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Objective

To examine endometrial cancer survivors' access to recommended obesity-related self-care resources.

Methods

Participants included women treated 2010–2015 for endometrial cancer at an academic medical center who lived in the surrounding 16 ZIP code area on Chicago's South Side. Demographic and health data were abstracted from medical records. A socioeconomic status (SES) score (SES-1?=?low, SES-5?=?high) was generated for each patient using census block group-level data. Self-care resources for exercise, healthy weight, and diet were obtained from a community resource census. Geospatial techniques assessed “walkable access” (~½-mile radius around a patient's home) to obesity-related resources. Multivariable logistic regression investigated associations between access to obesity-related resources and patient characteristics.

Results

Of 195 endometrial cancer survivors, 81% identified as Black/African American and 34% lived in an SES-1 census block. Two thirds (68%) had Stage I or II endometrial cancer. Nearly two thirds (62%) were obese (BMI?≥?30?kg/m2). Obesity was inversely associated with SES (p?=?0.05). Two thirds of survivors had access to at least one of all three recommended resource types. Access was lower in low SES regions and among Black/African American women. Lower SES was associated with lower odds of walkable access to recommended resources (AOR for access to two of each resource type 0.75, 95%CI 0.59, 0.97; AOR for access to three or more of each 0.44, 95%CI 0.32, 0.61).

Conclusions

Obesity rates were higher and access to recommended resources was lower for Black/African American endometrial cancer survivors living in high poverty areas in Chicago.  相似文献   
58.
The epidermal growth factor receptor (EGFR) regulates multiple patterning events in Drosophila limb development, but its role in vertebrate limb morphogenesis has received little attention. The EGFR and several of its ligands are expressed in developing vertebrate limbs in manners consistent with potential patterning roles. To gain insight into functions of EGFR signaling in vertebrate limb development, we expressed a constitutively active EGFR in developing chick limbs in ovo. Expression of activated EGFR causes pre- and postaxial polydactyly, including mirror-image-type digit duplication, likely due to induction of ectopic expression and/or modulation of genes involved in anterior-posterior (AP) patterning such as Sonic hedgehog (Shh), dHand, Patched (Ptc), Gli3, Hoxd13, Hoxd11, bone morphogenetic protein 2 (Bmp2), Gremlin, and FGF4. Activation of EGFR signaling dorsalizes the limb and alters expression of the dorsal-ventral (DV) patterning genes Wnt7a, Lmx, and En1. Ectopic and/or extended FGF8 expressing apical ectodermal ridges (AERs) are also seen. Interdigital regression is inhibited and the digits fail to separate, leading to syndactyly, likely due to antiapoptotic and pro-proliferative effects of activated EGFR signaling on limb mesoderm, and/or attenuation of interdigital Bmp4 expression. These findings suggest potential roles for EGFR signaling in AP and DV patterning, AER formation, and cell survival during limb morphogenesis.  相似文献   
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Gelatinous marrow transformation (GMT) is an uncommon and poorly recognized condition characterized by deposition of seromucinous gelatinous material in the bone marrow stroma. Forty-three cases of GMT were studied in a period of 4 years. There was male preponderance. Fourteen cases were in pediatric age group (less than 12 years). Majority of patients had a preceding history of anorexia, malnutrition and chronic debility. All the patients had anemia. Bone marrow biopsy revealed focal or diffuse GMT. Bone marrow aspirate showed metachromatic dense mucoid material with a few entrapped hematopoietic cells on Giemsa staining. The gelatinous material stained with alcian blue at pH 2.5.  相似文献   
60.
Heme oxygenase-1 (HO-1) is a stress-induced enzyme that catalyses the oxidation of heme to biliverdin. The primary deficiency of this enzyme has been shown in HO-1 knockout mice, and is characterized by intrauterine death and chronic inflammation. The first case of human HO-1 deficiency was reported in 1999. Human HO-1 deficiency has been observed to involve the endothelial cells more severely, resulting in hemolysis and disseminated intravascular coagulation. We report another case of human HO-1 deficiency in a young girl with congenital asplenia, who presented with severe hemolysis, inflammation, nephritis, which was refractory to therapy with corticosteroids, cyclophosphamide, and rituximab.  相似文献   
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