Responses of immature pullets to repeated cycles of gradual increases and abrupt decreases in photoperiod

1. Growing pullets were reared on constant 8, 11 or 14 h photoperiods or given 12 daily increments of 30 min followed by an abrupt 6 h decrease in photoperiod in 14 d cycles from 2 d of age to sexual maturity. 2. Birds on the experimental lighting programme matured earlier than constant 8-h controls, later than 11-h controls but at the same age and body weight as constant 14-h controls. 3. Weight of the first egg was correlated with age at first egg. 4. It is assumed that potential advances in maturity for the experimental birds from the 30 min increments in photoperiod were cancelled by the retarding influences of 6 h decreases in photoperiod, resulting in their maturity being similar to that of birds reared on a constant daylength equal to the longest photoperiod reached during the cycle.     

Pregnancy-related impairments and the Americans with Disabilities Act

Congress passed the Americans with Disabilities Act (ADA) in 1990. The ADA's overriding purpose is to provide a national mandate for the elimination of discrimination against individuals with disabilities. This article addresses the emerging relationship between pregnancy-related disabilities and the employment provisions of the ADA, set forth in title I of the Act. In view of the high percentage of women who will become pregnant and their potential need for workplace accommodations during and after pregnancy, it is crucial that health professionals understand the impact of the ADA's employment provisions.     

Dorsal horn cells connected to the lissauer tract and their relation to the dorsal root potential in the rat

We have examined the role of dorsal horn cells that respond to Lissauer tract stimulation in regulating primary afferent depolarization (PAD). PAD was monitored by recording the dorsal root potential (DRP) in the roots of the lumbar cord. Recordings were made of the discharges of Lissauer tract-responsive cells, and their discharges were correlated with the DRPs occurring spontaneously and those evoked by stimulation. Electrical microstimulation of the Lissauer tract (<10 microA; 200 micros) was used to activate the tract selectively and evoke a characteristic long-latency DRP. Cells that were excited by Lissauer tract stimulation were found in the superficial laminae of the dorsal horn. They exhibited low rates of ongoing discharge and responded to Lissauer tract stimulation typically with a burst of impulses with a latency to onset of 5.6 +/- 2.7 ms (mean +/- SD) and to termination of 13.6 +/- 4.1 ms (n = 105). Lissauer tract-responsive cells in L5 were shown to receive convergent inputs from cutaneous and muscle afferents as they responded to stimulation of the sural nerve (100%, n = 19) and the nerve to gastrocnemius (95%, n = 19). The latency of the response to sural nerve stimulation was 3.7 +/- 1.5 ms and to gastrocnemius nerve stimulation, 8.3 +/- 3.6 ms. Stimulation through a microelectrode at a depth of 1.5 mm in the sensorimotor cortex (100 microA, 200 micros) evoked a response in 17 of 31 Lissauer tract-responsive cells (55%) with a latency to onset of 21.9 +/- 2.8 ms (n = 17). Stimulation of the sural nerve, nerve to gastrocnemius or sensorimotor cortex was shown to depress the response of Lissauer tract-responsive cells to a subsequent Lissauer tract stimulus. The ongoing discharges of Lissauer tract-responsive cells were correlated to the spontaneous DRP using spike-triggered averaging. Of 123 cells analyzed in this way, 117 (95%) were shown to be correlated to the DRP. In addition, the peaks of spontaneous negative DRPs in spinally transected animals were detected in software. Perievent time histograms triggered from these peaks showed the discharge of Lissauer tract-responsive cells to be correlated to the spontaneous DRPs in 57 of 62 cells (92%) recorded. We conclude that these data provide compelling evidence that the Lissauer tract, and the dorsal horn cells that it excites, mediate the PAD evoked from multiple neural pathways.     

Glomerular endothelial cells synthesize collagens but little gelatinase A and B

Mesangial sclerosis is a major feature of progressive renal disease. The mesangium contains mesangial cells and is bounded by the peripheral glomerular basement membrane and endothelial cells. Mesangial cells synthesize and degrade extracellular matrix. Whereas both mesangial and endothelial cells synthesize extracellular matrix components, the degradative pathway, well studied in the former, has not been investigated in endothelial cells. This study examines lines of all three glomerular cell types derived from female B6SJLF1/J mice, as well as mRNA levels for collagens alpha1(I), alpha1(IV), alpha3 (IV), alpha5 (IV), and alpha1 (VI), laminin, tenascin, matrix metalloproteinase-2 (MMP-2), and MMP-9. Type I and IV collagen synthesis was confirmed by enzyme-linked immunosorbent assay. MMP-2 and MMP-9 enzyme activity was measured by zymography. It was found that glomerular endothelial cells are a significant source of collagens, laminin, and tenascin. However, they express only low levels of MMP-2 and no detectable MMP-9. Stimulation with exogenous transforming growth factor-beta1 leads to a significant increase in collagen I, tissue inhibitors of metalloproteinase-1, and MMP-9 in conditioned media. These data suggest that glomerular endothelial cells may play an active role in extracellular matrix remodeling in glomerular disease.     

Molecular analysis of the PDS gene in Pendred syndrome

Pendred syndrome is an autosomal recessive disorder characterized by the association between sensorineural hearing loss and thyroid swelling or goitre and is likely to be the most common form of syndromic deafness. Within the thyroid gland of affected individuals, iodide is incompletely organified with variable effects upon thyroid hormone biosynthesis, whilst the molecular basis of the hearing loss is unknown. The PDS gene has been identified by positional cloning of chromosome 7q31, within the Pendred syndrome critical linkage interval and encodes for a putative ion transporter called pendrin. We have investigated a cohort of 56 kindreds, all with features suggestive of a diagnosis of Pendred syndrome. Molecular analysis of the PDS gene identified 47 of the 60 (78%) mutant alleles in 31 families (includes three homozygous consanguineous kindreds and one extended family segregating three mutant alleles). Moreover, four recurrent mutations accounted for 35 (74%) of PDS disease chromosomes detected and haplotype analysis would favour common founders rather than mutational hotspots within the PDS gene. Whilst these findings demonstrate molecular heterogeneity for PDS mutations associated with Pendred syndrome, this study would support the use of molecular analysis of the PDS gene in the assessment of families with congenital hearing loss.