Study of vestibular evoked myogenic potentials in patients affected by Meniere's disease treated with endolymphatic mastoid shunt.

Objectives: We recorded and compared the vestibular evoked myogenic potentials (VEMPs) before use of an endolymphatic mastoid shunt (EMS) and 1, 12, and 48 months after placement of the shunt.

Methods: Air-conducted VEMPs were recorded in 28 patients affected by intractable Meniere's disease and treated with placement of an EMS.

Results: One month and 12 months after the surgery, VEMPs were not detectable in the operated ear in 100% and 86% of the patients, respectively.

The interactome of the histone gene regulatory factor HiNF-P suggests novel cell cycle related roles in transcriptional control and RNA processing.

HiNF-P is a recently identified histone H4 subtype specific transcriptional regulator that associates with the conserved cell cycle control element in the proximal promoter regions of histone H4 genes. HiNF-P interacts with the global histone gene regulator and direct cyclin E/CDK2 substrate p220(NPAT) to potently upregulate histone H4 gene transcription at the G1/S phase transition in response to cyclin E/CDK2 signaling. To gain insight into the function of HiNF-P in a broader cellular context, we performed a yeast two-hybrid screen to identify its novel interacting proteins.

HiNF-P directly links the cyclin E/CDK2/p220NPAT pathway to histone H4 gene regulation at the G1/S phase cell cycle transition.

Genome replication in eukaryotic cells necessitates the stringent coupling of histone biosynthesis with the onset of DNA replication at the G1/S phase transition. A fundamental question is the mechanism that links the restriction (R) point late in G1 with histone gene expression at the onset of S phase. Here we demonstrate that HiNF-P, a transcriptional regulator of replication-dependent histone H4 genes, interacts directly with p220(NPAT), a substrate of cyclin E/CDK2, to coactivate histone genes during S phase.

Treatment of benign positional vertigo in the elderly: a randomized trial.

Objectives/hypothesis: The objective of the study was to evaluate the efficacy of three therapeutic strategies (Semont maneuver, flunarizine, and no treatment) in patients with benign paroxysmal positional vertigo.

Study Design: Randomized prospective trial.

Methods: One hundred fifty-six consecutive patients older than 60 years of age who were affected by benign paroxysmal positional vertigo of the posterior semicircular canal were enrolled.

Tumor suppressor pRB functions as a co-repressor of the CCAAT displacement protein (CDP/cut) to regulate cell cycle controlled histone H4 transcription.

The CCAAT displacement protein (CDP-cut/CUTL1/cux) performs a key proliferation-related function as the DNA binding subunit of the cell cycle controlled HiNF-D complex. HiNF-D interacts with all five classes (H1, H2A, H2B, H3, and H4) of the cell-cycle dependent histone genes, which are transcriptionally and coordinately activated at the G(1)/S phase transition independent of E2F. The tumor suppressor pRB/p105 is an intrinsic component of the HiNF-D complex.

The tumor suppressor interferon regulatory factor 1 interferes with SP1 activation to repress the human CDK2 promoter.

Cell growth control by interferons (IFNs) involves up-regulation of the tumor suppressor interferon regulatory factor 1 (IRF1). To exert its anti-proliferative effects, this factor must ultimately control transcription of several key genes that regulate cell cycle progression. Here we show that the G1/S phase-related cyclin-dependent kinase 2 (CDK2) gene is a novel proliferation-related downstream target of IRF1.