Independent and court-ordered forensic neuropsychological examinations: Official statement of the National Academy of Neuropsychology

Independent forensic neuropsychological examinations are performed by neuropsychologists who are hired as independent contractors by third parties to make determinations regarding neuropsychological functioning. The responsibilities of neuropsychologists when performing independent or court-ordered forensic examinations differ from those of clinical examinations. Because neuropsychological training typically occurs in clinical contexts, the transition to forensic contexts may result in uncertainty about how to negotiate the unique responsibilities of the forensic examiner role. Neuropsychologists are responsible for maintaining the highest standards of professional practice when performing independent and court-ordered forensic examinations. To reach and maintain the highest standards of practice, neuropsychologists must understand the unique relationships with retaining parties and examinees and strive to maintain true independence and objectivity. Although a true neuropsychologist-patient relationship is not considered to exist within the context of a forensic neuropsychological evaluation, neuropsychologists have ethical responsibilities to both the retaining party and the examinee.     

Oral tolerance in EAE: reversal of tolerance by T helper cell cytokines

Oral administration of myelin basic protein (MBP) inhibits clinical and histopathological manifestations of experimental autoimmune encephalomyelitis (EAE), but only partially reduces serum anti-MBP antibody titers. We report here that orally administered MBP alters the isotypic distribution of anti-MBP antibody-forming cells (AFC) among various lymphoid tissues, with the most profound differences seen in mucosal tissues. We observed an isotype-selective reduction in anti-MBP IgA but not IgM AFC frequencies in Peyer's patches. The anti-MBP IgA AFC frequencies could be reconstituted by addition of interleukin 4 (IL-4) and interleukin 5 (IL-5). The cytokines did not appear to generate de novo responses since no increases in anti-MBP IgA AFC frequencies were observed in control cultures. These results indicate that decreased antibody production, as a result of oral antigen administration, can be reversed by exposure to the appropriate cytokines.     

Increased recognition of IgA nephropathy in African-American children

Based upon the percentage of cases of IgA nephropathy (IgAN) in biopsy series, a lower prevalence has been assumed for African-Americans compared with Americans of European descent. This may be due to a racial difference in the basic underlying pathology of IgAN or to racial differences in patterns of referral and biopsy selection practices. Over the past decade (1985 – 1994), we have found similar incidences of IgAN in Caucasian and African-American children from Shelby County, Tennessee. The incidence was 3.0 cases per million per year for Caucasian and 5.7 cases per million per year for African-American children. IgAN may be more common in African-American children than previously appreciated. Population-based incidence studies will be necessary to determine whether or not our experience has become a more widespread phenomenon. Received August 21, 1996; received in revised form and accepted December 18, 1996     

Inhibition of hog liver folylpolyglutamate synthetase by 5-substituted 5,8-dideaza analogues of folic acid bearing a terminal L-ornithine residue.

Five new N alpha-(5,8-dideazapteroyl)-L-ornithines have been prepared using multistep synthetic sequences. These include N alpha-[5-(trifluoromethyl)-5,8-dideazapteroyl]-L-ornithine, 3, as well as N alpha-[5-(trifluoromethyl)-5,8-dideazaisopteroyl]-L-ornithine, 4, and its 5-fluoro and 5-chloro analogues. Both of the compounds containing a 5-(trifluoromethyl) group (3 and 4) were found to be excellent inhibitors of homogeneous hog liver folylpolyglutamate synthetase, having Ki values in the same range as N alpha-(5-chloro-5,8-dideazapteroyl)-L-ornithine, 2, (approximately 10 nM). However, the bridge-reversed isomer of 2 was 60-fold less inhibitory than 2.     

Images of liposarcoma using technetium-99m bleomycin and technetium (V)-99m DMSA

The effectiveness of Tc-99m bleomycin (BLM) and Tc(V)-99m DMSA are compared with that of Ga-67 citrate, which is currently the most widely used agent. In four patients with lipomatous tumors, the clinical significance of tumor imaging with each of these three agents is discussed and compared. Results indicate that both Tc-99m BLM and Tc(V)-99m DMSA are superior in detecting the extension or localization of liposarcomas.     

ACUTE EFFECT OF ETHANOL ON RENAL ELECTROLYTE TRANSPORT IN THE RAT

1. Despite human and animal studies, the direct effect of ethanol on renal water and electrolyte transport is poorly understood. The acute effect of increasing plasma concentrations of ethanol was evaluated in a water diuretic anaesthetized rat model which inhibits endogenous arginine vaso-pressin (AVP) release. 2. Ethanol at a plasma concentration of 1.69 ±0.28 mmol/L produced an immediate increase in urine flow (174 ± 11 μL/min pre-ethanol and 189 ± 13 and then 206 ± 12 μL/min during the ethanol infusion; P<0.001) as well as an increase in fractional sodium excretion (0.17 ± 0.04 to 0.28 ± 0.05 and 0.27 ± 0.05%; P<0.001). There was also a brief phosphaturia. These increases in electrolyte excretion had returned to control values by 20 min despite a further increase in the plasma ethanol concentration. 3. The urinary excretion of potassium, calcium and magnesium was not altered nor was glomerular filtration rate or renal plasma flow. 4. Ethanol at a mean concentration of 1.60 mmol/L did not alter the action of a maximal concentration of AVP (75 ng/kg) on water or electrolyte transport. However, the antidiuretic effect of a submaximal concentration of AVP (7.5 ng/kg) was augmented by ethanol at concentrations of 1.63 and 0.98 mmol/L. 5. These studies suggest that the ethanol induced diuresis commonly ascribed to inhibition of AVP secretion may also be due to other intrarenal effects of ethanol, possibly acting within the proximal tubule. These results also confirm recent in vitro findings that while ethanol does not inhibit the action of a maximal concentration of AVP, it does modulate the effects of lower AVP concentrations.