What bycatch tells us about the diet of harbor and gray seals and overlap with commercial fishermen

Northwest Atlantic harbor (Phoca vitulina vitulina) and gray (Halichoerus grypus atlantica) seal populations are recovering from early to mid-20th century exploitation, increasing their biological interactions and bycatch in Northeastern US commercial fisheries. We evaluated the seals’ diet composition and compared their prey to commercial catches to assess trophic overlap and potential competition with commercial fisherman target catches. We obtained 148 harbor and 178 gray seal stomach samples from bycatch events that occurred between 2004 and 2018. We learned from the hard part remains that the majority of seals bycaught are young-of-the-year (≤12 months old) that consume a wide breadth of prey across three trophic groups. There was a general dichotomy in extrinsic factors associated with seal diet in which 45% trophic niche separation was explained by non-overlapping harbor and gray seal phenology and pup haul-out locations that are adjacent to active fishing areas. Prey size estimated from fish otoliths and squid beaks recovered from stomach contents showed that gray seals consumed larger prey than harbor seals and prey sizes from both seals showed limited overlap with prey sizes caught by commercial gillnet fishermen. The most important prey to both seals included large (>20 cm) and small (≤20 cm) silver hake (Merluccius bilinearis), (≤40 cm) red hake (Urophycis chuss), gulf stream flounder (Citharichthys arctifrons), medium (21–40 cm) white hake (Urophycis tenuis), and (<50 cm) Atlantic cod (Gadus morhua). Important prey to harbor seals that did not overlap with gray seals were Acadian redfish (Sebastes fasciatus), Atlantic herring (Clupea harengus), longfin (Doryteuthis pealeii), and shortfin squid (Illex illecebrosus). They contrasted with prey important to gray seals that did not overlap with harbor seals: yellowtail flounder (Limanda ferruginea), sand lance (Ammodytes spp.), Urophycis spp., and fourspot flounder (Hippoglossina oblonga). Despite the potential bias associated with opportunistic bycatch sampling, this study demonstrates the importance and value of utilizing carcasses retained from bycatch events, is complimentary to newer methodologies (i.e., DNA meta-barcoding), and fills data gaps in our understanding of the role recovering harbor and gray seal populations have on Northeastern US regional food webs

Pediatric Cushing disease: disparities in disease severity and outcomes in the Hispanic and African-American populations.

BackgroundLittle is known about the contribution of racial and socioeconomic disparities to severity and outcomes in children with Cushing disease (CD).MethodsA total of 129 children with CD, 45 Hispanic/Latino or African-American (HI/AA) and 84 non-Hispanic White (non-HW), were included in this study. A 10-point index for rating severity (CD severity) incorporated the degree of hypercortisolemia, glucose tolerance, hypertension, anthropomorphic measurements, disease duration, and tumor characteristics. Race, ethnicity, age, gender, local obesity prevalence, estimated median income, and access to care were assessed in regression analyses of CD severity.ResultsThe mean CD severity in the HI/AA group was worse than that in the non-HW group (4.9±2.0 vs. 4.1±1.9, P=0.023); driving factors included higher cortisol levels and larger tumor size. Multiple regression models confirmed that race (P=0.027) and older age (P=0.014) were the most important predictors of worse CD severity. When followed up a median of 2.3 years after surgery, the relative risk for persistent CD combined with recurrence was 2.8 times higher in the HI/AA group compared with that in the non-HW group (95% confidence interval: 1.2-6.5).ConclusionOur data show that the driving forces for the discrepancy in severity of CD are older age and race/ethnicity. Importantly, the risk for persistent and recurrent CD was higher in minority children

Diurnal Plasma Cortisol Measurements Utility in Differentiating Various Etiologies of Endogenous Cushing Syndrome

