This study investigated mitochondrial respiratory activity in Huntington's disease (HD) brain. Mitochondrial membranes from caudate and cortex of HD and non-HD autopsied brains were assayed for succinate oxidation, cytochrome oxidase activity, and cytochromes b, cc1, and aa3. There was a significant decrease in HD caudate mitochondrial respiration, cytochrome oxidase activity, and cytochrome aa3, whereas cytochromes b and cc1 were normal. These findings are consistent with the hypothesis that mitochondrial dysfunction may contribute to the localized hypometabolism and progressive atrophy of the HD caudate.

A series of typical (chlorpromazine, haloperidol and thioridazine) and atypical (risperidone, quetiapine, clozapine and olanzapine) antipsychotics were tested for effects on integrated bioenergetic functions of isolated rat liver mitochondria. Polarographic measurement of oxygen consumption in freshly isolated mitochondria showed that electron transfer activity at respiratory complex I is inhibited by chlorpromazine, haloperidol, risperidone, and quetiapine, but not by clozapine, olanzapine, or thioridazine. Chlorpromazine and thioridazine act as modest uncouplers of oxidative phosphorylation. The typical neuroleptics inhibited NADH-coenzyme Q reductase in freeze-thawed mitochondria, which is a direct measure of complex I enzyme activity. The inhibition of NADH-coenzyme Q reductase activity by the atypicals risperidone and quetiapine was 2-4 fold less than that for the typical neuroleptics. Clozapine and olanzapine had only slight effects on NADH-coenzyme Q reductase activity, even at 200 microM. The relative potencies of these neuroleptic drugs as inhibitors of mitochondrial bioenergetic function is similar to their relative potencies as risk factors in the reported incidence of extrapyramidal symptoms, including tardive dyskinesia (TD). This suggests that compromised bioenergetic function may be involved in the cellular pathology underlying TD.

Whole blood serotonin levels and platelet counts were studied in 14 families, representing 57 family members and 15 probands who met DSM III criteria for infantile autism. High serotonin appeared to segregate in families. When two parents had high serotonin, the serotonin level in their offspring was twice the parental level. When one parent had high serotonin, the serotonin level in the offspring approximated the level of serotonin in either the high serotonin parent or the low serotonin parent. For the case where both parents had low serotonin, in one family the children had low serotonin and in a second family, high serotonin levels were present in the autistic proband, and a sibling with severe mental retardation. Mean serotonin levels were higher for both male and female, autistics and family members, in the four black families than in the 10 Caucasian families.

The ability of fibroblasts to reproduce and attach to teeth is of paramount importance in re-establishing the lost connective tissue attachment after periodontal therapy. This study examined the effect of nicotine, a major component of the particulate phase of tobacco smoke, on human gingival fibroblast (HGF) reproduction and attachment to tissue culture surfaces. Pooled HGF cultures made from explants of gingival biopsies were utilized between passages 5 and 10 and plated in 96-well plates at 1.0 x 10(4) cells per well. Cell numbers were determined using 3-(4,5-dimethylthiazol-2-y)-2,5-diphenyl tetrazolium bromide (MTT), which is a reflection of mitochondrial dehydrogenase activity. The concentrations of nicotine used were 0.025, 0.05, 0.1, 0.2, and 0.4 microM, the average serum concentration for a smoker being approximately 0.1 microM. The effect of continuous nicotine exposure on HGF reproduction was determined by incubating cell cultures and media containing nicotine for up to 48 hours. Residual toxicity was determined by preincubating cells with nicotine for 1 or 6 hours. HGF suspensions and increasing concentrations of nicotine were added together to determine the effect on attachment. Results showed an enhanced effect of nicotine on HGF attachment, with increasing numbers of cells attaching with increasing nicotine concentrations, compared to the control. Low concentrations of nicotine had a stimulatory effect on cell replication, while higher concentrations of nicotine appear to have no significant effect on HGF reproduction. The responses of cells to some concentrations of nicotine may persist after its removal.

