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At least 343 records · Page 19Linked to original sources
PubMed2004

Cytotoxic effects of gingival retraction cords on human gingival fibroblasts in vitro.

The objective of this study was to determine the cytocompatibility of three different extracts of gingival retraction cords and to compare the cytotoxic effect of these materials on human gingival fibroblasts. Gingival retraction cords impregnated with aluminium sulphate (Gingi-Aid), dl-adrenaline HCl (Gingi-Pak) and non-drug-impregnated cord (Gingi-Plain) were eluted with culture medium for 10 min and 24 h. Cytotoxicity was judged using a tetrazolium bromide reduction assay. Our data demonstrated that gingival retraction cords applied alone almost completely inhibited cell viability (P < 0.05). In addition, the results also showed that the eluates from aluminium sulphate-impregnated cord, dl-adrenaline HCl-impregnated cord and non-drug-impregnated cord were cytotoxic to primary human gingival fibroblast cultures (P < 0.05). The cell viability of incubation of gingival fibroblasts containing 10-min eluates of aluminium sulphate, dl-adrenaline HCl and non-drug-impregnated cord was 61, 21 and 70%, respectively. The cell viability of incubation of gingival fibroblasts containing 24 h eluates of aluminium sulphate, dl-adrenaline HCl and non-drug-impregnated cord was 68, 58 and 72%, respectively. It was found that dl-adrenaline HCl-impregnated gingival retraction cord was the most toxic gingival retraction cord among the materials tested in all cultures (P < 0.05). The cytotoxicity decreased in an order of dl-adrenaline HCl-impregnated cord > aluminium sulphate-impregnated cord > non-drug-impregnated cord. The extent or degree of the cytotoxicity depended on the materials tested. Gingival retraction cords have significant potential for gingival toxicity. Careful management of gingiva retraction cords would lower the risk of potential gingival tissue damage during clinical application procedure and thus increase the success of prosthodontic procedures.

Alum Compounds↗
PubMed2000

Motor neuronal death in sporadic amyotrophic lateral sclerosis (ALS) is not apoptotic. A comparative study of ALS and chronic aluminium chloride neurotoxicity in New Zealand white rabbits.

Whether diseased motor neurones in sporadic amyotrophic lateral sclerosis (ALS) die via apoptosis is unknown. Because this relates primarily to difficulties in utilizing post-mortem tissue from end-stage disease, motor neurone degeneration in ALS spinal cord was compared with that of a model of a chronic motor neurone degeneration. Degenerating motor neurones in ALS, identified by ubiquitin immunoreactivity, did not demonstrate the morphological characteristics of apoptosis and were not c-Jun immunoreactive or TUNEL positive. A temporal analysis of spinal motor neurone death in the chronic AlCl3 neurotoxicity model of motor neurone degeneration was also undertaken. AlCl3 was administered intracisternally every 4 weeks and, at intervals of 51, 107, 156 and 267 days, evidence of apoptosis was sought by morphology, TUNEL hybridization or DNA laddering. Double-labelling immunostudies were also performed with antibodies to either c-Jun, ubiquitin or high molecular weight neurofilament (NFH) with TUNEL hybridization. Although significant neurone loss was evident, apoptosis was not found. These studies demonstrate a lack of apoptosis in ALS spinal motor neurones and suggest that this observation does not relate to the utilization of post-mortem tissue in which apoptotic neurones may have been lost.

Adult↗
PubMedDate not supplied

Acrodermatitis enteropathica with Pseudomonas aeruginosa sepsis.

Acrodermatitis enteropathica is characterized by eczematous and scaly plaques on the face, scalp, acral, and anogenital regions. In addition to typical lesions, unusual prominent vesiculobullous lesions are also described. We report a full-term, 9-month-old boy who has acrodermatitis enteropathica and Pseudomonas sepsis. In this patient there were clinical findings of sepsis and eczematous vesiculobullous lesions on the periorificial and acral areas. Serum zinc level was extremely low. Pseudomonas aeruginosa was identified in cultures of blood and fluid which was aspirated from the bullous lesions. After oral zinc sulfate and intravenous antibiotic treatment his condition improved within 2 weeks.

