University of Arkansas for Medical Sciences

About: University of Arkansas for Medical Sciences is a education organization based out in Little Rock, Arkansas, United States. It is known for research contribution in the topics: Population & Health care. The organization has 14077 authors who have published 26012 publications receiving 973592 citations. The organization is also known as: UAMS.

The nonrandom distribution of facial hemangiomas.

Abstract: Objective To map sites of occurrence of facial infantile hemangiomas and correlate these with pattern of tumor growth, clinical complications, and proximity to structural and developmental landmarks. Design A retrospective medical record review of 205 patients diagnosed with facial infantile hemangioma. Setting Arkansas Children's Hospital, Little Rock, a 250-bed teaching hospital affiliated with the University of Arkansas for Medical Sciences. Patients Based on their clinical photographs, 232 of the hemangiomas were mapped on a facial schematic. Each lesion was encoded with a number reflective of its location, and this number was shared by other lesions occurring at the same site. Frequencies of complicating ulceration and airway obstruction were determined by medical record review. Results Two patterns of tumor growth were evident among the hemangiomas analyzed: focal (177 lesions [76.3%]) and diffuse (55 lesions [23.7%]). The focal hemangiomas mapped to 22 sites of occurrence, all near lines of mesenchymal or mesenchymal-ectodermal embryonic fusion. The 55 diffuse hemangiomas showed a segmental tissue distribution and thus were designated as frontonasal (15 lesions [27%]), maxillary (19 lesions [35%]), or mandibular (21 lesions [38%]). Ulceration was 3 times more common in patients with diffuse hemangiomas (21 [51%] of 41) than in patients with focal hemangiomas (28 [17%] of 164). Airway obstruction was characteristic of diffuse mandibular hemangiomas. Conclusions Facial infantile hemangiomas occurred in 2 distinct patterns of tissue involvement: a focal type with a tumorlike appearance and a less common diffuse type with a plaquelike appearance. The diffuse lesions were more likely to be complicated by ulceration or airway obstruction and showed a strikingly segmental distribution pattern. Focal hemangiomas, in contrast, showed a predilection for regions of embryological fusion.

Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice.

Abstract: Aging or glucocorticoid excess decrease bone strength more than bone mass in humans and mice, but an explanation for this mismatch remains elusive. We report that aging in C57BL/6 mice was associated with an increase in adrenal production of glucocorticoids as well as bone expression of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1, the enzyme that activates glucocorticoids. Aging also decreased the volume of the bone vasculature and solute transport from the peripheral circulation to the lacunar-canalicular system. The same changes were reproduced by pharmacologic hyperglucocorticoidism. Furthermore, mice in which osteoblasts and osteocytes were shielded from glucocorticoids via cell-specific transgenic expression of 11beta-HSD type 2, the enzyme that inactivates glucocorticoids, were protected from the adverse effects of aging on osteoblast and osteocyte apoptosis, bone formation rate and microarchitecture, crystallinity, vasculature volume, interstitial fluid, and strength. In addition, glucocorticoids suppressed angiogenesis in fetal metatarsals and hypoxia inducible factor-1alpha transcription and vascular endothelial growth factor production in osteoblasts and osteocytes. These results, together with the evidence that dehydration of bone decreases strength, reveal that endogenous glucocorticoids increase skeletal fragility in old age as a result of cell autonomous effects on osteoblasts and osteocytes leading to interconnected decrements in bone angiogenesis, vasculature volume, and osteocyte-lacunar-canalicular fluid.

Inclusion of Sarcopenia Within MELD (MELD-Sarcopenia) and the Prediction of Mortality in Patients With Cirrhosis

Abstract: Inclusion of Sarcopenia Within MELD (MELD-Sarcopenia) and the Prediction of Mortality in Patients With Cirrhosis

APOBEC family mutational signatures are associated with poor prognosis translocations in multiple myeloma

Abstract: We have sequenced 463 presenting cases of myeloma entered into the UK Myeloma XI study using whole exome sequencing. Here we identify mutations induced as a consequence of misdirected AID in the partner oncogenes of IGH translocations, which are activating and associated with impaired clinical outcome. An APOBEC mutational signature is seen in 3.8% of cases and is linked to the translocation-mediated deregulation of MAF and MAFB, a known poor prognostic factor. Patients with this signature have an increased mutational load and a poor prognosis. Loss of MAF or MAFB expression results in decreased APOBEC3B and APOBEC4 expression, indicating a transcriptional control mechanism. Kataegis, a further mutational pattern associated with APOBEC deregulation, is seen at the sites of the MYC translocation. The APOBEC mutational signature seen in myeloma is, therefore, associated with poor prognosis primary and secondary translocations and the molecular mechanisms involved in generating them.

A meta-analysis identifies new loci associated with body mass index in individuals of African ancestry.

Abstract: Genome-wide association studies (GWAS) have identified 36 loci associated with body mass index (BMI), predominantly in populations of European ancestry. We conducted a meta-analysis to examine the association of >3.2 million SNPs with BMI in 39,144 men and women of African ancestry, and followed up the most significant associations in an additional 32,268 individuals of African ancestry. We identified one novel locus at 5q33 (GALNT10, rs7708584, p=3.4×10−11) and another at 7p15 when combined with data from the Giant consortium (MIR148A/NFE2L3, rs10261878, p=1.2×10−10). We also found suggestive evidence of an association at a third locus at 6q16 in the African ancestry sample (KLHL32, rs974417, p=6.9×10−8). Thirty-two of the 36 previously established BMI variants displayed directionally consistent effect estimates in our GWAS (binomial p=9.7×10−7), of which five reached genome-wide significance. These findings provide strong support for shared BMI loci across populations as well as for the utility of studying ancestrally diverse populations.