The purpose of this pilot study was to determine if lost osseous support adjacent to root form implants could be regenerated using a guided tissue regeneration technique. Three fixtures were placed in each edentulous mandibular bicuspid region of two micro pigs. A total of 6 fixtures were placed in each pig. Due to the presence of a pathologic condition, which was in no way related to the research, the results of one pig were not evaluated. Following osseointegration, peri-implantitis were induced by the use of ligatures and a soft diet. Three modalities of treatment were performed. Utilizing a surgical flap approach, one third of the fixtures (one per quadrant) were covered with expanded polytetrafluoroethylene (ePTFE) membrane and submerged under the soft tissue complex. The second group of fixtures were submerged under the soft tissue complex with no ePTFE membrane. The control fixtures along with their abutments were debrided and remained non-submerged. All fixtures were debrided using an air-abrasive polishing system. The osseous defects around the fixtures were measured from a fixed reference point at the time of surgery and after obtaining block sections.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was 2-fold to: 1) evaluate in vitro the surface texture of titanium implant abutments after exposure to plastic scalers, an air-powder abrasive system, rubber cup polishing with flour of pumice, and untreated control abutments; and 2) compare plaque accumulation in humans on abutments treated with the above methods. In part I, 5.5 mm abutments were instrumented for 30 seconds per 90 degrees segment with the respective methods. The surface character was compared to untreated controls using SEM at 260X magnification. The control abutments revealed prominent milling marks and small pits; plastic scalers slightly smoothed the milling marks and created microscratches; the air-powder abrasive largely obliterated the milling marks and caused some surface pitting; the rubber cup with flour of pumice removed the milling marks and created a smooth swirl pattern. None of the instrumentation appeared to roughen the surface. In the clinical experiment (part II), four abutments, one of each type, were placed in 12 patients for a period of 7 days, during which the patients performed no oral hygiene. At the end of 7 days, the abutments were retrieved and processed for SEM. A digitizer and software program were used to determine the percent of total abutment surface area covered by plaque. The demarcation of supragingival and subgingival plaque was well delineated. The total mean percent surface area of plaque ranged from 52.06% for the air-powder abrasive to 55.29% for the plastic scalers.(ABSTRACT TRUNCATED AT 250 WORDS)

Proteins from 5- to 7-wk-old lean and obese Zucker rats were separated by one-dimensional sodium dodecyl sulfate (SDS) and two-dimensional SDS-isoelectric focusing-polyacrylamide gel electrophoresis. Laser densitometry revealed an obesity-related decrease in the concentration of a 28-kDa cytosolic adipocyte protein, the most abundant protein in adipocytes from lean Zucker rats. Microsequencing revealed the identity of this protein to be carbonic anhydrase III (CA III). The identity and obesity-related decrease was further confirmed using isoform-specific antisera and CA III enzyme activity measurements made by 18O mass spectrometry. Immunoblotting studies also revealed that CA III is present in at least two charge isoforms in adipocytes. Our data indicate that lean Zucker rat adipocytes may represent the richest source of CA III in nature (24% of the cytosolic protein content). An obesity-related decrease in both the concentration and activity of CA III was observed in two lipogenic tissues, liver and white fat, but not in soleus muscle. Adipocyte CA III activity was no longer depressed when hyperinsulinemic obese rats were made insulin deficient by streptozotocin injection. This suggests that the obesity-related decrease in CA III may be related to the hyperinsulinemia as well as to the insulin hyperresponsiveness that adipocytes from obese Zucker rats of this age display.

We examined ZO-1 protein content in cultured retinal vascular endothelial cells to test the hypothesis that histamine alters tight-junction-protein expression. Histamine (10(-9) -10(-4) M) causes a reversible concentration-dependent reduction of ZO-1 protein content, mediated by both H1 and H2 receptors. Histamine reduces ZO-1 expression within the time associated with increased paracellular permeability. Tight-junction-protein alterations may be a novel explanation for the mechanism by which vasoactive agents increase microvascular permeability.