High-fidelity encoding of mechanostimuli by tactile food-sensing neurons requires an ensemble of ion channels.

The nematode C. elegans uses mechanosensitive neurons to detect bacteria, which are food for worms. These neurons release dopamine to suppress foraging and promote dwelling.

An automated clinical mass spectrometric method for identification and quantification of variant and wild-type amyloid-β 1-40 and 1-42 peptides in CSF.

Introduction: We developed an automated liquid chromatography-tandem mass spectrometry high performance liquid chromatography tandem mass spectrometry (HPLC-MS/MS) method for multiplex quantification of wild-type (wt) amyloid β (Aβ) peptides 1-40 (Aβ40) and 1-42 (Aβ42) and detection of variant Aβ peptides in cerebrospinal fluid.

Methods: The multiplex Aβ HPLC-MS/MS assay was validated in a clinically accredited laboratory following regulatory guidelines, with Aβ42 calibration assigned to the ERM/IFCC certified reference material; sequence variants were additionally multiplexed into the method.

Results: Sample preparation was fully automated on a liquid handler.

The F-actin bundler α-actinin Ain1 is tailored for ring assembly and constriction during cytokinesis in fission yeast.

The actomyosin contractile ring is a network of cross-linked actin filaments that facilitates cytokinesis in dividing cells. Contractile ring formation has been well characterized in Schizosaccharomyces pombe, in which the cross-linking protein α-actinin SpAin1 bundles the actin filament network. However, the specific biochemical properties of SpAin1 and whether they are tailored for cytokinesis are not known.

MicroRNAs targeting Nicastrin regulate Aβ production and are affected by target site polymorphisms.

Despite the growing number of genome-wide association studies, the involvement of polymorphisms in microRNA target sites (polymiRTS) in Alzheimer's disease (AD) remains poorly investigated. Recently, we have shown that AD-associated single-nucleotide polymorphisms (SNPs) present in the 3' untranslated region (3'UTR) of amyloid precursor protein (APP) could directly affect miRNA function. In theory, loss of microRNA (miRNA) function could lead to risk for AD by increasing APP expression and Aβ peptide production.

Evaluation of late-onset Alzheimer disease genetic susceptibility risks in a Canadian population.

We performed case-control studies using 2 Canadian cohorts to examine the role of 10 promising Alzheimer's disease (AD) loci identified in recent genomewide association studies. Patients age 65 years and older diagnosed with AD at baseline (prevalent cases) or who developed AD during follow-up assessments (incident cases) were compared with control subjects with no cognitive impairment. Our prevalent case study comparing prevalent AD cases (n = 428) with participants with no cognitive impairment (n = 524) revealed a significant association of rs6656401 and rs3818361 (CR1), rs2075650 (TOMM40), rs7561528 (BIN1), and rs3865444 (CD33) with late-onset AD that were robust to adjustment with age and apolipoprotein E ε4 genotype.

Clinical and pathological features of familial frontotemporal dementia caused by C9ORF72 mutation on chromosome 9p.

Frontotemporal dementia and amyotrophic lateral sclerosis are closely related clinical syndromes with overlapping molecular pathogenesis. Several families have been reported with members affected by frontotemporal dementia, amyotrophic lateral sclerosis or both, which show genetic linkage to a region on chromosome 9p21. Recently, two studies identified the FTD/ALS gene defect on chromosome 9p as an expanded GGGGCC hexanucleotide repeat in a non-coding region of the chromosome 9 open reading frame 72 gene (C9ORF72).

Clinical and pathological features of amyotrophic lateral sclerosis caused by mutation in the C9ORF72 gene on chromosome 9p.

Two studies recently identified a GGGGCC hexanucleotide repeat expansion in a non-coding region of the chromosome 9 open-reading frame 72 gene (C9ORF72) as the cause of chromosome 9p-linked amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). In a cohort of 231 probands with ALS, we identified the C9ORF72 mutation in 17 familial (27.4%) and six sporadic (3.

Three-dimensional nanocrystal superlattices grown in nanoliter microfluidic plugs.

We studied the self-assembly of inorganic nanocrystals (NCs) confined inside nanoliter droplets (plugs) into long-range ordered superlattices. We showed that a capillary microfluidic platform can be used for the optimization of growth conditions for NC superlattices and can provide insights into the kinetics of the NC assembly process. The utility of our approach was demonstrated by growing large (up to 200 μm) three-dimensional (3D) superlattices of various NCs, including Au, PbS, CdSe, and CoFe(2)O(4).

rs5848 polymorphism and serum progranulin level.

Objective: To assess the influence of rs5848 polymorphism in serum progranulin (PGRN) level in a cohort of subjects with Alzheimer and related dementias from a tertiary referral clinic.

Background: Mutations in the GRN gene cause autosomal dominant frontotemporal dementia (FTD) with TDP-43 pathology (FTLD-TDP) through haploinsufficiency. It has recently been shown that homozygous carriers of the T allele of rs5848 have an elevated risk of developing FTD, and this polymorphism may play a role in the pathogenesis of other dementia by modifying progranulin level.

Digital PCR on a SlipChip.

This paper describes a SlipChip to perform digital PCR in a very simple and inexpensive format. The fluidic path for introducing the sample combined with the PCR mixture was formed using elongated wells in the two plates of the SlipChip designed to overlap during sample loading. This fluidic path was broken up by simple slipping of the two plates that removed the overlap among wells and brought each well in contact with a reservoir preloaded with oil to generate 1280 reaction compartments (2.

Interaction between endothelin and angiotensin II in the up-regulation of vasopressin messenger RNA in the inner medullary collecting duct of the rat.

Recent studies in our laboratory have demonstrated that angiotensin (ANG) II and endothelin (ET) 1 up-regulate the expression of arginine vasopressin V(2) receptor in the inner medullary collecting duct (IMCD) of the rat. The present studies were performed to explore the interaction between ANG II and ET-1 in up-regulating the expression of arginine vasopressin V(2) receptor in the IMCD of the rat. Two sets of studies were done.