Adolescent childbearing revisited: the age of inner-city mothers at delivery is a determinant of their children's self-sufficiency at age 27 to 33

OBJECTIVES: Data from recent interviews with 1758 inner-city children, born between 1960 to 1965 and followed with their mothers in the Pathways to Adulthood Study to age 27 to 33 years, were used to address two related questions. 1) Is maternal age, across the reproductive age range, a determinant of child's adult outcome? and 2) Do covariates of maternal age at delivery reduce or eliminate the effect of maternal age on child's adult outcome? METHODS: An intergenerational life course model of development identified significant maternal and child characteristics at birth associated with the child's self-sufficient outcomes in adulthood: education (more than or equal to a high school diploma); financial independence of public support; and delay of first birth until age 20 or older. Bivariate and multiple logistic regression techniques were used to identify independent relationships between dependent and independent variables and to adjust the outcomes to compensate for the effect of possible confounding of maternal age at delivery by maternal education, parity, poverty status, and the child's race and gender. RESULTS: Each covariate was independently associated with maternal age at delivery. Adjustment for their effects reduced, but did not eliminate, the association between maternal age at birth and the child's outcome at age 27 to 33 years. As a group, children of the oldest mothers (>/=25 years of age) had the most favorable outcomes, and those of teenage mothers (<20 years of age) had the least favorable outcomes; 22% of daughters and 6% of sons of the oldest mothers versus 38% and 18%, respectively, of the youngest mothers became teenage parents. CONCLUSION: The mother's age at delivery is an independent determinant of the child's adult status.     

Time course comparison of cell-cycle protein expression following partial hepatectomy and WY14,643-induced hepatic cell proliferation in F344 rats

During recent years, there has been an extensive research focus in the area of cell-cycle control in eukaryotes and the relationship that exists between cell proliferation and cancer. The eukaryotic cell-cycle is governed by signal transduction pathways mediated by complexes of cyclin dependent kinases (CDK) and their partner cyclin proteins. This study was performed to identify differences in cell-cycle control protein expression following physical and chemical stimuli of hepatic cell growth. Protein levels of cell cycle mediators, cyclin dependent kinases (CDK 1,2,4,5), cyclin proteins (A,B,D1-D3 and E), proliferating cell nuclear antigen (PCNA), tumor suppressor proteins (p53 and Rb), and CDK inhibitory proteins (p16Ink4, p21Waf1 and p27Kip1) were examined in F344 rats following 70% partial hepatectomy or a single dose of WY14,643 over 96- and 48-h time courses, respectively. CDK1 (p34cdc2) and PCNA protein concentrations, quantified by ELISA, were significantly increased beginning at the 24-h time point and maximal at 48 h (6.9- and 3.7-fold for partial hepatectomy and 4.2- and 3.3-fold for WY14,643, respectively). Differential effects were observed with the G1 cell-cycle mediators CDK4, CDK5, and cyclin D3, p21Waf1 and p27Kip1 CDK inhibitory protein concentrations rose in accordance with the induction of DNA synthesis and histone H1 kinase activity. In addition, there were dramatic differences in p53 protein expression patterns following partial hepatectomy versus WY14,643 dosing. Because non-genotoxic hepatocarcinogens are known to induce cellular proliferation, data generated from this study may aid in elucidating the specific hepatocarcinogenic signal transduction pathways stimulated by non-genotoxic carcinogens.      

The elevation of blood levels of zinc protoporphyrin in mice following whole body irradiation

Elevation of zinc protoporphyrin (ZPP) levels in the blood has served as an indicator of lead poisoning and iron deficiency anemia for many years. We have discovered that sublethal doses of whole body irradiation with x-rays also elevates ZPP 2-3-fold over normal levels. The ZPP level does not begin to increase until days 12-14 postirradiation and peaks between days 18 and 20 before returning to normal levels between days 28 and 35. Increasing the radiation dose delays the onset of the rise in ZPP, but does not affect the magnitude of the elevation. At lethal doses, ZPP elevation is not observed. Neither of the two previously described mechanisms that cause elevations of ZPP, namely iron deficiency and inhibition of ferrochelatase, are responsible for the radiation-induced elevation of ZPP. The elevation of ZPP appears to be correlated with the recovery of the hematopoietic system from radiation injury.     

Chemical transformation of mouse liver cells results in altered cyclin D-CDK protein complexes

