337 research outputs found
Rethinking Legislative Consent Law?
This book is designed to be used as a supplemental text in children's literature and reading/language art courses at the pre-service and graduate levels. The text contains seven chapters: three of wich set the stage for teaching effectively with childern's literature and four of wich provide examples of activities using specific children's books.xv, 164 p.; ill.: 28 c
Parenting and Attachment among Low-Income African-American and Caucasian Preschoolers
Despite a plethora of research on parenting and infant attachment, much less is known about the contributions of parenting to preschool attachment, particularly within different racial groups. This study seeks to build on the extant literature by evaluating whether similar associations between parenting and attachment can be observed in African American and Caucasian families, and whether race moderates them. Seventy-four primary caregivers and their preschool children (51% African American, 49% Caucasian, 46% male) from similar urban, low income backgrounds participated in two visits four weeks apart when children were between four and five years of age. Attachment was scored from videotapes of the Strange Situation paradigm using the preschool classification system developed by Cassidy, Marvin, and the MacArthur Working Group. Parenting was assessed using a multi-method, multi-context approach: in the child’s home, in the laboratory, and via parent-report. Seventy-three percent of the children were classified as securely attached. Warm, responsive parenting behavior (but not race) predicted attachment. Although parents of African American and Caucasian children demonstrated some significant differences in parenting behaviors, race did not moderate the relationship between parenting and child attachment. These findings highlight the direct role that parenting plays over and above race in determining attachment security during the preschool period
Machine Learning and Irresponsible Inference: Morally Assessing the Training Data for Image Recognition Systems
Just as humans can draw conclusions responsibly or irresponsibly, so too can computers. Machine learning systems that have been trained on data sets that include irresponsible judgments are likely to yield irresponsible predictions as outputs. In this paper I focus on a particular kind of inference a computer system might make: identification of the intentions with which a person acted on the basis of photographic evidence. Such inferences are liable to be morally objectionable, because of a way in which they are presumptuous. After elaborating this moral concern, I explore the possibility that carefully procuring the training data for image recognition systems could ensure that the systems avoid the problem. The lesson of this paper extends beyond just the particular case of image recognition systems and the challenge of responsibly identifying a person’s intentions. Reflection on this particular case demonstrates the importance (as well as the difficulty) of evaluating machine learning systems and their training data from the standpoint of moral considerations that are not encompassed by ordinary assessments of predictive accuracy
Thresholds and timing of pre-operative thrombocytosis and ovarian cancer survival: analysis of laboratory measures from electronic medical records
Obesity-Induced Peritoneal Dissemination of Ovarian Cancer and Dominant Recruitment of Macrophages in Ascites
One-fifth of cancer deaths are associated with obesity. Because the molecular mechanisms by which obesity affects the progression of ovarian cancer (OC) are poorly understood, we investigated if obesity could promote the progression of OC cells using the postmenopausal ob/ob mouse model and peritoneal dissemination of mouse ID8 OC cells. Compared to lean mice, obese mice had earlier OC occurrence, greater metastasis throughout the peritoneal cavity, a trend toward shorter survival, and higher circulating glucose and proinflammatory chemokine CXCL1 levels. Ascites in obese mice had higher levels of macrophages (Mφ) and chemokines including CCL2, CXCL12, CXCL13, G-CSF and M-CSF. Omental tumor tissues in obese mice had more adipocytes than lean mice. Our data suggest that obesity may accelerate the peritoneal dissemination of OC through higher production of pro-inflammatory chemokines and Mφ recruitment
More than maternal sensitivity shapes attachment : infant coping and temperament
The aim of this longitudinal studywas to investigate the effect of a set of factors from multiple levels of influence: infant temperament, infant regulatory behavior, and maternal sensitivity on infant’s attachment.
Our sample consisted of 48 infants born prematurely and their mothers. At 1 and 3 months of age, mothers described their infants’behavior using the Escala de Temperamento do Beb´e. At 3 months of
age, infants’ capacity to regulate stress was evaluated during Tronick’s Face-to-Face Still-Face (FFSF) paradigm. At 9 months of age, mothers’ sensitivity was evaluated during free play using the CARE-Index.
