False memories based on indirect associations of gender stereotypes of occupations

This study examined whether false memories, as revealed by the Deese-Roediger-McDermott (DRM) paradigm, can arise from indirect stereotype associations, as proposed by Lenton, Blair, and Hastie (2001). We found significant indications of stereotype-evoked false memories. The participants in our experiment reported that they were unaware of the gender theme of the studied list, suggesting that the false memories were due to implicit associative processes. Although we could not replicate an increase in the false recognition of stereotypically gender-congruent occupations, we detected a gender-congruent effect partially by the analyses of the "Remember" responses and the participants' egalitarian attitudes against the gender role. Moreover, analyses of the "Know" responses indicated that participants' attitudes toward gender roles potentially moderate the degree that they form occupational gender stereotypes. Implications of the results for basic/applied research on the interactions between stereotype and memory are discussed.     

Radiosynthesis and preliminary biodistribution in mice of 6‐deoxy‐6‐[131I]iodo‐L‐ascorbic acid

An ascorbate analog labeled with iodine‐131, 6‐deoxy‐ 6‐[¹³¹I]iodo‐L ‐ascorbic acid was prepared for evaluation as an in vivo tracer of L ‐ascorbic acid. The no‐carrier‐added radiosynthesis was conducted by nucleophilic bromine–iodine exchange between the brominated precursor and sodium [¹³¹I]iodide in 2‐pentanone at 130–140°C. HPLC purification using a reverse‐phase column gave 6‐deoxy‐6‐[¹³¹I]iodo‐L ‐ascorbic acid in radiochemical yield of 36–60% with high radiochemical purity and satisfactory‐specific radioactivity in a total preparation time of 90 min. Biodistribution studies in fibrosarcoma‐bearing mice showed a high uptake in the adrenal glands, accompanied by low activity of tumor accumulation, accumulation properties similar to previous results obtained with ¹⁴C‐labeled ascorbic acid and 6‐deoxy‐6‐[¹⁸F]fluoro‐L ‐ascorbic acid, in spite of high level of deiodination. Copyright © 2009 John Wiley & Sons, Ltd.     

D-Serine and a glycine transporter inhibitor improve MK-801-induced cognitive deficits in a novel object recognition test in rats

Compounds enhancing N-methyl-d-aspartate (NMDA) glutamate receptor function have been reported to improve cognitive deficits. Since cognitive deficits are considered to be the core symptom of schizophrenia, enhancing NMDA receptor function represents a promising approach to treating schizophrenia. In the present study, we investigated whether d-serine or a glycine transporter inhibitor N-[3-(4'-fluorophenyl)-3-(4'-phenylphenoxy)propyl]sarcosine (NFPS), both of which enhance NMDA receptor function, could improve MK-801-induced cognitive deficits in rats, and compared their effects with those of the atypical antipsychotic clozapine and of the typical antipsychotic haloperidol. To assess cognitive function, we used a novel object recognition test in rats that measured spontaneous exploratory activity of a novel object when paired with a familiar object. We then evaluated the effects of the compounds on cognitive deficits induced by treatment with MK-801, the NMDA receptor antagonist. Pretreatment with clozapine (1, 5 mg/kg, i.p.) but not haloperidol (0.03, 0.1 mg/kg, i.p.) significantly improved MK-801-induced cognitive deficits. Pretreatment with D-serine at 800 mg/kg (i.p.) or NFPS (0.3, 1 mg/kg, i.p.) significantly improved MK-801-induced cognitive deficits under this test paradigm. These findings suggest that impaired preference for novel objects induced by MK-801 in the novel object recognition test could be a useful animal model for evaluating the efficacy of compounds targeting the cognitive deficits observed in schizophrenic patients. The results also suggest that enhancing NMDA receptor function is an effective way for treating the cognitive deficits associated with schizophrenia.     

