Over the course of ontogenesis, the human brain and human cognitive abilities develop in parallel, resulting in a phenotype strikingly distinct from that of other primates. Here, we used microarrays and RNA-sequencing to examine human-specific gene expression changes taking place during postnatal brain development in the prefrontal cortex and cerebellum of humans, chimpanzees, and rhesus macaques. We show that the most prominent human-specific expression change affects genes associated with synaptic functions and represents an extreme shift in the timing of synaptic development in the prefrontal cortex, but not the cerebellum. Consequently, peak expression of synaptic genes in the prefrontal cortex is shifted from <1 yr in chimpanzees and macaques to 5 yr in humans. This result was supported by protein expression profiles of synaptic density markers and by direct observation of synaptic density by electron microscopy. Mechanistically, the human-specific change in timing of synaptic development involves the MEF2A-mediated activity-dependent regulatory pathway. Evolutionarily, this change may have taken place after the split of the human and the Neanderthal lineages.

Human brain transcriptome analysis revealed widespread age-related splicing changes in the prefrontal cortex and cerebellum. While most of the splicing changes take place in development, approximately one-third of them extends into aging.

Acoustic rhinometry evaluates the geometry of the nasal cavity with acoustic reflections and provides information about nasal cross-sectional area and nasal volume within a given distance. Variations in internal nasal diameters have attracted increased interest since the advent of endoscopic surgical techniques. Race is known to be one of the most important factors affecting the nasal structure. In this study, we evaluated 106 healthy adult volunteers with acoustic rhinometry to determine internal nasal diameters and volumes and obtained normative data for four racial/ethnic groups. The data were analyzed with regard to race, sex, height, and weight. All measurements were made before and after the application of a topical nasal decongestant so that the effects of the nasal cycle were eliminated by decongestion.

miR-26a suppresses proinflammatory cytokine production via inactivating NF-κB, whereas NF-κB inhibits miR-26a production through binding to miR-26a promoter. We identified a reciprocal inhibition between miR-26a and NF-κB in obesity-related chondrocytes, providing a potential mechanism linking obesity to osteoarthritis.

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Acoustic rhinometry (AR) was used to objectively measure the success of septoplasty in relieving nasal obstruction caused by septal deviation. In addition, the patients were given a questionnaire to subjectively assess symptoms of congestion, rhinorrhea, and sneezing. Patients diagnosed with a septal deviation requiring surgery to eliminate obstruction were enrolled in this study. A septal deviation often results in concomitant sinonasal or respiratory problems that require septoplasty plus other surgeries to treat the patient effectively. AR measurements for patients who underwent septoplasty or septoplasty plus other surgeries were taken before and after surgery. To avoid confounding results caused by different levels of congestion, we used only postdecongestant values to analyze the data and only the side of the nose with the smaller volume for analysis. Patients in the septoplasty-only group showed a statistically significant (P < 0.01) increase in volume as measured by AR, a decrease in the symptom of congestion, and a decrease in the symptom of rhinorrhea. Patients who had septoplasty plus other sinonasal procedures showed significant increases in volume and cross-sectional area (CSA) 3, whereas CSAs 1 and 2 increased also, but not significantly.

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