Acrodermatitis↗
PubMed2002

The effects of zinc supplementation on serum zinc and cholesterol concentrations in hemodialysis patients.

OBJECTIVE: To examine the effect of zinc sulfate supplementation on the concentrations of serum zinc and serum cholesterol in hemodialysis (HD) patients. SETTING: Outpatient dialysis center in a large metropolitan city. DESIGN: Randomized, double-blind, before-after trial. PATIENTS: Twenty-eight maintenance HD patients were selected. Twenty (15 women and 5 men) completed the study. Subjects were identified for inclusion in the study by the following criteria: HD treatment for a minimum of 6 months, no signs of gastrointestinal disorders, and no record of hospitalizations for reasons other than vascular access complications within the last 3 months. INTERVENTIONS: Patients were given a daily supplement of 7.7 micromol zinc sulfate (50 mg elemental zinc) or a cornstarch placebo capsule for 90 days. Patients completed 2-day food records, at day 0 and day 90 of the study, which included 1 dialysis day and 1 nondialysis day. MAIN OUTCOME MEASURE: Fasting, predialysis serum samples were collected on days 0, 40, and 90 to determine serum zinc and total cholesterol (TCHOL) concentrations. Dietary parameters, including zinc, protein, and energy intake, were also analyzed on days 0 and 90. RESULTS: Initial concentrations of serum zinc indicated subjects were below the normal range for serum zinc standards (12 micromol/L [80 microg/dL]). After supplementation, subjects in the zinc-supplemented group showed significant increases in serum zinc concentrations from 0.79 microg/mL at day 0 to 0.96 microg/mL at day 90. Serum TCHOL concentrations were initially low among subjects in the control (2.914 +/- 0.158 mmol/L [112.7 +/- 6.1 mg/dL]) and zinc-supplemented (3.155 +/- 0.354 mmol/L [122.0 +/- 13.7 mg/dL]) groups. Serum TCHOL concentrations in the control group increased slightly throughout the study period but did not reach statistical significance. A progressive increase in serum TCHOL concentration was observed in the zinc-supplemented group from the beginning (3.155 +/- 0.354 mmol/L [122.0 +/- 13.7 mg/dL]) to the end (4.445 +/- 0.478 mmol/L [171.9 +/- 18.5 mg/dL]) of the study (r =.63, P <.05). Mean serum high-density lipoprotein (HDL) cholesterol concentrations for the zinc-supplemented group were 0.959 mmol/L +/- 0.11 (37.1 mg/dL +/- 4.3), 0.825 mmol/L +/- 0.08 (31.9 mg/dL +/- 3.2), and 0.908 mmol/L +/- 0.10 (35.1 mg/dL +/- 3.9) from the beginning to the end of the experimental period. The mean serum HDL cholesterol concentrations for the control group were 0.760 mmol/L +/- 0.075 (29.4 mg/dL +/- 2.9), 0.760 +/- 0.08 (29.4 mg/dL +/- 3.0), and 0.799 mmol/L +/- 0.13 (30.9 mg/dL +/- 4.9) from the beginning to the end of the experimental period. A progressive increase in low-density lipoprotein (LDL) cholesterol concentration was observed for the zinc-supplemented group throughout the study. Mean LDL cholesterol concentrations for the zinc-supplemented group were 2.19 mmol/L +/- 0.39 (85 mg/dL +/- 15.0), 3.30 mmol/L +/- 0.36 (127.8 mg/dL +/- 14.1), and 3.53 mmol/L +/- 0.53 (136.7 mg/dL +/- 20.6) from the beginning to the end of the study period. When serum zinc concentration was correlated with serum LDL cholesterol concentration, a significant correlation was found (r =.62, P <.03) for the zinc-supplemented group and no significant difference was found for the control group. No significant differences in LDL cholesterol concentrations were found within the control group from the beginning to the end of the study. Dietary intake of zinc, cholesterol, total fat, and saturated fat remained constant and did not statistically influence serum values. Reported energy intake increased significantly in the zinc-supplemented group from 5,799 kJ/24 h (1,385 kcal/d) at day 0 to 7,042 kJ/24 h (1,682 kcal/d) at day 90. CONCLUSION: Zinc supplementation is an effective means of improving serum levels of zinc and cholesterol in the HD patient.

