Abstract Study Objective Few studies have examined the effects of maternal depressive symptoms among adolescent women. The purpose of this study was to investigate the impact of depressive symptoms ...on birth outcomes of infants born to adolescent mothers. Design The medical records of pregnant adolescent patients were examined. Information about maternal depressive symptoms and birth outcomes was collected. Setting Data were collected at Washington Hospital Center, a nonprofit, community-based hospital that serves residents throughout the Washington, DC area. Participants Participants were 294 African-American and Latina adolescent mothers. Mean age was 16.2 years (standard deviation SD 1.4). Based on self-reports of depressive symptoms, adolescents were categorized by the following: no reported symptoms, depressive symptoms without SI/SA (suicidal ideation or attempt), and depressive symptoms with SI/SA. Main Outcome Measures Infant birth weight and gestational age at delivery. Results Over one-quarter of pregnant adolescents in this study reported symptoms of depression. Adolescents reporting depressive symptoms with SI/SA delivered babies that weighed 239.5 grams (98.3% confidence interval CI 3.9 to 475.1) less than babies born to mothers reporting depressive symptoms without SI/SA. There was no association between reported symptoms and gestational age. Conclusions Results suggest that compared to nonpregnant teens and adults, pregnant teens may have an increased risk for depression. Additionally, pregnant adolescents with suicidal ideation are at greater risk for delivering infants of lower birth weight compared with teens reporting depressive symptoms without SI/SA and teens reporting no symptoms. This study supports the need for early screening and treatment of depression for young pregnant women.
A major limitation to the use of rat hepatocytes in the study of drug metabolism and toxicity is the rapid loss of CYPs. We demonstrate that the culture of rat hepatocytes results in a rapid loss of ...liver-specific CYP2C11 mRNA and transcripts encoding the general housekeeping gene copper-zinc superoxide dismutase (CuZnSOD) as well as poly(A(+)) mRNA. These losses are accelerated by fibronectin, which has no effect on the transcription of CYP2C11 and CuZnSOD. However, fibronectin, an extracellular matrix protein involved in cell adhesion and spreading, induces ribonuclease (RNase) activity. Fibronectin also increases hepatocyte diameter and data are presented that cell spreading is involved in the loss of both CYP2C11 and CuZnSOD mRNAs. The use of functional blocking antibodies demonstrates that fibronectin is operating through its alpha(5)beta(1) integrin receptor and genistein, a tyrosine kinase inhibitor, prevents hepatocyte spreading, RNase induction, and CYP2C11 mRNA loss. Collectively, the data indicate that hepatocytes in vitro actively promote the extinction of their phenotype via the autocrine effects of fibronectin rather than the current consensus that they simply lose differentiated function, such as CYP2C11 expression, through the absence of extracellular matrix proteins. The substrate specificity of the ribonuclease induced is also considered.
Background It is unknown whether intellectual disability (ID) is more familially related to psychotic mood disorders or schizophrenia. L. S. Penrose's large sample of families with two or more ...members admitted to psychiatric hospitals provided a unique opportunity to investigate the familial relationship between mild ID, schizophrenia and psychotic affective disorders.
Method There were 183 affected relative pairs comprising probands with mild ID (95 male, 88 female) and their first or second degree relatives with schizophrenia or psychotic affective disorder.
Results There were nearly twice as many relatives with a diagnosis of schizophrenia (n = 121) as relatives with affective disorders (n = 62) among the intellectually impaired probands. This excess of schizophrenia was statistically significant, even after accounting for the increased risk of hospitalization for schizophrenia (P = 0.005), and was fairly constant across the different relative types. First‐degree relatives with either mental illness were more likely to be parents (n = 77) than siblings (n = 51) or children (n = 3), but there was no excess of mother–son pairs.
Conclusions These results suggest a stronger familial relationship of ID with schizophrenia than psychotic affective disorder, and lend some support to the neurodevelopmental hypothesis of schizophrenia.
