Effects of photoperiod and intermittent lighting on reproduction in pheasant hens

Forty 28-wk-old ring-necked pheasant hens were equally distributed among 5 treatment groups and exposed to the following light schedules for 36 wk: Treatment 1 - 16L:8D; Treatment 2 - 1L:11D:4L:8D; Treatment 3 - 1L:13D:2L:8D; Treatment 4 - 1L:14D:1L:8D; and Treatment 5 - 1L:14.5D:0.5L:8D. The number of days from stimulatory lighting to the first egg was significantly (P<0.05) greater under the intermittent schedules (20.3, 29.5, 40.3, 44.4, and 57.7 d, respectively) when the subjective daylength was shorter than 13 h. Despite the delay in initiation of laying, average egg production was higher under intermittent lighting (23.0, 36.0, 48.6, 43.8, and 42.3% or 58.0, 93.0, 122.5, 110.4, and 106.6 eggs). Patterns of oviposition indicated a tendency in the birds exposed to intermittent lighting to have synchronized laying, with the period opposite the longest scotoperiod provided by their light schedule; thus subjective daylengths of 13, 11, 10 and 9.5 h, respectively, were created. Fertility was significantly (P<0.05) lower under intermittent lighting and was apparently associated with a high proportion of eggs in the late stages of oviducal development at the time of insemination.     

Mutations in CUL4B, which encodes a ubiquitin E3 ligase subunit, cause an X-linked mental retardation syndrome associated with aggressive outbursts, seizures, relative macrocephaly, central obesity, hypogonadism, pes cavus, and tremor

We have identified three truncating, two splice-site, and three missense variants at conserved amino acids in the CUL4B gene on Xq24 in 8 of 250 families with X-linked mental retardation (XLMR). During affected subjects' adolescence, a syndrome emerged with delayed puberty, hypogonadism, relative macrocephaly, moderate short stature, central obesity, unprovoked aggressive outbursts, fine intention tremor, pes cavus, and abnormalities of the toes. This syndrome was first described by Cazebas et al., in a family that was included in our study and that carried a CUL4B missense variant. CUL4B is a ubiquitin E3 ligase subunit implicated in the regulation of several biological processes, and CUL4B is the first XLMR gene that encodes an E3 ubiquitin ligase. The relatively high frequency of CUL4B mutations in this series indicates that it is one of the most commonly mutated genes underlying XLMR and suggests that its introduction into clinical diagnostics should be a high priority.     

Current progress in use of adipose derived stem cells in peripheral nerve regeneration

Unlike central nervous system neurons; those in the peripheral nervous system have the potential for full regeneration after injury. Following injury, recovery is controlled by schwann cells which replicate and modulate the subsequent immune response. The level of nerve recovery is strongly linked to the severity of the initial injury despite the significant advancements in imaging and surgical techniques. Multiple experimental model shave been used with varying successes to augment the natural regenerative processes which occur following nerve injury. Stem cell therapy in peripheral nerve injury may be an important future intervention to improve the best attainable clinical results. In particular adipose derived stem cells(ADSCs) are multipotent mesenchymal stem cells similar to bone marrow derived stem cells, which are thought to have neurotrophic properties and the ability to differentiate into multiple lineages. They are ubiquitous within adipose tissue; they can form many structures resembling the mature adult peripheral nervous system. Following early in vitro work; multiple small and large animal in vivo models have been used in conjunction with conduits, autografts and allografts to successfully bridge the peripheral nerve gap. Some of the ADSC related neuroprotective and regenerative properties have been elucidated however much work remains before a model can be used successfully in human peripheral nerve injury(PNI). This review aims to provide a detailed overview of progress made in the use of ADSC in PNI, with discussion on the role of a tissue engineered approach for PNI repair.