重庆市两所大学学生营养知识、态度及行为的基线调查

目的:了解重庆市某两所大学学生的营养知识、态度和行为现况,为开展营养教育效果评价提供基线数据。方法:选取重庆渝中区某学院为干预学校,文理科各一个系,整群抽取一年级9个班的学生,共289人;选取九龙坡区某学院为对照学校,选择与干预学校相匹配的文理科各一个系,整群抽取9个班的学生,共344人。于2005-03采用自编调查问卷,对以上633名在校学生进行营养知识、态度和行为的调查。问卷内容包括一般人口统计学资料、营养知识、态度、行为情况,营养知识获取途径等,其中知识问题满分16分,有关态度问题满分9分,行为问题满分40分,得分越高越好。结果:发放问卷650份,回收有效问卷633份,有效率97.4%。①两组学生一般人口学特征和家庭背景均有可比性(P>0.05)。②干预学校学生营养知识、态度和行为得分分别为(9.04±2.43),(7.13±1.20),(16.27±3.53)分,对照学校得分分别为(9.23±2.22),(6.96±1.28),(16.38±3.39)分,两组比较无差异。③只有30.33%的同学每天吃早餐,只有37.91%的学生在选择食物时考虑了营养价值或自己的营养需要,不常吃水果,常吃零食现象严重。大部分学生都有良好的求知欲望,希望通过多种途径获得营养知识。结论:①大学生对营养知识缺乏全面深入的了解,大部分学生营养态度端正,行为良好,但部分学生也存在一些问题。②两所学校营养知识、态度与行为无显著差异。     

Monocytoid differentiation of freshly isolated human myeloid leukemia cells and HL-60 cells induced by the glutamine antagonist acivicin

Previously we showed that starvation of HL-60 promyelocytic leukemia cells for a single essential amino acid induced irreversible differentiation into more mature monocyte-like cells. Although not an essential amino acid, glutamine is important in the growth of normal and neoplastic cells. The glutamine analogue, alpha S,5S-alpha-amino-3- chloro-4,5-dihydro-5-isoxazoleacetic acid (acivicin) inhibits several glutamine-utilizing enzymes and therefore depletes cells of certain metabolic end products. The current study was designed to examine in vitro the effects of acivicin on growth and differentiation of several established human myeloid leukemia cell lines, including the HL-60 cell line, and of freshly isolated cells from patients with acute nonlymphocytic leukemia (ANLL). Four-day culture of HL-60 cells with acivicin at concentrations of 0.1 to 10.0 micrograms/mL (0.56 to 56 nmol/L) decreased cell growth by 33% to 88% as compared with untreated control cells. Viability of cells was greater than 92% for untreated cells and 93% to 41% for acivicin-treated cells. Cells treated with acivicin differentiated along a monocytic pathway as shown by increased H2O2 production and alpha-naphthyl butyrate esterase (NSE) content. Differentiation was time and dose dependent, and was irreversible. Changes in H2O2 production and NSE content were partially abrogated by co-culture with 10 mmol/L exogenous cytidine and guanosine but not by co-culture with other nucleosides or glutamine. At these concentrations of acivicin, differentiation was associated with expression of the N- formyl-methyl-leucyl-phenylalanine-receptor (FMLP-R) on 8% to 29% of cells as compared with 8% for control cells. Acivicin potentiated the differentiating effects of interferon-gamma, tumor necrosis factor, dihydroxyvitamin D3, dimethylsulfoxide, and retinoic acid. Culture of cells from the U937 (monoblastic), K562 (erythroleukemia), and KG-1 (myeloblastic) cell lines resulted in decreased growth and viability, but not consistently in differentiation. Acivicin decreased survival of freshly isolated ANLL cells and increased their H2O2 production and NSE content. These results suggest that the glutamine analogue acivicin may be useful as a differentiating agent with antileukemia activity in patients with ANLL.     

Anatomic determinants of sleep-disordered breathing across the spectrum of clinical and nonclinical male subjects

OBJECTIVES: We wished to determine the independent contribution of craniofacial dimensions of the upper airway to sleep-disordered breathing (SDB) in subjects who spanned the entire continuum of SDB. We also determined the interactive effects of body mass index (BMI) and age on the relationship between airway dimensions and SDB. DESIGN AND SUBJECTS: We studied 142 nonclinical male subjects in a working community population (average age, 47 years; average BMI, 29; average +/- SD apnea/hypopnea index [AHI], 20 +/- 20/h), and 62 patients with obstructive sleep apnea (average age, 47 years; average BMI, 32; average +/- SD AHI, 48 +/- 35/h. We determined the AHI from overnight polysomnography and the number of oxygen desaturations (> or = 2%) per hour of sleep. We used lateral facial cephalometric radiographs to measure 41 anatomic landmarks and 55 dimensions in the upper airway. SETTING: A university hospital and a sleep-disorders clinic. DATA ANALYSIS: We used stepwise regression analysis to determine the independent contributions of measured variables to SDB. MEASUREMENTS AND RESULTS: In the entire study population (n = 204), variations in BMI and six measures of craniofacial morphology accounted equally for one half of the total variance in AHI, and their interactive effects accounted for an additional 15%. Membership in the clinical or nonclinical group per se had no significant influence on these relationships. The single most important cephalometric variable in predicting AHI severity was the horizontal dimension of the maxilla (ie, porion vertical to supradentale [PV-A] distance). When the PV-A distance was relatively narrow (< 97 mm) the probability of having mild (AHI, 15 to 30/h) to severe (AHI > 30/h) SDB increased fivefold to sevenfold in nonobese subjects and threefold in obese subjects. Thus, in nonobese subjects (average BMI, 25 +/- 2) and in subjects with narrow upper airway dimensions, four cephalometric dimensions were the dominant predictors of AHI, accounting for 50% of the variance. However, in subjects with a large anteroposterior facial dimension, BMI was the major predictor of AHI and a BMI > 28 increased the probability of moderate-to-severe sleep apnea by approximately fivefold. Finally, the combination of cephalometric dimensions and BMI accounted for an increasing amount of the variance in AHI as the severity of AHI increased. CONCLUSIONS: Across the population spectrum of SDB, four cephalometric dimensions of the upper airway in combination with BMI accounted independently for up to two thirds of the variation in AHI; and the relative contribution of these two sets of determinants of AHI varied depending on airway size, obesity, and the amount of SDB.     