At 12 months of age, infants’ attachment security was assessed during Ainsworth’s Strange Situation. A total of 16 infants were classified as securely attached, 17 as insecure-avoidant, and 15 as insecure-resistant. Mothers of securely attached infantswere more likely than mothers of insecure infants to describe their infants as less difficult and to be more sensitive
to their infants in free play. In turn, secure infants exhibited more positive responses during the Still-Face. Infants classified as insecureavoidant were more likely to self-comfort during the Still-Face and had mothers who were more controlling during free play. Insecure-resistant exhibited higher levels of negative arousal during the Still-Face and had mothers who were more unresponsive in free play. These findings show that attachment quality is influenced bymultiple factors, including infant temperament, coping behavior, and maternal sensitivity
High-Fat Diet-Induced Obese Effects of Adipocyte-Specific CXCR2 Conditional Knockout in the Peritoneal Tumor Microenvironment of Ovarian Cancer
Obesity contributes to ovarian cancer (OC) progression via tumorigenic chemokines. Adipocytes and OC cells highly express CXCR2, and its ligands CXCL1/8, respectively, indicating that the CXCL1/8-CXCR2 axis is a molecular link between obesity and OC. Here, we investigated how the adipocyte-specific CXCR2 conditional knockout (cKO) affected the peritoneal tumor microenvironment of OC in a high-fat diet (HFD)-induced obese mouse model. We first generated adipocyte-specific CXCR2 cKO in mice: adipose tissues were not different in crown-like structures and adipocyte size between the wild-type (WT) and cKO mice but expressed lower levels of CCL2/6 compared to the obese WT mice. HFD-induced obese mice had a shorter survival time than lean mice. Particularly, obese WT and cKO mice developed higher tumors and ascites burdens, respectively. The ascites from the obese cKO mice showed increased vacuole clumps but decreased the floating tumor burden, tumor-attached macrophages, triglyceride, free fatty acid, CCL2, and TNF levels compared to obese WT mice. A tumor analysis revealed that obese cKO mice attenuated inflammatory areas, PCNA, and F4/80 compared to obese WT mice, indicating a reduced tumor burden, and there were positive relationships between the ascites and tumor parameters. Taken together, the adipocyte-specific CXCR2 cKO was associated with obesity-induced ascites despite a reduced tumor burden, likely altering the peritoneal tumor microenvironment of OC
CXCR2 is a negative regulator of p21 in p53-dependent and independent manner via Akt-mediated Mdm2 in ovarian cancer
Ovarian cancer (OC) has the highest rate of mortality among gynecological malignancy. Chemokine receptor CXCR2 in OC is associated with poor outcomes. However, the mechanisms by which CXCR2 regulates OC proliferation remain poorly understood. We generated CXCR2-positive cells from parental p53 wild-type (WT), mutant and null OC cells, and assessed the roles of CXCR2 on proliferation of OC cells in p53-dependent and independent manner. CXCR2 promoted cell growth rate: p53WT \u3e mutant = null cells. Nutlin-3, a p53 stabilizer, inhibited cell proliferation in p53WT cells, but had little effect in p53-mutant or null cells, indicating p53-dependence of CXCR2-mediated proliferation. CXCR2 decreased p53 protein, a regulator of p21, and downregulated p21 promoter activity only in p53WT cells. The p53 responsive element (RE) of p21 promoter played a critical role in this CXCR2-mediated p21 downregulation. Moreover, CXCR2-positive cells activated more Akt than CXCR2-negative cells followed by enhanced murine double minute (Mdm2). Silencing Mdm2 or Akt1 upregulated p21 expression, whereas Akt1 overexpression downregulated p21 at the promoter and protein levels in p53WT cells. Cell cycle analysis revealed that CXCR2 decreased p21 gene in p53-null cells. Interestingly, romidepsin (histone deacetylase inhibitor)-induced p21 upregulation did not involve the p53 RE in the p21 promoter in p53-null cells. Romidepsin decreased the protein levels of Akt1 and Mdm2, leading to induction of p21 in p53-null cells. CXCR2 reduced romidepsin-induced p21 upregulation by activating Akt-induced Mdm2. Taken together, CXCR2 enhances cell proliferation by suppressing p21 through Akt-Mdm2 signaling in p53-dependent and independent manner
School support, chaos, routines, and parents' mental health during COVID-19 remote schooling
Remote schooling due to Coronavirus Disease 2019 (COVID-19) created profound challenges for families. In this investigation, we examined parents' depression and anxiety during remote schooling and their associations with parents' reports of school support. We also evaluated indirect and interactive (i.e., moderation) associations. Participants were parents (N = 152, 92.8% mothers, 65.1% Black) from an urban area with high rates of COVID-19. Of the 152 parents, 27.6% reported elevated levels of depression and 34.2% reported elevated anxiety. Regression analyses showed that school support was negatively associated with parents' depression (β = -.33, p < .01) and anxiety (β = -.21, p < .01). There was an indirect association between school support and parents' mental health via household chaos and daily routines. Reported COVID-19 impact moderated the direct association between school support and parental depression and anxiety. There was a statistically significant association between school support and parents' depression and anxiety when COVID-19 impact was low or moderate, but not when COVID-19 impact was high. These results may suggest that for parents who were not highly impacted by the pandemic, school support buffered the association between stress and parents' mental health problems; parents most impacted by COVID-19 may need additional support. (PsycInfo Database Record (c) 2022 APA, all rights reserved).K01 MH110600 - NIMH NIH HHS; L40 MH117714 - NIMH NIH HHSAccepted manuscrip
BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers
Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers.
Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided.
Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed.
Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations
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