EEG correlates of the development of infant joint attention skills

The development of the capacity for social attention coordination, or "joint attention," is a major milestone of infancy. Data from a recent study of handicapped infants have raised the hypothesis that the tendency to initiate bids for joint attention may reflect processes associated with the frontal cortex to a greater extent than other forms of infant attention coordination (R. Caplan et al., 1993). This hypothesis was examined in a longitudinal study of 32 normally developing infants. The results indicated that EEG data at 14 months indicative of left frontal, as well as left and right central cortical activity, was associated with the tendency to initiate joint attention bids (IJA) at 14 and 18 months. In contrast, a pattern of left parietal activation and right parietal deactivation at 14 months was associated with the development of the capacity to respond to the joint attention bids (RJA) of others at 14 and 18 months. These results were interpreted to be consistent with a general anterior-posterior model of attention development (M. Posner & S. Petersen, 1990). The implications of these results for current conceptualizations of joint attention development, as well as for understanding the disturbance of joint attention skill development in autism are discussed.     

Phosphorylated KDR is expressed in the neoplastic and stromal elements of human renal tumours and shuttles from cell membrane to nucleus

Vascular endothelial growth factor (VEGF)-A is an important angiogenic factor in establishing the vasculature in renal cell carcinomas (RCCs). Since little is known about VEGF signalling in RCCs, the profile of phosphorylated KDR (pKDR) has been investigated and the intracellular location of the receptor has been examined in the present study. Using two monoclonal antibodies raised against the phosphorylated KDR epitopes (Y1059 and Y1214) known to mediate different VEGF functions, together with a commercial anti-KDR antibody and immunohistochemistry, the expression of pKDR was investigated in a series of normal (n = 25) and neoplastic kidneys (n = 54; clear cell n = 35; papillary n = 10; oncocytomas n = 8). pKDR was present in many tissue elements of both normal and neoplastic renal tissues, with strong expression in the cell membrane, cytoplasm, and nuclei of normal kidney and tumour cells, as well as endothelial cells in tumours of all histological types. Patterns and intensity were similar using both anti-pKDR antibodies. There was no significant correlation in clear cell carcinomas between pKDR expression and age (p = 0.57), tumour size (p = 0.2), gender (p = 0.59), grade (p = 0.2) or histological type (p = 0.36). To delineate further the intracellular processing that might account for the cellular distribution, confocal microscopy was also performed. Antibodies to the different phosphorylated epitopes demonstrated different intracellular staining patterns. This study shows that pKDR is present in a wide variety of renal tumours, suggesting that anti-VEGF therapy might have direct effects on tumour cells. It further suggests that cells traffic pKDR depending on the precise KDR tyrosines that are autophosphorylated in a manner that enables receptor activation to result in different functions.     

Slow and fast fiber isoform gene expression is systematically altered in skeletal muscle of the Sox6 mutant, p100H.

We have previously demonstrated that p100H mutant mice, which lack a functional Sox6 gene, exhibit skeletal and cardiac muscle degeneration and develop cardiac conduction abnormalities soon after birth. To understand the role of Sox6 in skeletal muscle development, we identified muscle-specific genes differentially expressed between wild-type and p100H mutant skeletal muscles and investigated their temporal expression in the mutant muscle. We found that, in the mutant skeletal muscle, slow fiber and cardiac isoform genes are expressed at significantly higher levels, whereas fast fiber isoform genes are expressed at significantly lower levels than wild-type. Onset of this aberrant fiber type-specific gene expression in the mutant coincides with the beginning of the secondary myotube formation, at embryonic day 15-16 in mice. Together with our earlier report, demonstrating early postnatal muscle defects in the Sox6 null-p100H mutant, the present results suggest that Sox6 likely plays an important role in muscle development.     

Identification of neurons with acetylcholinesterase and NADPH-diaphorase activities in the centrifugal visual system of the chick

The isthmo-optic nuclei (ION) and ectopic neurons, which constitute the centrifugal visual system (CVS), are thought to be cholinoceptive and nitrergic. However, it is not clear which neurons express these markers, namely the ones that project to the retina rather than in neurons that only participate in a local circuit. Therefore, to characterize the neurochemical patterns of the centrifugal visual system in the post-hatched chick, retinopetal cells of the isthmo-optic nuclei and the ectopic region were identified via immunolabeling for cholera toxin, a neuronal tracer, which has been injected in the ocular globe. Then, double labeled with acetylcholinesterase histochemistry to reveal cholinergic synapses, or NADPH-diaphorase histochemistry as a nitrergic marker. Briefly, acetylcholinesterase activity was present mainly in cholera toxin labeled cell bodies of the isthmo-optic nucleus and the ectopic region indicating that retinal projecting neurons of centrifugal visual system comprise a cholinoceptive pathway. On the other hand, NADPH-diaphorase histochemistry was present in the neuropile and sparse cell bodies inside of the isthmo-optic nucleus and in ectopic neurons which were not cholera toxin positive suggesting their role in an intrinsic circuit of the centrifugal visual system. These data support the idea that these two neurochemical systems are present in distinct neuronal populations in the centrifugal visual system.     

Laser induced thermal injury of rabbit cornea and treatment with anti-inflammatory agents

A moderately severe thermal injury of the central cornea of 48 Dutch-belted rabbit eyes was produced with a carbon (CO₂) laser. The lesions were photographed with a slit lamp (SL) camera immediately following the injury and at 1, 2, 4, 7, 14, 21, 30 and 60 days after the exposure. Lesion size, opaqueness, and depth were graded clinically by SL biomicroscopy at the same intervals. No significant differences were found (p 0.05) between groups of eyes treated with flurbiprofen (0.03%), prednisolone acetate (1%), and vehicle control four-times-a-day for three weeks following injury. Additionally, eyes were studied histopathologically at 3 and 60 days following injury by light and transmission electron microscopy, and clinically at 30 and 60 days by endothelial specular microscopy. Important clinical and histopathological findings included coagulative necrosis of the corneal epithelium, epithelial sloughing, fusion of stromal collagen, stromal edema and inflammatory cell infiltration, stromal scar formation, corneal thinning, endothelial hyperplasia and metaplasia, fibrinous anterior chamber reaction with hypopyon, and retrocorneal fibrous membrane formation.