Commonly Associated Disorders with Complete Scalp Alopecia in Early Childhood: A Review.

Complete scalp hair loss can be a source of distress for affected children and their families. In addition to infectious and trauma-related causes of hair loss, infants and children may present with total scalp alopecia arising from a range of genetic predispositions. Our objective with this review was to identify the common genetic conditions in children with complete scalp alopecia. The PubMed Database was reviewed for all articles from 1962 to 2019 containing the search terms related to genetic alopecia. The conditions with at least five reported cases in the literature were considered for the inclusion. All clinical trials, retrospective studies, and cases on human subjects and written in English were included. Six genetic conditions related to complete scalp alopecia were included in this review. The most common genetic conditions associated with total scalp hair loss include: alopecia totalis/Alopecia universalis (AU), atrichia with papular lesions, AU congenita, hereditary Vitamin D-resistant rickets type IIA, alopecia with mental retardation, and pure hair and nail ectodermal dysplasia. In children presenting with total scalp hair loss, a myriad of genetic and environmental factors may be the underlying cause. Increased awareness of potential genetic conditions associated with total scalp hair loss may assist in diagnosis, with improved the prognosis for the children.

3D bioprinting of cardiac tissue: current challenges and perspectives.

Demand for donor hearts has increased globally due to cardiovascular diseases. Recently, three-dimensional (3D) bioprinting technology has been aimed at creating clinically viable cardiac constructs for the management of myocardial infarction (MI) and associated complications. Advances in 3D bioprinting show promise in aiding cardiac tissue repair following injury/infarction and offer an alternative to organ transplantation. This article summarizes the basic principles of 3D bioprinting and recent attempts at reconstructing functional adult native cardiac tissue with a focus on current challenges and prospective strategies.

Required growth facilitators propel axon regeneration across complete spinal cord injury.

Transected axons fail to regrow across anatomically complete spinal cord injuries (SCI) in adults. Diverse molecules can partially facilitate or attenuate axon growth during development or after injury1-3, but efficient reversal of this regrowth failure remains elusive4. Here we show that three factors that are essential for axon growth during development but are attenuated or lacking in adults-(i) neuron intrinsic growth capacity2,5-9, (ii) growth-supportive substrate10,11 and (iii) chemoattraction12,13-are all individually required and, in combination, are sufficient to stimulate robust axon regrowth across anatomically complete SCI lesions in adult rodents. We reactivated the growth capacity of mature descending propriospinal neurons with osteopontin, insulin-like growth factor 1 and ciliary-derived neurotrophic factor before SCI14,15; induced growth-supportive substrates with fibroblast growth factor 2 and epidermal growth factor; and chemoattracted propriospinal axons with glial-derived neurotrophic factor16,17 delivered via spatially and temporally controlled release from biomaterial depots18,19, placed sequentially after SCI. We show in both mice and rats that providing these three mechanisms in combination, but not individually, stimulated robust propriospinal axon regrowth through astrocyte scar borders and across lesion cores of non-neural tissue that was over 100-fold greater than controls. Stimulated, supported and chemoattracted propriospinal axons regrew a full spinal segment beyond lesion centres, passed well into spared neural tissue, formed terminal-like contacts exhibiting synaptic markers and conveyed a significant return of electrophysiological conduction capacity across lesions. Thus, overcoming the failure of axon regrowth across anatomically complete SCI lesions after maturity required the combined sequential reinstatement of several developmentally essential mechanisms that facilitate axon growth. These findings identify a mechanism-based biological repair strategy for complete SCI lesions that could be suitable to use with rehabilitation models designed to augment the functional recovery of remodelling circuits.