Dysregulated cell proliferation is one phenotypic change associated with neoplasia. Key protein complexes involved in regulating cell division are composed of cyclins, cyclin-dependent kinases (CDK) and CDK inhibitors (CDI). Many virally transformed cells in culture exhibit disrupted cyclin-CDK-CDI complexes, suggesting that such changes may play a mechanistic role in viral transformation. To determine whether similar alterations may be involved in chemical carcinogenesis we characterized cyclin D1-CDK-CDI protein complexes in a non-tumorigenic mouse liver cell line and investigated whether complexes were altered after transformation with the genotoxic carcinogens N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) or 3-methylcholanthrene (MC). In non- tumorigenic mouse liver cells cyclin D1 associated with CDK6, CDK4 or CDK2 to form binary (cyclin D1-CDK), tertiary (cyclin D1-CDK-p27KIP1) or quaternary (cyclin D1-CDK-p21WAF1-PCNA) complexes. After chemical transformation of mouse liver cells with either MC or MNNG, select cyclin D1-CDK-CDI protein complexes were altered. In MC-transformed cells formation of various binary, tertiary and quaternary cyclin D1- CDK-(CDI) protein complexes was reduced, resulting in decreased CDK4 kinase activity. Interestingly, CDK6 kinase activity was dramatically elevated due to high levels of cyclin D3 in association with CDK6. In MNNG-transformed cells select cyclin D1-CDK6-CDI and cyclin D1-CDK2-CDI protein complexes were altered but CDK6 and CDK4 kinase activity remained unaffected. Distinct changes in cyclin D1-CDK-CDI complexes found between the two chemically transformed mouse liver cell lines suggest that each cell line harbored unique mutations or alterations that differentially contributed to stabilization of cyclin D1-CDK-CDI holoenzymes. p53 gene mutations were not detected in the MC- or MNNG- transformed mouse liver cell lines and thus were not involved in disrupting cyclin D1-CDK-CDI protein complexes. In summary, this study presents evidence that D-type CDK protein complexes can be altered physically and functionally after chemical transformation with genotoxic carcinogens, suggesting that components of the cell cycle machinery can be targeted during chemical carcinogenesis.      

Tissue characterization of the testes using ultrasonic CT. Work in progress

Ultrasonic computed tomography (UCT) can aid in characterizing tissue for the detection and diagnosis of leukemic infiltration of the testes. Preliminary studies in 6 healthy adults and 26 patients (3-20 years old) with leukemia or non-Hodgkin lymphoma suggest that elevated speed of sound in the testis may be an indicator of leukemic infiltration. UCT may become an important screening method for detecting testicular involvement. In long-term follow-up, UCT can be performed more frequently and easily than biopsy, which is the current screening method.     

跆拳道运动员运动损伤的调查

目的:调查分析跆拳道运动员发生运动损伤的常见部位和损伤原因及损伤发生率。方法:于2005-03选择南京体育学院运动系跆拳道专选队学生33人,男20人,女13人,年龄21～25岁,专项训练平均年限3.5年。纳入对象均对调查项目知情同意。由被调查者自行填写自拟调查问卷,该问卷主要内容为损伤的部位、损伤的原因。结果:学生33名均进入结果分析。共发放问卷33份,收回填写完整、准确的问卷33份,收回率100%。①损伤部位:踝关节损伤、膝关节损伤、足损伤、大腿损伤、腰损伤、小腿损伤、肘损伤、手损伤分别为24人次(25%),21人次(21.9%),15人次(15.6%),9人次(9.4%),15人次(15.6%),8人次(8.3%),2人次(2.1%),2人次(2.1%)。②损伤发生率:纳入跆拳道运动员33名均发生运动损伤,损伤率100%,损伤96人次,人均受伤2.91次。③损伤原因:跆拳道损伤多发生在专项训练和比赛时,占38.49%;身体素质差引起的运动损伤,占19.67%;准备活动不科学也是造成运动损伤不容忽视的因素,占12.97%。结论:跆拳道运动损伤部位以踝关节和膝关节为主,损伤多发生于专项训练和比赛时。     

Characteristics of elderly blood donors

The aging of our society will result in an increased demand for blood components, but it also has the potential to produce a large group of blood donors, the elderly. To study the effects of regular donation by older persons, a randomized, controlled trial is being conducted among 244 healthy, elderly volunteers. This report focuses on the efficacy of the recruiting efforts for that study and describes the resultant population in terms of their demographics, medical status, and donation safety. Of 325 potential subjects, 18 percent were disqualified and 7 percent refused entry into the study. After medical evaluation, only 2 persons were disqualified for conditions not detected by the usual blood services screening protocols. The resultant elderly donor population (n = 244) was well-educated, middle-income, and, for the most part, married. The group reported more past and present medical conditions, past surgical procedures, and current medications than would be expected in a younger donor group. Reactions to donation were infrequent and mild. With current screening and donation procedures, blood donation by the elderly appears to be safe and practical.     

The emerging syndrome of envenoming by the New Guinea small-eyed snake Micropechis ikaheka

The New Guinea small-eyed or Ikaheka snake, <it>Micropechis ikaheka</it>, which occurs throughout New Guinea and some adjacent islands, is feared by the indigenes. The first proven human fatality was in the 1950s and this species has since been implicated in many other cases of severe and fatal envenoming. Reliable attribution of envenoming to this species in victims unable to capture or kill the snake recently became possible by the use of enzyme immunoassay. Eleven cases of proven envenoming by <it>M. ikaheka</it>, with two fatalities, were identified in Papua New Guinea and Irian Jaya. Five patients showed no clinical signs of envenoming by other Australasian elapids: mild local swelling, local lymphadenopathy, neurotoxicity, general myalgia, spontaneous systemic bleeding, incoagulable blood and passage of dark urine (haemoglobinuria or myoglobinuria). Two patients developed hypotension and two died of respiratory paralysis 19 and 38 h after being bitten. <it>In vitro</it> studies indicate that the venom is rich in phospholipase A2, is indirectly haemolytic, anticoagulant and inhibits platelets, but is not procoagulant or fibrinolytic. It shows predominantly post-synaptic neurotoxic and myotoxic activity. Anecdotally, Commonwealth Serum Laboratories' (CSL) death adder antivenom has proved ineffective whereas CSL polyvalent antivenom may be beneficial. Anticholinesterase drugs might prove effective in improving neuromuscular transmission and should be tested in patients with neurotoxic envenoming.