Adaptive assessment of the capacity of cognitive control.

Cognitive control, although it has limited capacity, serves an essential role in supporting a broad range of cognitive functions. The backward masking majority function task (MFT-M) is a validated behavioural method for measuring the capacity of cognitive control (CCC), but the administration is lengthy. We tested the relative efficiency of administering the MFT-M using an adaptive method based on the principles of computerised adaptive testing (CAT). Participants were 40 healthy young adults aged 18-26. Scores on the adaptive version were highly correlated with scores based on the original approach to administration and showed high test-retest reliability. In addition, compared with the original task of 864 trials (about 86 min), less than 216 trials (20 min) were required in the adaptive version. The results suggest that CAT is a valid and more efficient method for assessing CCC than the MFT-M. This study provides an example of adaptive trial selection in task administration, an approach that can advance the methodology of behavioural science.

Down-regulation of ABCG2 and ABCB4 transporters in the placenta of rats exposed to cadmium.

As a maternal and developmental toxicant, cadmium (Cd) possesses weak penetrability through the placental barrier. However, the underlying mechanism remains unclear. To gain insight into the protein molecules associated with Cd toxicity in placenta and explore their roles in Cd transportation, a reproductive animal experiment was carried out using Sprague-Dawley rats. We performed proteomic analysis of the placenta by Difference Gel Electrophoresis (DIGE) combined with Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Tandem Mass Spectroscopy (MALDI-TOF/TOF MS). The DIGE assay identified 15 protein spots that were differentially expressed with a greater than 1.5-fold change in placenta of Cd-treated rats compared to the control rats. Based on the expression patterns and biological functions of the proteins, we selected the ABCG2 and ABCB4 transporter proteins for further analysis. Western blot analysis showed that Cd exposure could down-regulate the expression of ABCG2 and ABCB4 in the placenta. There was a negative dose-response relationship between Cd exposure and the expression of ABCG2 or ABCB4 protein. These results indicated that down-regulation of ABCG2 and ABCB4 transporters may regulate Cd across through placenta and thus affect the in vivo toxic effect of Cd to fetus.

Occupational trichloroethylene hypersensitivity syndrome: human herpesvirus 6 reactivation and rash phenotypes.

BACKGROUND: Trichloroethylene (TCE) is an industrial solvent which can cause severe generalized dermatitis, i.e., occupational TCE hypersensitivity syndrome. Reactivation of latent human herpesvirus 6 (HHV6) can occur in such patients, which has made TCE known as a causative chemical of drug-induced hypersensitivity syndrome (DIHS). OBJECTIVE: This study aimed to clarify HHV6 status, cytokine profiles and their association with rash phenotypes in patients with TCE hypersensitivity syndrome. METHODS: HHV6 DNA copy numbers, anti-HHV6 antibody titers, and cytokines were measured in blood prospectively sampled 5-7 times from 28 hospitalized patients with the disease. RESULTS: The patients (19 had exfoliative dermatitis (ED) and 9 had non-ED type rash) generally met the diagnostic criteria for DIHS. Viral reactivation defined as increases in either HHV6 DNA (≥100 genomic copies/10(6) peripheral blood mononuclear cells) or antibody titers was identified in 24 (89%) patients. HHV6 DNA, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-5, IL-6 and IL-10 concentrations were remarkably higher in the patients than in the healthy workers (p<0.01). Positive correlations between HHV6 DNA, TNF-α, IFN-γ, IL-6 and IL-10 were significant (p<0.05) except for that between HHV6 DNA and IFN-γ. An increase in HHV6 DNA was positively associated with an increase in TNF-α on admission (p<0.01). HHV6 DNA, the antibody titers, TNF-α and IL-10 concentrations were significantly higher in ED than in the non-ED type (p<0.05). CONCLUSION: Reactivated HHV6 and the increased cytokines could be biomarkers of TCE hypersensitivity syndrome. The higher-level reactivation and stronger humoral responses were associated with ED-type rash.

[High expression of LIP1 in Pichia pastoris].

