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SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
The limbs develop from small protrusions (the limb buds) that arise from the body wall of the embryo. Positioning and patterning the limb involves cellular interactions between the ectoderm surrounding the limb bud (apical ectodermal ridge) and the mesenchymal cells that form the core of the limb bud.
Hands
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
Apical ectodermal ridge (AER). The mesoderm of the limb bud induces the overlying ectodermal cells to elongate, become pseudostratified and form the AER. Both the AER and the underlying mesoderm are required for limb development – removal of the AER or loss of contact of the AER with limb bud mesoderm prevents limb development. Removing the AER early results in a severely truncated limb (e.g. formation of a humerus only).
Skeletal Embryology and Limb Growth
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Rick Brown, Anish Sanghrajka, Deborah Eastwood
The ectoderm covering the distal tip of the limb bud, under the influence of bone morphogenetic protein (BMP), thickens to form the apical ectodermal ridge (AER). The AER is essential for growth and development of the limb, particularly its width and dorsoventral axis. Beneath the AER is the progress zone (PZ), in which undifferentiated mesenchymal cells rapidly proliferate resulting in longitudinal outgrowth of the limb (proximodistal axis). The anteroposterior axis (thumb to little finger) is regulated by the zone of polarizing activity (ZPA), a mass of cells within the posterior aspect of the limb bud. The dorsoventral axis (dorsal to volar) is regulated by a complex interaction between Wnt (dorsal) and engrailed (ventral) proteins.
Baseline anxiety disorders are associated with progression of diabetic kidney disease in type 2 diabetes
Published in Renal Failure, 2023
Bin Han, Ling Wang, Yueyue Zhang, Lijie Gu, Weijie Yuan, Wei Cao
Kidney status was evaluated on the basis of AER in at least two of three overnight or consecutive timed 24-h urine collections. Accordingly, participants were divided into four classifications: normal AER (<30 mg/24 h or <20 μg/min), microalbuminuria (≥30 but <300 mg/24 h or ≥20 but <200 µg/min), macroalbuminuria (≥300 mg/24 h or ≥200 μg/min), and kidney failure (having received a kidney transplantation or undergoing dialysis). DKD progression was identified as the transition from one AER stage to the next stage or the development of kidney failure (i.e., from normal AER at baseline to either microalbuminuria, macroalbuminuria, or kidney failure; or from microalbuminuria at baseline to either macroalbuminuria, or kidney failure; or from macroalbuminuria at baseline to kidney failure). Data on progression were derived from the medical records during the follow-up period.
Neurologic disorders in long-term survivors of neuroblastoma – a population-based cohort study within the Adult Life after Childhood Cancer in Scandinavia (ALiCCS) research program
Published in Acta Oncologica, 2020
Filippa Nyboe Norsker, Catherine Rechnitzer, Elisabeth Wreford Andersen, Karen Markussen Linnet, Line Kenborg, Anna Sällfors Holmqvist, Laufey Tryggvadottir, Laura-Maria Madanat-Harjuoja, Ingrid Øra, Halldora K. Thorarinsdottir, Kim Vettenranta, Andrea Bautz, Henrik Schrøder, Henrik Hasle, Jeanette Falck Winther
Considering both relative and absolute numbers, highest risks were within the main groups of episodic and paroxysmal disorders (RR: 3.4 95% CI 2.5–4.5; AER: 3.9); nerve, nerve root and plexus disorders (RR: 3.3 95% CI 2.0–5.5; AER: 1.2); paralytic syndromes (RR: 40.1 95% CI 27.5–58.7; AER: 3.4); hydrocephalus, Horner’s syndrome and other disorders of the nervous system (RR: 18.1 95% CI 12.3–26.6; AER: 2.9); and diseases within the sensory organs (RR: 2.6 95% CI 2.1–3.1; AER: 8.5) (Table 1); all together, constituting 96% of all excess hospital contacts for neurologic disorders in survivors.
Cyclooxygenase-2 interacts with MMP and FGF pathways to promote epimorphic regeneration in lizard Hemidactylus flaviviridis
Published in Growth Factors, 2018
Pranav R. Buch, Isha Ranadive, Isha Desai, Suresh Balarakrishnan
The blastema stage is characterized by accumulation of progenitor cells beneath the AEC. This is effected by the migration of cells from distal stump tissues, which requires restructuring of the ECM framework (Yang & Bryant, 1994). While MMP2 transcript and protein levels were significantly reduced in COX-2-inhibited blastemas in our study, the effect on mmp9, mmp14 and timp2 was not biologically significant. The mid blastemal stage involves intense proliferative activity in the constituent cells and as the MMPs can promote proliferation of tumor cells (Bergers et al., 2000; Itoh et al., 1998; Zhou et al., 2000), they may be helping blastemal cell proliferation as well. Another outcome of MMP-mediated ECM degradation is the liberation of growth factors that remain embedded in it (Houck et al., 1992). FGFs are such factors which associate with matrix proteoglycans in the extracellular space. Xenopus and Axolotl limb blastemas are known to express FGF8 and FGF10 (Christensen et al., 2002; Han et al., 2001; Yokoyama et al., 2000). During embryonic limb development too, FGF2, FGF8 and FGF10 are able to induce a limb-bud in the absence of an apical ectodermal ridge, which otherwise maintains their levels (Cohn et al., 1995; Fallon et al., 1994; Niswander et al., 1993; Vogel et al., 1996). Over and above these, fgf20 has also been implicated in blastemal formation during zebrafish fin regeneration (Whitehead et al., 2005). The expression of each of fgf2, fgf8, fgf10 and fgf20 was severely hit by etoricoxib administration, clearly indicating a role for COX-2 as one of the top regulators of blastema formation in lizards. Additionally, as for the wound epithelium stage, FGFR1 was significantly reduced in the treatment group animals. The effects of FGFR1 inhibitor SU5402 on the progression of wound healing and blastema formation are similar to the ones seen for etoricoxib in this model (Pillai et al., 2013; Sharma & Suresh, 2008), giving credence to the notion that COX-2 influence on regenerative outcome is mediated through FGFR1 signaling. Nevertheless, concluding the role of an FGFR3-based pathway in relaying the effects of COX-2 warrants further investigation.