Meta-analytic methods were used to synthesize the results of published randomized, controlled-outcome studies of psychosocial interventions with adult cancer patients. Forty-five studies reporting 62 treatment-control comparisons were identified. Samples were predominantly White, female, and from the United States. Beneficial effect size ds were .24 for emotional adjustment measures, .19 for functional adjustment measures, .26 for measures of treatment- and disease-related symptoms, and .28 for compound and global measures. The effect size of .17 found for medical measures was not statistically significant for the few reporting studies. Effect sizes for treatment-control comparisons did not significantly differ among several categories of treatment: behavioral interventions, nonbehavioral counseling and therapy, informational and educational methods, organized social support provided by other patients, and other nonhospice interventions.

Recent studies suggest that noninvasive positive pressure ventilation (NPPV) administered by nasal or oronasal mask avoids the need for endotracheal intubation, rapidly improves vital signs, gas exchange, and sense of dyspnea, and may reduce mortality in selected patients with acute respiratory failure, but few controlled trials have been done. The present study used a randomized prospective design to evaluate the possible benefits of NPPV plus standard therapy versus standard therapy alone in patients with acute respiratory failure. Patients to receive NPPV were comfortably fitted with a standard nasal mask connected to a BiPAP ventilatory assist device (Respironics, Inc., Murrysville, PA) in the patient flow-triggered/time-triggered (S/T) mode, and standard therapy consisted of all other treatments deemed necessary by the primary physician, including endotracheal intubation. The need for intubation was reduced from 73% in the standard therapy group (11 of 15 patients) to 31% in the NPPV group (5 of 16 patients, p < 0.05). Among chronic obstructive pulmonary disease (COPD) patients, the reduction was even more striking, with 8 of 12 (67%) control patients requiring intubation compared with 1 of 11 (9%) NPPV patients (p < 0.05). Heart and respiratory rates were significantly lower in the NPPV group than in control patients within 1 h, and PaO2 was significantly improved in the NPPV group for the first 6 h. Dyspnea scores and maximal inspiratory pressures were better in the NPPV than in control patients at 6 h, and nurses and therapists spent similar amounts of time at the bedside for both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Gibbons are small arboreal apes that display an accelerated rate of evolutionary chromosomal rearrangement and occupy a key node in the primate phylogeny between Old World monkeys and great apes. Here we present the assembly and analysis of a northern white-cheeked gibbon (Nomascus leucogenys) genome. We describe the propensity for a gibbon-specific retrotransposon (LAVA) to insert into chromosome segregation genes and alter transcription by providing a premature termination site, suggesting a possible molecular mechanism for the genome plasticity of the gibbon lineage. We further show that the gibbon genera (Nomascus, Hylobates, Hoolock and Symphalangus) experienced a near-instantaneous radiation ~5 million years ago, coincident with major geographical changes in Southeast Asia that caused cycles of habitat compression and expansion. Finally, we identify signatures of positive selection in genes important for forelimb development (TBX5) and connective tissues (COL1A1) that may have been involved in the adaptation of gibbons to their arboreal habitat.

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Mobile elements have created structural variation in the human genome through their de novo insertions and post-insertional genomic rearrangements. L1 elements are a type of long interspersed element (LINE) that is dispersed at high copy numbers within most mammalian genomes. To determine the magnitude of L1 recombination-associated deletions (L1RADs), we computationally extracted L1RAD candidates by comparing the human and chimpanzee genomes and verified each of the L1RAD events by using wet-bench analyses. Through these analyses, we identified 73 human-specific L1RAD events that occurred subsequent to the divergence of the human and chimpanzee lineages. Despite their low frequency, the L1RAD events deleted Ϸ450 kb of the human genome. One L1RAD event generated a large deletion of Ϸ64 kb. Multiple alignments of prerecombination and postrecombination L1 elements suggested that two different deletion mechanisms generated the L1RADs: nonallelic homologous recombination (55 events) and nonhomologous end joining between two L1s (18 events). In addition, the position of L1RADs throughout the genome does not correlate with local chromosomal recombination rates. This process may be implicated in the partial regulation of L1 copy numbers by the finding that Ϸ60% of the DNA sequences deleted by the L1RADs consist of L1 sequences that were either directly involved in the recombination events or located in the intervening sequence between recombining L1s. Overall, there is increasing evidence that L1RADs have played an important role in creating structural variation.LINE-1 ͉ nonallelic homologous ͉ nonhomologous end joining ͉ retrotransposon L ong interspersed elements (LINE-1s or L1s) are universal constituents of mammalian genomes and account for Ϸ17% of the human genome (1). They have expanded to Ϸ 520,000 copies over the last 150 million years (1, 2). Full-length L1s are Ϸ6 kb long, and encode two ORFs (ORF1 and ORF2), which code for a 40-kDa RNA-binding protein with nucleic acid chaperone activity (3) and a 150-kDa protein with both endonuclease (EN) and reverse transcriptase (RT) activities (4-6). L1s mobilize via an RNA intermediate to integrate themselves into genomic DNA at the target site. However, Ϸ99.8% of L1s in the human genome are unable to retrotranspose (7), either because of point mutations or structural deficiencies (e.g., 5Ј truncations, 5Ј inversions, or other internal rearrangements) (8 -10). Consequently, only 80 -100 retrotranspositioncompetent L1s capable of autonomous retrotransposition are located in the human genome (7,11).Homologous recombination between closely related DNA fragments occurs in all living organisms (12, 13). A recent study of human genomic deletions caused by unequal homologous recombination between two Alu elements showed that 492 human-specific deletion events resulted in a total of Ϸ400 kb DNA being lost since the divergence of the human and chimpanzee lineages (14). Similar to the Alu elements, L1s may have been a source of recombination-associated genomic deletion throughou...