The gene of LIP1, the most important isoenzyme of Candida rugosa lipase (CRL), was artificially synthesized according to its mature peptide sequence. It consisted of 20 codons of preference in Pichia pastoris. The artificial gene was cloned into methanol-inducible expression vector pPICZalphaA, and constitutive expression vector pGAPZalphaA, respectively. The linearized recombinant plasmids were transformed into chromosome of Pichia pastoris SMD1168H strain by electroporation. The abilities of expressing LIP1 in both transformed yeasts had been compared, and the yeast transformed with pGAPZalphaA was more efficient than pPICZalphaA. A recombinant yeast strain named CHT-II expressed LIP1 constitutively, and was the most efficient one. Some enzymatic properties of the recombinant LIP1 were also determined. CHT-II secreted LIP1 into supernate at a level of 2.00x10(5) u/L after 72 h (the cells had been transferred to fresh culture medium at the 24th h). After optimizing the conditions for high cell-density fermentation, the selected yeast strain could secrete LIP1 into supernate at a level of 1.395x10(6) u/L after 72 h. The results indicated that this modification of lip1 gene was successful.

Guinea pig maximization test for trichloroethylene and its metabolites.

OBJECTIVES: To study the contact allergenic activities of trichloroethylene (TCE) and its three metabolites trichloroacetic acid, trichloroethanol and chloral hydrate. METHODS: A modified guinea pig maximization test (GPMT) was adopted. The skin sensitization (edema and erythema) was observed in trichloroethylene, trichloroacetic acid, trichloroethanol, chloral hydrate and 2,4-dinitrochlorobenzene. RESULTS: The allergenic rate of TCE, trichloroacetic acid and 2,4-dinitrochlorobenzene was 71.4%, 58.3% and 100.0% respectively, and that of trichloroethanol and chloral hydrate was 0%. The mean response score of TCE, trichloroacetic acid and 2,4-dinitrochlorobenzene was 2.3, 1.1, 6.0 respectively. The histopathological analysis also showed an induction of allergenic transformation in guinea pig skin by both TCE and trichloroacetic acid. CONCLUSION: TCE appears to be a strong allergen while trichloroacetic acid a moderate one. On the other hand, both trichloroethanol and chloral hydrate are weak sensitization potentials. Immunologic reaction induced by TCE might be postulated as the pathological process of this illness. Consequently, it is suggested that in the mechanism of Occupational Dermatitis Medicamentose-Like (ODML) induced by TCE, the chemical itself might be the main cause of allergy. As one of its metabolic products, trichloroacetic acid might be a subordinate factor.

Studies on hypokalemia induced by trimethyltin chloride.

OBJECTIVES: To determine the possible relationship between plasma potassium concentration and severity of acute trimethyltin chloride (TMT) poisoning and to assess the mechanism of TMT induced hypokalemia. METHODS: SD rats were treated with various dosages of TMT (i.p.). All the indices were measured and analysed for determining their possible relations with plasma K+. RESULTS: With increase of dosage, the plasma K+ level dropped rapidly, and deaths appeared more quickly. The LD50 of TMT (i.p.) was 14.7 mg/kgbw. In the low dosage group (10 mg/kgbw), the plasma K+ level dropped slowly with the lowest dosage on day 6 (4.85 mmol/L). It rose again on day 11 (5.06 mmol/L), and recovered on day 28. The poisoning signs corresponded with decline of the span of K+ level. The plasma Na+ level dropped half an hour after TMT treatment, but recovered 24 h later. In the high dosage group (46.4 mg/kgbw), the levels of plasma K+ and Na+ fell rapidly within half an hour (P < 0.05), the intracellular potassium concentration of RBC did not decrease obviously (P > 0.05), the activities of Na(+)-K(+)-ATPase and Mg(2+)-ATPase in RBC membrane were depressed remarkably (P < 0.01, P < 0.05, respectively), the plasma aldosterone concentrations rose as high as tenfold (P < 0.01), the arterial blood pH fell from 7.434 to 7.258 (P < 0.01), pCO2 was raised from 29.62 to 45.33 mmHg (P < 0.01). In the 24 h urine test, when rats were treated with TMT (21.5 mg/kgbw, i.p.), urine volume, urinary potassium, sodium and chloride increased significantly in comparison with those in the controls (P < 0.01). CONCLUSION: TMT could induce hypokalemia in SD rats. The available evidence suggests that TMT can induce acute renal leakage of potassium. At the same time, a significant rise of plasma aldosterone may play an important role in promoting potassium leakage from kidney to result in severe hypokalemia with inhaling acid-base abnormalities produced, which aggravate the poisoning symptoms. In the end the rats would die of respiratory failure.