Astringents↗
PubMed1999

Effectiveness of different anticalcification treatments for stentless aortic bioprostheses.

BACKGROUND: New anticalcification treatments for stentless bioprostheses have not yet been compared independently. MATERIAL AND METHODS: The No-reacts (Biocor), AOA (Medtronic Freestyle), and BiLinx (SJM Toronto SPV II) methods were studied and compared with a control group. Aortic valve leaflet and aortic root tissue was subcutaneously implanted in 60 male, 21-days-old Sprague-Dawley rats. Calcium content was quantified using inductively coupled plasma spectrophotometry. RESULTS: No infections occurred. Low levels of calcium were measured in aortic valve leaflet tissue for all methods (0.4 to 1.5 mg/g dry weight) in comparison to the control group (225 mg/g), p < 0.01. Calcification of aortic root tissue was low in the Bilinx group (2.4 mg/g, p < 0.01), whereas calcium levels were high in all other groups (104 to 127 mg/g). CONCLUSIONS: Calcification of aortic valve leaflets was significantly reduced by all new anticalcification treatments, whereas aortic root calcification was only reduced by inhibition of cellular calcification (BiLinx). Maximum anticalcification properties of both leaflet and aortic root are important, as these are considered a functional unit in stentless bioprostheses.

Aluminum Chloride↗
PubMed1992

[Therapy of Frey's syndrome with an anhidrotic gel].

In recent years we treated 53 patients suffering from Frey's syndrome with an antihidrotic gel. The active ingredient we used was aluminiumtrichloridhexahydrate. In addition to presenting a historic review we will also demonstrate and discuss our results. The study concludes, that this gel is effective in treating Frey's syndrome.

Adolescent↗
PubMed2001

Aquagenic palmoplantar keratoderma.

Aquagenic palmoplantar keratoderma is an acquired condition characterized by burning and edema limited to the hands after brief immersion in water. The 3 patients described possess a striking similarity to those with transient reactive papulotranslucent acrokeratoderma. All 3 patients manifested the "hand-in-the-bucket" sign, having presented to a physician with a hand immersed in a bucket of water to more promptly demonstrate the physical findings. Aluminum chloride hexahydrate represents a potentially valuable therapeutic option for this unusual condition.

Adolescent↗
PubMed2002

Electron microscopic analysis of the effects of chemical retraction agents on cultured rat keratinocytes.

STATEMENT OF PROBLEM: Chemical retraction agents used in fixed prosthodontics for temporary displacement of free gingival tissue before impression making can cause injury to the gingival tissue cells. PURPOSE: This study evaluated changes in cultured rat keratinocytes treated with 2 chemical agents used for gingival retraction. Treated cultures were compared with untreated cultures. MATERIAL AND METHODS: Keratinocytes of rat gingiva were grown in a specific medium for 10 days. After treating 1 group of specimens with 0.05% tetrahydrozoline and another group with 25% aluminum chloride, both for 10 minutes, the cultured cells were examined with scanning and transmission electron microscopy and compared with control specimens. RESULTS: Twenty-five percent aluminum chloride produced a significantly greater extent of cellular damage than 0.05% tetrahydrozoline, which caused only mild changes in the cultured cells. CONCLUSION: On the basis of the morphologic and ultrastructural changes in primary cell cultures of rat keratinocytes observed in this study, it was concluded that 25% aluminum chloride was significantly more aggressive than 0.05% tetrahydrozoline.

Aluminum Chloride↗
PubMed2003

In vitro kinetic study of absorbency of retraction cords.

