SUMMARYPathologies of retinal blood vessels are among the major causes of blindness worldwide. A key cell type that regulates retinal vascular development is the astrocyte. Generated extrinsically to the retina, astrocytes migrate into the retina through the optic nerve head. Even though there is a strong correlation between astrocyte distribution and retinal vascular development, the factors that guide astrocytes into the retina remain unclear. In this study, we show that astrocytes migrate within a laminin-containing basement membrane -the inner limiting membrane. Genetic deletion of the laminin β2 and γ3 chains affects astrocyte migration and spatial distribution. We show that laminins act as haptotactic factors in vitro in an isoform-specific manner, inducing astrocyte migration and promoting astrocyte differentiation. The addition of exogenous laminins to laminin-null retinal explants rescues astrocyte migration and spatial patterning. Furthermore, we show that the loss of laminins reduces β1 integrin expression in astrocytes. Culturing lamininnull retinal astrocytes on laminin substrates restores focal localization of β1 integrin. Finally, we show that laminins containing β2 and γ3 chains regulate subsequent retinal blood vessel growth and maintain vascular integrity. These in vivo and in vitro studies demonstrate clearly that laminins containing β2 and γ3 chains are indispensable for migration and spatial organization of astrocytes and that they play a crucial role during retinal angiogenesis in vivo. RESEARCH ARTICLELaminins regulate angiogenesis treatment with exogenous laminins rescues astrocyte migration and spatial patterning phenotype ex vivo. Together, these data support the hypothesis that β2-and γ3-containing laminins are important cues in retinal vascular development.

Neurovascular pathologies of the central nervous system (CNS), which are associated with barrier dysfunction, are leading causes of death and disability. The roles that neuronal and glial progenitors and mature cells play in CNS angiogenesis and neurovascular barrier maturation have been elucidated in recent years. Yet how neuronal activity influences these processes remains largely unexplored. Here, we discuss our current understanding of how neuronal and glial development affects CNS angiogenesis and barriergenesis, and outline future directions to elucidate how neuronal activity might influence these processes. An understanding of these mechanisms is crucial for developing new interventions to treat neurovascular pathologies.

Percutaneous endoscopic gastrostomy (PEG) has been used for providing enteral access to patients who require long-term enteral nutrition for years. Although generally considered safe, PEG tube placement can be associated with many immediate and delayed complications. Buried bumper syndrome (BBS) is one of the uncommon and late complications of percutaneous endoscopic gastrostomy (PEG) placement. It occurs when the internal bumper of the PEG tube erodes into the gastric wall and lodges itself between the gastric wall and skin. This can lead to a variety of additional complications such as wound infection, peritonitis, and necrotizing fasciitis. We present here a case of buried bumper syndrome which caused extensive necrosis of the anterior abdominal wall.

A tetra-nuclear, star-shaped hetero-metallic copper(II)-manganese(II) complex, [{CuL(H(2)O)}(2)(CuL)Mn](ClO(4))(2) (1) has been synthesized by reacting the "complex as ligand" [CuL] with Mn(ClO(4))(2) where H(2)L is the tetradentate di-Schiff base derived from 1,3-propanediamine and 2-hydroxyacetophenone. Upon treatment with the polyatomic anions azide, cyanate, or thiocyanate in methanol medium, complex 1 transforms into the corresponding trinuclear species [(CuL)(2)Mn(N(3))(2)] (2), [(CuL)(2)Mn(NCO)(2)] (3) and [(CuL)(2)Mn(NCS)(2)] (4). All four complexes have been structurally and magnetically characterized. In complex 1 the central Mn(II) ion is encapsulated by three terminal [CuL] units through the formation of double phenoxido bridges between Mn(II) and each Cu(II). In complexes 2-4 one of the CuL units is replaced by a couple of terminal azide, N-bonded cyanate or N-bonded thiocyanate ions respectively and the central Mn(II) ion is connected to two terminal Cu(II) ions through a double asymmetric phenoxido bridge. Variable temperature magnetic susceptibility measurements show the presence of moderate ferrimagnetic exchange interactions in all the cases mediated through the double phenoxido bridges with J values (H = -JS(i)S(i + 1)) of -41.2, -39.8 and -12.6 cm(-1) (or -40.5 and -12.7 cm(-1) if we use a model with two different exchange coupling constants) for the tetranuclear MnCu(3) cluster in compound 1 and -20.0, -17.3 and -32.5 cm(-1) for the symmetric trinuclear MnCu(2) compounds 2-4. These ferrimagnetic interactions lead to spin ground states of 1 (5/2 - 3*1/2) for compound 1 and 3/2 (5/2 - 2*1/2) for compounds 2-4.