Post-translational phosphorylation of the slow/β myosin heavy chain isoform in adult rabbit masseter muscle

Four different phenotypes of slow muscle fibers, characterized by differential epitope expression in the slow/ myosin heavy chain (MyHC) isoform, have been identified in adult rabbit masseter muscle. We investigated the role of post-translational phosphorylation in the expression of these four phenotypes. Serial cryostat sections were treated either with alkaline phosphatase to dephosphorylate proteins in the tissue, or with a brain kinase solution and ATP to phosphorylate them, and then stained, using four antibodies that bind specifically to the slow/ MyHC isoform. In sections pre-treated with phosphatase, immunoreactivity to antibody A4.840 was abolished, but it could be restored by subsequent kinase/ATP treatment or ATP alone, indicating that the expression of its epitope requires phosphorylation. Phosphatase treatment resulted in an exposure of the epitope for antibody A4.951 in cells that normally bind this antibody only weakly or not at all, but since heat treatment alone produced similar effects, the role of phosphorylation in this enhancement is less certain. Immunoreactivity to antibodies S58 and BA-D5 were not influenced by phosphatase pre-treatment. Kinase/ATP treatment was only effective in changing antibody binding when tissues already had been phosphatase treated. We interpret these results to mean that sites of potential phosphorylation may already be occupied by O-linked glycosylation.     

A de novo translocation t(3;17)(q26.3;q23.1) in a child with Cornelia de Lange syndrome.

A female infant with Cornelia de Lange syndrome and severe limb reduction defects is described. Chromosome analysis showed a de novo translocation with breakpoints at 3q26.3 and 17q23.1. This is the first reported case of a de novo translocation associated with this syndrome.     

Blepharophimosis sequence and diaphragmatic hernia associated with interstitial deletion of chromosome 3 (46,XY,del(3)(q21q23)).

A case of blepharophimosis, ptosis, and epicanthus inversus (BPES) associated with prenatally diagnosed diaphragmatic hernia and interstitial deletion of the long arm of chromosome 3, del(3)(q21q23), is reported. Comparison with other cases of BPES resulting from 3q rearrangements indicate that this disorder, previously assigned to 3q2, can now be more accurately mapped to 3q23.     

现代派文学的"世纪末"综合症

19世纪末的文学忧郁和悲观等病症对20世纪现代派文学的影响是深远的,现代派文学经历了从以丑为美到迷惘、异化、荒诞和虚无的文学创作轨迹,显示了从19世纪末传染到的综合症状以及作家们改革和拓荒的勇气.现代派文学对心灵的解剖是深刻的,语言形式的反叛也是彻底的.     

Melatonin and adjustment to phase shift

The pineal hormone melatonin has clear circadian phase-shifting effects in humans which have recently been formalized as a phase response curve. Its potential use in circadian rhythm disorders has been investigated in field studies of jet lag and shift work and in simulated phase shift. A substantial amount of information indicates that in the majority of subjects it hastens adaptation of both subjective and objective measures to forced shifts in time cues with few reported side-effects. Field studies of its use in adaptation to shift work are sparse and preliminary but the first indications are positive. In some blind subjects with sleep disturbance it can stabilize sleep onset time without necessarily entraining all circadian rhythms and it can advance sleep timing in delayed sleep-phase insomnia. Acute suppression of core body temperature may be an integral part of the phase-shifting mechanism.     

Microglial proliferation in cortical neural cultures exposed to feline immunodeficiency virus

Microglia are thought to play an important role in neurodegenerative changes due to infection with human or animal immunodeficiency viruses. Using feline immunodeficiency virus and cat neural cultures, we observed a dramatic increase in the accumulation of microglia from a basal rate of 5-7% day(-1) to 25-126% day(-1). Both live virus and heat-inactivated virus induced proliferation. Negligible proliferation was seen in purified microglial cultures. Conditioned medium from astrocytes or mixed neural cultures treated with feline immunodeficiency virus stimulated the proliferation of purified microglia. Disease progression may be facilitated by early non-infectious interactions of lentiviruses with neural tissue that promote the activation and proliferation of microglia.