STATEMENT OF PROBLEM: The soaking time required for liquid uptake by retraction cords is a crucial factor in the successful gingival retraction procedure. PURPOSE: The aim of this investigation was to determine the optimal soaking time for 3 retraction cords of different thickness to ensure adequate uptake of the hemostatic solution. MATERIAL AND METHODS: Braided ULTRAPAC retraction cords of 3 different thicknesses (No. 00, No. 0, and No. 1) with identical lengths (35 mm) were used. The capability of the cords to absorb liquids was measured by a gravimetric method. Different sulcus retraction solutions (epinephrine, aluminum chloride, and ferric sulfate) were tested, with physiological saline solution used as the control. The cords were soaked for various time intervals (2 seconds; 1, 5, and 60 minutes; and 24 hours) in the medicament solutions at room temperature. Immediately before immersion, air inclusions that may have inhibited the inner moistening of the cords were manually pressed out. In each of the 4 treatment groups, 75 pieces of cord were tested by determining the grams of fluid absorbed by grams of dry cord (gram/gram). Before the cord was weighed, excess fluid accumulating on the outer surface of the cord was removed by filter paper saturated in the corresponding test solution. The data were analyzed by F test analysis, and P<.05 was regarded as significant. RESULTS: In each group, regardless of the cord type (No. 00, No. 0, or No. 1) or medicament solutions tested, the amount of fluid absorbed increased with the soaking time, but to different extents. A logarithmic relationship in a linear plot between the amount of fluid absorbed and the soaking time was demonstrated. The relationship established offered an exact determination of both the rate and the saturation level of liquid uptake. The rate of liquid uptake calculated from the saturation equations exhibited significant correlation with the cord thickness (P<.05). The saturation levels of the solutions did not show correlation with the cord thickness (P>.30). CONCLUSION: Within the limitations of this study, the results indicated that 20 minutes of soaking time was necessary for saturation of the cords before use, provided that air trapped within the cords was removed. In addition to the soaking time, the saturation of the cords with the solutions largely depended on the wetting of the cords.

Absorption↗
PubMed1986

Absorption, deposition and distribution of dietary aluminium in immature rats: effects of dietary vitamin D3 and food-borne chelating agent.

We report the levels of aluminium, calcium and potassium in selected tissues of growing rats administered dietary or subcutaneous aluminium, and also the effect of dietary aluminium in combination with cholecalciferol, or with lactose plus a dietary chelating agent. Dietary aluminium decreased the growth rate of normal rats and increased the deposition of aluminium in the tissues. Animals given lactose with a dietary chelator showed a 17 - 100% increase in brain, heart, and muscle aluminium concentration in comparison with those fed aluminium alone. Animals fed both aluminium with cholecalciferol also showed increased levels (12-39%) of aluminium, chiefly in muscle and heart in comparison with those fed aluminium alone. Aluminium deposition was correlated positively with Ca2+ and K+ levels among each of these tissues. We conclude that in normal growing rats aluminium deposition is increased in heart and muscle in the presence of vitamin D3 and in brain, heart and muscle in the presence of lactose and a dietary chelating agent.

Aging↗
PubMed1993

Dietary aluminum chloride reduces the amount of intestinal calbindin D-28K in chicks fed low calcium or low phosphorus diets.

The mechanism of aluminum (Al) toxicity may involve disturbances in calcium (Ca) metabolism. Aluminum compounds have been reported to reduce vitamin D-dependent Ca absorption in chicks, rats and humans. To investigate the mechanism by which Al reduces Ca absorption, we studied the effect of dietary aluminum chloride (AlCl3) on the relative amounts of intestinal calbindin D-28K in chicks fed diets varying in Ca and phosphorus concentration. AlCl3 was added so that Al constituted 0, 0.15 or 0.3 g/100 g of diets that were either adequate, low in Ca, low in P, or contained supplemental P. Diets were fed for 2 wk. Intestinal calbindin D-28K levels were assayed using SDS-PAGE and 45Ca binding to Western blots. Added dietary Al greatly reduced the amount of intestinal calbindin in chicks fed adequate diets, low Ca diets, or low P diets. When diets with supplemental P were fed, little calbindin was evident with or without added Al. Tibia ash, body weight and food intake were also reduced (P < 0.05) by added Al. These results indicate that dietary AlCl3 inhibits vitamin D-dependent Ca absorption by reducing the amount of intestinal calbindin D-28K. Aluminum, therefore, may interfere with the body's ability to regulate intestinal calbindin D-28K levels. This could have implications for other tissues that contain substantial levels of calbindin D-28K.

