The relationship between the dose of dentogingival plaque and the in vitro lymphoproliferative response in subjects with periodontal disease

The in vitro lymphoblastic response to autologous dentogingival plaque (DGP) extract at nine concentrations was measured in 28 individuals (Periodontal Index (Russell 1956] 0.8–7.4). Significantly elevated responses were obtained in 25 of the patients but the levels of the peak responses were unrelated to the severity of the disease. There was a significant (n=28, r=?.734) negative linear relationship between the PI of the individuals studied and the logarithmic concentration of DGP producing the peak lymphoblastic response. Lower concentrations of DGP extract would appear to be required to achieve peak responses in patients with severe periodontal disease.     

The effects of flurazepam hydrochloride on brain electrical activity during sleep.

To further evaluate the effects of flurazepam on EEG during sleep, following 7 nights of placebo baseline, flurazepam (30 mg) was administered to 6 young adult poor sleepers for 10 additional nights while 6 other young adult poor sleepers continued to receive placebo capsules in a double-blind paradigm. Three placebo follow-up nights were recorded 2--3 weeks post-treatment. Twelve good sleepers received only placebo capsules for the first 7 nights. Delta waves, 0.5--2 c/sec, and sleep spindles were counted on-line by a phasic detector. Delta activity was also analyzed off-line by PDP-12 computer for only the first 4 h of sleep and involved a comparison over stages of sleep. Click-evoked K-complexes during NREM sleep were analyzed for 6 good sleepers and 11 poor sleepers. Repeated use of flurazepam caused a gradual decrease in delta amplitude and count, and a gradual increase in sleep spindle rate. The decrease in delta amplitude was seen in all sleep stages, but the decrease was significant only during SWS and stage 2. The decrease in delta amplitude was significant by the 3rd drug night, but the rate of amplitude decrease tended to slow with continued treatment. The decrease in delta count was less pronounced and more gradual over drug nights than the rate of decrease in amplitude. Flurazepam also significantly reduced evoked K-complex amplitude but did not affect latency. Sleep spindle rate was significantly increased by drug night 5. Results of this study indicate that the reduction of SWS with flurazepam during the initial drug nights is due primarily to the decrease in delta amplitude, but, with continued use, the decrease in delta count also contributes to the decrease in stage 4 sleep.     

Phenytoin-Induced Gingival Overgrowth Resulting in Delayed Eruption of the Primary Dentition: A Case Report

A case of delayed eruption of the primary dentition secondary to Phenytoin therapy in a 4-year-old child is reported. The patient had been on phenytoin therapy since the first months of life. Radiographs revealed that alveolar but not gingival emergence had occurred. Surgical excision of the excess gingival tissue was accomplished under general anesthesia. Oral hygiene procedures were stressed and parental cooperation solicited. Three- and ninemonth postoperative visits revealed no regrowth of gingival tissue and continued eruption of the primary dentition.     

Brain-stem auditory evoked potentials in the rat: effects of gender, stimulus characteristics and ethanol sedation

Rat BAEPs varied significantly as a function of gender and ethanol sedation as well as stimulus intensity and repetition rate. All BAEP wave latencies decreased and amplitudes increased with increasing stimulus intensity. Contrary to the prevailing view, the I-IV interpeak latency changed significantly as a function of stimulus intensity. In terms of repetition rate, all BAEP wave latencies increased and amplitudes decreased with increasing repetition rate. Male rats, compared to females, had significantly longer latencies for several BAEP components and interpeak latencies as well as smaller wave II amplitudes across a broad range of stimulus intensities. Males, compared to females, also had longer BAEP wave IV latencies and I-IV interpeak latencies at a slow stimulus repetition rate (8 clicks/sec) but shorter wave IV and I-IV latencies at a fast repetition rate (120 clicks/sec). These gender-dependent differences indicate that male and female rat BAEP data should not be combined indiscriminantly. Ethanol sedation had a statistically significant effect on the I-IV interpeak latency that was judged to be largely independent of core temperature changes. This finding suggests that while sedatives and anesthetics used to immobilize animals may have apparently minor temperature-independent effects on BAEP latencies, these effects can be statistically significant.     

Bursting response to current-evoked depolarization in rat CA1 pyramidal neurons is correlated with lucifer yellow dye coupling but not with the presence of calbindin-D28k

Calbindin-D28k (CaBP) immunohistochemistry has been combined with electrophysiological recording and Lucifer Yellow (LY) cell identification in the CA1 region of the rat hippocampal formation. CaBP is shown to be contained within a distinct sub-population of CA1 pyramidal cells which is equivalent to the superficial layer described by Lorente de Nó (1934). The neurogenesis of these CaBP-positive neurons occurs 1-2 days later than the CaBP-negative neurons in the deep pyramidal cell layer, as shown by 3H-thymidine autoradiography. No correlation could be found between the presence or absence of CaBP and the type of electrophysiological response to current-evoked depolarizing pulses. The latter could be separated into bursting or non-bursting types, and the bursting-type response was nearly always found to be associated with the presence of LY dye coupling. Furthermore, when dye coupling involved three neurons, a characteristic pattern was observed which may represent the coupling of phenotypically identical neurons into distinct functional units within the CA1 pyramidal cell layer. In this particular case the three neurons were all likely to be CaBP-positive.     

The effect of methyltransferase inhibitors on histamine release from human dispersed lung mast cells activated with anti-human IgE and calcium ionophore A23187

Inhibitors of adenosylmethionine (AdoMet)-dependent methyltransferases reduce histamine release from enzymatically dispersed human lung mast cells activated with either anti-human IgE or calcium ionophore A23187. The IC25 values for adenosine and 3-deazaadenosine (DZA) inhibiting anti-IgE-induced histamine release were 395 microM and 301 microM respectively. The addition of homocysteine thiolactone (Hcy) potentiated the effects of adenosine and DZA, reducing their IC25 values to 32 microM and 10.5 microM respectively. The adenosine deaminase (adenosine aminohydrolase EC 3.5.4.4) inhibitors erythro-9-(2-hydroxy-3-nonyl)-adenine (EHNA) inhibited anti-IgE-induced histamine release with an IC50 of 162 microM. This inhibition was not potentiated by Hcy. The combination of DZA and Hcy effectively inhibited histamine release induced by concentrations of A23187 which released a similar amount of histamine to anti-IgE. However the combination was 17 times less potent against A23187-compared with anti-IgE-induced release. These observations suggest that AdoMet-dependent methyltransferases play an important role in IgE-dependent histamine release from human lung mast cells but their role in A23187-induced release is less clear.