Cortisol diurnal variation may be abnormal among patients with endogenous Cushing syndrome (CS). The study objective was to compare the plasma cortisol AM/PM ratios between different etiologies of CS. This is a retrospective cohort study, conducted at a clinical research center. Adult patients with CS that underwent adrenalectomy or trans-sphenoidal surgery (n=105) were divided to those with a pathologically confirmed diagnosis of Cushing disease (n=21) and those with primary adrenal CS, including unilateral adrenal adenoma (n=28), adrenocortical hyperplasia (n=45), and primary pigmented nodular adrenocortical disease (PPNAD, n=11). Diurnal plasma cortisol measurements were obtained at 11:30 PM and midnight and at 7:30 and 8:00 AM. The ratios between the mean morning levels and mean late-night levels were calculated. Mean plasma cortisol AM/PM ratio was lower among CD patients compared to those with primary adrenal CS (1.4±0.6 vs. 2.3±1.5, p<0.001, respectively). An AM/PM cortisol ratio≥2.0 among patients with unsuppressed ACTH (>15 pg/ml) excludes CD with a 85.0% specificity and a negative predictive value (NPV) of 90.9%. Among patients with primary adrenal CS, an AM/PM cortisol≥1.2 had specificity and NPV of 100% for ruling out a diagnosis of PPNAD. Plasma cortisol AM/PM ratios are lower among patients with CD compared with primary adrenal CS, and may aid in the differential diagnosis of endogenous hypercortisolemia

Medullary thyroid cancer, leukemia, mesothelioma and meningioma associated with germline APC and RASAL1 variants: A new syndrome?

Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor hereditary in 35% of cases. The most common syndromic form is in the context of the multiple endocrine neoplasia type 2 (MEN 2) syndromes in association with other tumors and due to germline RET mutations. We describe a 57-year-old female patient diagnosed with sporadic MTC. The patient had a history of other neoplasias, such as acute myeloid leukemia, for which she had received chemotherapy, and two other solid tumors, peritoneal mesothelioma and meningioma. Genetic analyses were carried out including whole exome and Sanger sequencing (WES and SS) and loss-of-heterozygosity (LOH) testing for the respective loci. Immunohistochemistry (IHC) was used for the detection of proteins of interest. WES showed two germline variants in the APC and RASAL1 genes confirmed by SS. In MTC tissue only there was a RET variant identified by SS; germline studies did not show any RET sequence changes. The pattern of tumors in this patient is unusual for either one of the APC- or RASAL1-associated neoplasms and her non-MEN 2-associated MTC contained a RET variant like other sporadic MTCs. As in other patients with more than one genetic variant predisposing to tumors, it is possible that this case represents a unique association. © 2018, Hellenic Endocrine Society. All rights reserved

PRKAR1A gene analysis and protein kinase A activity in endometrial tumors

PRKAR1A codes for the type 1a regulatory subunit (RI alpha) of the cAMP-dependent protein kinase A (PKA), an enzyme with an important role in cell cycle regulation and proliferation. PKA dysregulation has been found in various tumors, and PRKAR1A-inactivating mutations have been reported in mostly endocrine neoplasias. In this study, we investigated PKA activity and the PRKAR1A gene in normal and tumor endometrium. Specimens were collected from 31 patients with endometrial cancer. We used as controls 41 samples of endometrium that were collected from surrounding normal tissues or from women undergoing gynecological operations for other reasons. In all samples, we sequenced the PRKAR1A-coding sequence and studied PKA subunit expression; we also determined PKA activity and cAMP binding. PRKAR1A mutations were not found. However, PKA regulatory subunit protein levels, both RI alpha and those of regulatory subunit type 2b (RII beta), were lower in tumor samples; cAMP binding was also lower in tumors compared with normal endometrium (P < 0.01). Free PKA activity was higher in tumor samples compared with that of control tissue (P < 0.01). There are significant PKA enzymatic abnormalities in tumors of the endometrium compared with surrounding normal tissue; as these were not due to PRKAR1A mutations, other mechanisms affecting PKA function ought to be explored. Endocrine-Related Cancer (2012) 19 457-46