Aluminum Chloride↗
PubMed2000

Beta-carotene and inhibitors of iron absorption modify iron uptake by Caco-2 cells.

A National fortification program instituted in Venezuela in 1993 reduced iron deficiency and anemia by half in only 1 y. The fortification mixture contained ferrous fumarate, vitamin A and other vitamins. We conducted experiments to characterize ferrous fumarate uptake by Caco-2 cells. Increasing amounts of ferrous fumarate, vitamin A, phytate, tannic acid and beta-carotene were added to incubation mixtures using a range of concentrations that included the molar ratios used in the Venezuelan fortification program. Cells were incubated for 1 h at 37 degrees C with 37 kBq (59)Fe and the compound to be evaluated. They were then rinsed, trypsinized and counted to measure uptake. Effects of ascorbic acid, days in culture and use of flasks or inserts were also evaluated. Optimal conditions for uptake experiments were pH 5.5, in the presence of ascorbic acid and at 16 d in culture. Use of flasks or inserts did not affect uptake. Vitamin A did not significantly increase iron uptake under the experimental conditions employed. However, beta-carotene (6 micromol/L) significantly increased iron uptake compared to no beta-carotene addition (114.9 +/- 6.3 and 47.2 +/- 5.9 pmol/mg cell protein, respectively). Moreover, in the presence of phytates or tannic acid, beta-carotene generally overcame the inhibitory effects of both compounds depending on their concentrations. We conclude that beta-carotene improves iron uptake and overcomes the inhibition by potent inhibitors of iron absorption. These experiments also validated the usefulness of Caco-2 cell model system to evaluate iron metabolism.

Absorption↗
PubMed2002

Aluminum chloride induces retinal changes in the rat.

We studied rat retinal changes due to aluminum (Al) toxicosis with a transmission electron microscope (TEM) and an energy dispersive X-ray analyzer (EDXA). Normal 4-week-old Wistar Kyoto rats were divided randomly into Al toxicosis and control groups. The Al toxicosis group was injected ip with 0.3 ml of 4% aluminum chloride (AlCl3) per day every day for 16 weeks. The retina was examined with a TEM and EDXA at 8, 12, and 16 weeks after starting injections with AlCl3. There was a statistically significant increase in the serum Al concentration in the Al toxicosis group (p < 0.001). We observed prominent pathologic changes at 16 weeks after the first injections. Thin retinal pigment epithelium (RPE), and disappearance of the photoreceptor outer and inner segments and nuclei were observed. There were high-density irregular granules in the outer and inner plexiform layers and in the inner nuclear layer. We found dense granules in the cells, which remained between the RPE and the inner nuclear layer. EDXA detected Al in the high-density irregular granules in these areas. Al injected ip caused accumulation of Al in the rat retina and the destruction of photoreceptor cells. These findings indicate that Al is toxic to the retina.

Aluminum Chloride↗
PubMed2001

Mitochondrial cytochrome c oxidase subunit III is selectively down-regulated by aluminum exposure in PC12S cells.

Aluminum (Al) has been implicated in several neurological diseases including dialysis dementia and Alzheimer's disease (AD). One possible mechanism of Al neurotoxicity could involve alteration of mitochondrial gene expression. We exposed PC12 cells to 0.1-100 microM AlCl3 for 6h at pH 7.4. Internalized Al, measured by atomic absorption spectrometry, was linearly proportional to the extracellular Al concentration. Northern blot analyses showed that cytochrome c oxidase subunit III (COX III) mRNA was significantly reduced by 70% after addition of 1 microM AlCl3. Higher concentrations of AlCl3 did not show a significant further effect. These results suggest that Al neurotoxicity involves a specific impairment of cytochrome c oxidase.

Aluminum Chloride↗