The introduction of effective antibacterial therapies for infectious diseases in the mid‐20th century completely revolutionized clinical practices and helped to facilitate the development of modern ...medicine. Many potentially life‐threatening conditions became easily curable, greatly reducing the incidence of death or disability resulting from bacterial infections. This overwhelming historical success makes it very difficult to imagine life without effective antibacterials; however, the inexorable rise of antibiotic resistance has made this a very real and disturbing possibility for some infections. The ruthless selection for resistant bacteria, coupled with insufficient investment in antibacterial research, has led to a steady decline in the efficacy of existing therapies and a paucity of novel structural classes with which to replace them, or complement their use. This situation has resulted in a very pressing need for the discovery of novel antibiotics and treatment strategies, the development of which is likely to be a key challenge to 21st century medicinal chemistry.
Resistance is futile: With bacterial resistance on the rise, a number of approaches are currently being explored to ensure that new drugs are being brought to the clinic. It is necessary for the next generation of antibacterials to not only have an improved drug profile but also overcome the latest bacterial resistance mechanisms. Insight into the current strategies being developed is discussed, in particular recent research within the area of quinolone quorum sensing modulators.
Leading scholars and publishers from ten countries have agreed a definition of predatory publishing that can protect scholarship. It took 12 hours of discussion, 18 questions and 3 rounds to reach.
Neuronal plasticity is a fundamental factor in cognitive outcome following traumatic brain injury. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, plays an important ...role in this process. While there are many ways to measure cognitive outcome, general cognitive intelligence is a strong predictor of everyday decision-making, occupational attainment, social mobility and job performance. Thus it is an excellent measure of cognitive outcome following traumatic brain injury (TBI). Although the importance of the single-nucleotide polymorphisms polymorphism on cognitive function has been previously addressed, its role in recovery of general intelligence following TBI is unknown. We genotyped male Caucasian Vietnam combat veterans with focal penetrating TBI (pTBI) (n = 109) and non-head injured controls (n = 38) for 7 BDNF single-nucleotide polymorphisms. Subjects were administrated the Armed Forces Qualification Test (AFQT) at three different time periods: pre-injury on induction into the military, Phase II (10-15 years post-injury, and Phase III (30-35 years post-injury). Two single-nucleotide polymorphisms, rs7124442 and rs1519480, were significantly associated with post-injury recovery of general cognitive intelligence with the most pronounced effect at the Phase II time point, indicating lesion-induced plasticity. The genotypes accounted for 5% of the variance of the AFQT scores, independently of other significant predictors such as pre-injury intelligence and percentage of brain volume loss. These data indicate that genetic variations in BDNF play a significant role in lesion-induced recovery following pTBI. Identifying the underlying mechanism of this brain-derived neurotrophic factor effect could provide insight into an important aspect of post-traumatic cognitive recovery.
Autosomal-dominant arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) causes sudden cardiac death and is characterized by clinical and genetic heterogeneity. Fifteen unrelated ARVC ...families with a disease-associated haplotype on chromosome 3p (ARVD5) were ascertained from a genetically isolated population. Identification of key recombination events reduced the disease region to a 2.36 Mb interval containing 20 annotated genes. Bidirectional resequencing showed one rare variant in transmembrane protein 43 (TMEM43 1073C→T, S358L), was carried on all recombinant ARVD5 ancestral haplotypes from affected subjects and not found in population controls. The mutation occurs in a highly conserved transmembrane domain of TMEM43 and is predicted to be deleterious. Clinical outcomes in 257 affected and 151 unaffected subjects were compared, and penetrance was determined. We concluded that ARVC at locus ARVD5 is a lethal, fully penetrant, sex-influenced morbid disorder. Median life expectancy was 41 years in affected males compared to 71 years in affected females (relative risk 6.8, 95% CI 1.3–10.9). Heart failure was a late manifestation in survivors. Although little is known about the function of the TMEM43 gene, it contains a response element for PPARγ (an adipogenic transcription factor), which may explain the fibrofatty replacement of the myocardium, a characteristic pathological finding in ARVC.
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