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For human hemoglobin, a pronounced dependence of oxygenation curves upon protein concentration can be demonstrated experimentally in the range between 10(-4) and 2 X 10(-6) M heme. The effects of such protein concentration dependence upon analysis of saturation curves have been explored using a model-independent linkage analysis which incorporates the dissociation of tetramers to dimers. We have carried out stimulations of oxygenation curves representing a variety of energy distributions designed to cover a wide range of values which are relevant to known hemoglobin systems and experimental conditions. The resulting simulated oxygenation curves were analyzed by least-squares minimization procedures in terms of the tetramer binding isotherm to yield the four apparent Adair constants. These derived constants were compared with the originally assumed values used in the simulation in order to assess the extent to which their values may be altered by the presence of dimer. For each energy distribution the analysis has been carried out over a wide range of protein concentration. We have found that the presence of even small amounts of dimer that are necessarily present at the low protein concentrations commonly employed may have a devastating effect upon the reliability of Adair constant determinations. In addition to these simulated cases, we have analyzed two sets of highly precise experimental data from the literature in order to assess the degree to which constants obtained may have been influenced by the presence of dimer.

SINCE THEIR FIRST description by Ehrlich, the distribution of tissue mast cells has been extensively studied. 1, 2 However, their presence and distribution in the oro-nasal region have remained controversial. Thus, Kelsall and Crabb 3 maintain that no literature exists regarding the distribution of mast cells in the oro-nasal region or in any other segments of the head and neck. Conversely, some investigators quoted by Michels 2 found a great number of these cells in the tongue. A large mast cell population has been reported in gingival connective tissue, 4, 5 decreasing in number in proximity to the gingival sulcus. 4Studies by other investigators 4-7 of the density of mast cells in inflamed gingiva have resulted in contradictory findings. These findings, together with McCutcheon's hypothesis 8 proposing increased mast cell counts in chronic inflammatory conditions elsewhere in the body induced us to undertake the present study. The purpose was to determine whether such an increase takes place in chronic destructive periodontal disease. MATERIALS AND METHODSBiopsies were taken from the upper buccal premolar area of 35 patients (age range 14-50 years) with chronic destructive periodontal disease (Group I). Pockets varying from 4 to 6 mm. in depth with bone resorption, but no tooth mobility, were present. The patients were not prescaled. Thirteen patients from 15 to 64 years of age with clinically healthy gingiva served as controls (Group 2). Papillary biopsies were taken from their upper buccal premolar area. A month prior to this procedure, the teeth of the controls were carefully scaled and polished, and the patients were instructed in oral home care.

The relation of acute thrombocytopenic purpura (TP) to the use of drugs was investigated in a case-control study conducted in eastern Massachusetts, Rhode Island, and the Philadelphia region; 62 cases over the age of 16 years with acute onset and with a rapid recovery were compared with 2,625 hospital controls. After control for confounding by multiple logistic regression, use of the following drugs in the week before the onset of symptoms was significantly associated: trimethoprim/sulfamethoxazole (relative risk [RR] estimate, 124), quinidine/quinine (101), dipyridamole (14), sulfonylureas (4.8), and salicylates (2.6). The overall annual incidence of acute TP was estimated to be 18 cases per million population. The excess risks for the associated drugs were estimated to be 38 cases per million users of trimethoprim/sulfamethoxazole per week, 26 per million for quinidine/quinine, 3.9 per million for dipyridamole, 1.2 per million for sulfonylureas, and 0.4 per million for salicylates. Associations with sulfonamides, quinidine/quinine, sulfonylureas, and salicylates have been previously reported, but the present study has provided the first quantitative measures of the risk. The association with dipyridamole was unexpected. In general, despite large RRs, the incidence rates attributable to the drugs at issue (excess risks) were low, suggesting that TP is not an important consideration in the use of the various drugs.

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The present study investigated the neuropsychometric correlates of the Mini-Mental State Examination. 12 consecutive neurological referrals were administered the Mini-Mental State Examination, the Wechsler Memory Scale, and the WAIS--R. Pearson product-moment correlations suggest moderate association between scores on the Mini-Mental State Examination and Wechsler Memory Scale but less robust relationships between scores on the Mini-Mental State Examination and WAIS--R Full Scale, Verbal, and Performance IQs.

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