Nonrandom inactivation of the X chromosome in early lineage hematopoietic cells in carriers of Wiskott-Aldrich syndrome

The Wiskott-Aldrich syndrome (WAS) is an X-linked (Xp11.22) recessive immunodeficiency syndrome characterized by susceptibility to opportunistic and pyogenic infections, thrombocytopenia, and eczema. Previous studies of obligate carriers of WAS documented that nonrandom inactivation of the X chromosome carrying the defective gene is observed in all peripheral blood cells. The existence of both abnormal platelets and lymphocytes is consistent with a defect that affects early hematopoietic precursors. We isolated CD34+ hematopoietic progenitor cells collected from obligate carriers of WAS by apheresis and used polymerase chain reaction analysis of a polymorphic variable number of repeats (VNTR) within the X-linked androgen receptor to document nonrandom inactivation. These data show that nonrandom inactivation of the X-chromosome in WAS-obligate carriers occurs early during hematopoietic differentiation.     

Alpha 4 beta 1 and alpha 5 beta 1 are differentially expressed during myelopoiesis and mediate the adherence of human CD34+ cells to fibronectin in an activation-dependent way

To study the receptors involved in the interaction between extracellular matrix proteins and hematopoietic progenitor cells, we analyzed the expression of beta 1 integrins on CD34+ bone marrow cells by means of immunoflowcytometry. Alpha 4 beta 1 and alpha 5 beta 1 were expressed, whereas alpha 1 beta 1, alpha 2 beta 1, alpha 3 beta 1, alpha 6 beta 1, and alpha v beta 1 were virtually absent. Furthermore, we assessed the alpha 4 and alpha 5 expression on committed myeloid progenitor cells. These colony-forming cells were detected in the alpha 4 dull fraction and the alpha 5 dull fraction. During myeloid differentiation, both in vivo and in vitro, a differential expression of alpha 4 beta 1 and alpha 5 beta 1 was observed. alpha 5 beta 1 was found to be lost at the myelocytic-metamyelocytic stage, before the loss of alpha 4 beta 1, at the band stage. Functional studies showed no binding of erythroid progenitor-depleted, CD34+ bone marrow cells to fibronectin. However, protein kinase C activation strongly induced fibronectin binding (68% of the cells). Inhibition experiments with specific antibodies and peptides showed the binding to be mediated by both alpha 4 beta 1 and alpha 5 beta 1. Also, colony-forming cells of granulocytes and macrophages were demonstrated to adhere to fibronectin in an activation-dependent way. During granulocyte colony-stimulating factor-induced in vitro maturation, the activation-dependent fibronectin binding capacity is gradually lost. We conclude that: (1) CD34+ bone marrow cells express alpha 4 beta 1 and alpha 5 beta 1; (2) the expression of alpha 4 beta 1 and alpha 5 beta 1 is differentially expressed during myeloid differentiation; and (3) binding of CD34+ bone marrow cells to fibronectin is activation dependent.     

Myeloperoxidase: an enzyme involved in intrinsic vincristine resistance in human myeloblastic leukemia

One of the differences between acute myeloblastic leukemia (AML) and acute lymphoblastic leukemia (ALL) is their sensitivity to vincristine. Although vincristine plays an important role in chemotherapeutic regimens for ALL, it does not possess clinically significant activity in AML. Horseradish peroxidase, a heme-centered peroxidase, oxidatively degrades Vinca derivatives and thereby abrogates their cytotoxic activity. This finding suggested that myeloperoxidase (MPO), a heme- centered peroxidase characteristically found in AML and not in ALL, might also degrade vincristine. We first examined the effects of MPO on vincristine in a cell-free system and demonstrated that this enzyme is capable of catalyzing vincristine's oxidative breakdown. We also observed that vincristine is more rapidly degraded in tissue culture by MPO-positive HL-60 cells than by a MPO-negative HL-60 subclone. The degree of MPO activity in these cell lines correlated in a positive manner with their degree of resistance to vincristine's cytotoxic activity. Moreover, the differential resistance to vincristine observed between these cell lines could be increased by increasing the concentration of H2O2 available to the enzyme. These data support the hypothesis that MPO-mediated oxidation of vincristine accounts in part for this drug's lack of activity in AML.