Use of mizoribine as a rescue drug for steroid-resistant pediatric IgA nephropathy

Recent clinical trials have shown a beneficial effect of mizoribine (Miz), an immunosuppressive drug, in the treatment of new-onset pediatric IgA nephropathy (IgAN). In this study, we evaluated the efficacy of Miz treatment in three children with established steroid-resistant IgAN. The patients had IgAN featuring persistent proteinuria and diffuse mesangial proliferation and had failed to respond to 2 years of treatment with prednisolone. Based upon the second biopsy results, patients were given methylprednisolone (mPSL) pulse therapy that induced a transient reduction in proteinuria, which was reversed when the mPSL dose was tapered. Miz therapy was then instigated in place of pulse mPSL. All three patients showed a substantial reduction in proteinuria and resolution of hematuria within 5 months. A follow-up biopsy in two of the patients showed a substantial reduction in the severity of glomerular lesions and a decrease in the number of activated macrophages. In conclusion, Miz therapy was found to be a safe and effective therapy in three cases of steroid-resistant pediatric IgAN. The ability of Miz to reduce the number of activated macrophages may be an important mechanism by which this drug ameliorated renal disease in these patients.     

JAK2-V617F mutation analysis of granulocytes and platelets from patients with chronic myeloproliferative disorders: advantage of studying platelets

There have been conflicting reports over the JAK2-V617F mutation status of platelets in chronic myeloproliferative diseases (CMPDs). The aim of this study was to analyse JAK2-V617F status, not only in granulocytes but also in platelets. The JAK2-V617F mutation was analysed in both granulocytes and platelets in 115 patients with CMPDs using direct sequencing. JAK2-V617F was detected in granulocytes from 71 of those patients, all 71 of whom also had platelet JAK2-V617F expression. The remaining 44 patients showed negative JAK2-V617F expression on granulocytes, but positive JAK2-V617F expression was detected on the platelets from nine of the 33 essential thrombocythaemia (ET) patients, one of the eight polycythaemia vera patients, and two of the three primary myelofibrosis patients. When ET patients were divided into three groups according to granulocyte and platelet JAK2-V617F status (both-positive, platelets-only positive and both-negative), the both-positive and platelets-only positive groups shared the clinical features of higher white blood cell count and frequent thrombosis. These results suggest that analysis of platelets is a more sensitive approach for detecting JAK2-V617F in CMPD patients than analysis of granulocytes. They also suggest that previous reports of the incidence of JAK2-V617F in CMPD patients, obtained using only analysis of granulocytes, could be underestimations.     

Haemodynamic evaluation of paraparetic transient ischaemic attacks in childhood moyamoya disease

Abstract

The haemodynamic mechanisms responsible for the appearance of paraparetic transient ischaemic attacks in ten patients with childhood moyamoya disease who subsequently underwent bifrontal omental transplantation were investigated. Cerebral perfusion (CP) was measured with ^99mTc-hexamethylene-propyleneamine oxime single photon computed tomography prior to and after administration of acetazolamide. Cerebral perfusion was obtained by dividing radioisotope uptake per pixel in regions of interest by that in cerebellum. Haemodynamic reserve was defined as [CP after acetazolamide - CP before acetazolamide]/CP before acetazolamide × 100. Amounts of CP in the anterior portion of the frontal lobe and in the paracentral lobule were 0.70±0.04 and 0.74 ±0.03, respectively, before appearance of the transient ischaemic attacks. The latter was significantly higher than the former (p <0.0001). Haemodynamic reserves were -11.1 ±2.8 and - 9.6 ± 3.0, respectively, at that time. These two parameters were significantly decreased just after paraparetic transient ischaemic attacks and two parameters in the paracentral lobule were more decreased than those in the anterior portion of the frontal lobe. But these increased again after bifrontal omental transplantation in these two regions. In summary, the watershed region was located anterior to the paracentral lobule before appearance of the transient ischaemic attacks, and widened and moved backward to include the paracentral lobule just before their appearance. [Neurol Res 1995; 17: 162-168]