitis (ACD) by haptens such as dinitrochlorobenzene (DNCB) in a significant proportion of individuals. By light microscopy, epidermal Langerhans cells (LC) have been reported to be depleted by UVB exposure as well as by epicutaneous hapten application, implying that LC may be the locus of action of the effects of both UVB and DNCB. However, light microscopy can not readily distinguish cell density changes secondary to LC necrosis from changes resulting from down-modulation of expression of LC surface molecules. Using a highly sensitive immunogold electron microscopic approach, we have evaluated the differential effects of UVB and/or DNCB on human epidermal LC. The results reveal that DNCB alone caused significant up-regulation of cell surface HLA class II expression on a very small number of LC, the major fraction of LC expressing normal levels of HLA class II. Furthermore, DNCB alone caused a modest reduction in the density of LC at the treated sites without evidence of cell necrosis. Treatment with UVB alone or UVB exposure followed by DNCB resulted in a reduction in the density of LC, with widespread evidence of LC necrosis. However, the few remaining intact LC were all intensely HLA class II-positive after UVB exposure followed by DNCB, whereas treatment with UVB alone did not result in changes in LC HLA class II expression. The findings that after DNCB painting only a small proportion of the LC were strongly HLA class II-positive, but after UVB exposure followed by DNCB all intact LC displayed significant up-regulation of cell surface HLA class II expression, imply that UVB exposure inhibits the migration of epidermal LC. This is consistent with the view that DNCB fails to induce ACD when hapten is painted on UVB-exposed skin because insufficient LC are available to initiate T cell activation in the draining lymph node.

Cell Count↗