硫酸锌对心肌慢反应电活动和哇巴因引起振荡后电位的影响

本文目的旨在观察硫酸锌对心肌慢反应电活动的影响,所得结果如下:(1) 0.1～0.3mmol硫酸锌能使高钾除极引起的豚鼠乳头肌慢反应动作电位APA和V_max降低,APD₅₀和APD₉₀)显著延长;(2) 0.1～0.3 mmol硫酸锌能抑制家兔离体窦房结细胞的自律性,使窦房结APA降低,APD₉₀延长,SP₀和SP₄减小;(3) 0.1 mmol硫酸锌可对抗0.4μmol哇巴因诱发的豚鼠心室肌振荡后电位,提高引起振荡后电位的哇巴因阈浓度。提示:锌抑制心肌慢反应电活动。     

Social adversity predicts ADHD‐medication in school children – a national cohort study

Aims: To test the hypothesis that psychosocial adversity in the family predicts medicated ADHD in school children. Method: ADHD‐medication during 2006 was identified in the Swedish Prescribed Drug Register in national birth cohorts of 1.1 million 6–19 year olds. Logistic regression models adjusted for parental psychiatric disorders were used to test our hypothesis. Results: There was a clear gradient for ADHD medication with level of maternal education, with an adjusted odds ratio of 2.20 (2.04–2.38) for the lowest compared with the highest level. Lone parenthood and reception of social welfare also implied higher risks of ADHD‐medication with adjusted ORs of 1.45 (1.38–1.52) and 2.06 (1.92–2.21) respectively. Low maternal education predicted 33% of cases with medicated ADHD and single parenthood 14%. Conclusions: Social adversity in the family predicts a considerable proportion of ADHD‐medication in school children in Sweden.     

Trends in hospital admission rates for anorexia nervosa in Oxford (1968–2011) and England (1990–2011): database studies

Objectives

To report on long-term trends in hospital admission rates for anorexia nervosa using two English datasets.

Design

We used data on hospital day-case and inpatient care across five decades in the Oxford Record Linkage Study (ORLS), and similar data for all England from 1990. We analysed rates of admission for anorexia nervosa in people aged 10–44 years, using hospital episodes (counting every admission) and first-recorded admissions (counting only the first record for each person).

Setting

Former Oxford NHS Region; and England.

Participants

None; anonymous statistical records were used.

Results

In the longstanding ORLS, the age-standardised first-recorded admission rate for women was 2.7 (95% confidence interval 1.6–3.8) per 100,000 female population aged 10–44 years in 1968–1971; 2.7 (2.1–3.3) in 1992–1996; and 6.3 (5.5–7.2) in 2007–2011. Male rates were zero in the 1960s; 0.07 (0.0–0.1) per 100,000 men in 1992–1996; and 0.4 (0.2–0.6) in 2007–2011. In England, female rates increased from 4.2 (4.0–4.4) in 1998–2001 to 6.9 (6.7–7.1) in 2007–2011; and the corresponding male rates were 0.2 (0.1–0.3) and 0.5 (0.4–0.6). Episode-based admission rates rose more than person-based rates. The highest rates by far were in girls and women aged 15–19 years.

Conclusions

In recent years, anorexia nervosa has become a greater burden on secondary care: not only have admission rates increased but so too have multiple admissions per person with anorexia nervosa. The increase in admission rates might reflect an increase in prevalence rates of anorexia nervosa in the general population, but other explanations, including lower clinical thresholds for admission, are possible and are discussed.     

Localization of the G-CSF gene on chromosome 17 proximal to the breakpoint in the t(15;17) in acute promyelocytic leukemia

The human granulocyte-colony stimulating factor gene (G-CSF) is localized at 17q11.2-q21, the region of one of the breakpoints in the 15;17 chromosome translocation specific for acute promyelocytic leukemia (APL). As G-CSF induces differentiation and loss of tumorigenicity in myeloid leukemic cells or cell lines, it was possible that the translocation in APL involved the DNA of the G-CSF coding region or its regulatory region. In situ hybridization to chromosomes with the t(15;17) from patients with the APL translocation using a G- CSF cDNA clone revealed that the coding region of this gene is proximal to the t(15;17) breakpoint on chromosome 17. Southern analysis of DNA from patients with the APL translocation showed no differences in hybridization between normal and leukemic cells. These results indicate that the G-CSF coding sequence is not disrupted by the chromosomal rearrangement characteristic of APL.     

Analysis of hematopoietic stem and progenitor cell populations in cytomegalovirus-infected mice

We have studied the effects of murine cytomegalovirus (MCMV) infection on bone marrow stem and progenitor cell populations to find an explanation for the defects in hematopoiesis that accompany CMV infections in patients. Sublethal MCMV infection of BALB/c mice resulted in a 5- to 10-fold decrease in the numbers of myeloid (colony- forming unit-granulocyte-macrophage [CFU-GM]) and erythroid (burst- forming unit-erythroid [BFU-E]) progenitor cells in the marrow, but not in primitive myeloerythroid progenitor cell (colony-forming unit-spleen [CFU-S]) numbers. In contrast, we observed a 10- to 20-fold reduction in CFU-S as well as CFU-GM and BFU-E in lethally infected mice. Depletion of marrow CFU-GM was less severe in C57BL/10 and C3H/HeJ mice, which are more resistant to the effects of MCMV infection. Treatment of bone marrow cells with MCMV preparations in vitro did not reduce the numbers of CFU-GM, although up to 10% of the cells were productively infected. This finding suggests that CFU-GM were not susceptible to lytic MCMV infection in vitro and are probably not eliminated by lytic infection in vivo. Increases in the frequencies of Sca-1+Lin- marrow cells, a population that includes cells with the characteristics of pluripotential stem cells, were observed in MCMV- infected BALB/c, C57BL/10, and DBA/2J mice. Increases in the frequencies of c-kit+Lin- marrow cells were only seen in DBA/2J mice. MCMV infection did not impair the function of pluripotential stem cells because transplantation of marrow from MCMV-infected donors into irradiated recipient mice resulted in successful reconstitution of the T, B, and myeloid cell lineages.