Electronic Noses and Tongues: Applications for the Food and Pharmaceutical Industries

The electronic nose (e-nose) is designed to crudely mimic the mammalian nose in that most contain sensors that non-selectively interact with odor molecules to produce some sort of signal that is then sent to a computer that uses multivariate statistics to determine patterns in the data. This pattern recognition is used to determine that one sample is similar or different from another based on headspace volatiles. There are different types of e-nose sensors including organic polymers, metal oxides, quartz crystal microbalance and even gas-chromatography (GC) or combined with mass spectroscopy (MS) can be used in a non-selective manner using chemical mass or patterns from a short GC column as an e-nose or “Z” nose. The electronic tongue reacts similarly to non-volatile compounds in a liquid. This review will concentrate on applications of e-nose and e-tongue technology for edible products and pharmaceutical uses

Reducing inflammation and rescuing FTD-related behavioral deficits in progranulin-deficient mice with α7 nicotinic acetylcholine receptor agonists.

Mutations in the progranulin gene cause frontotemporal dementia (FTD), a debilitating neurodegenerative disease that involves atrophy of the frontal and temporal lobes and affects personality, behavior, and language. Progranulin-deficient mouse models of FTD exhibit deficits in compulsive and social behaviors reminiscent of patients with FTD, and develop excessive microgliosis and increased release of inflammatory cytokines. Activation of nicotinic acetylcholine receptors (nAChRs) by nicotine or specific α7 nAChR agonists reduces neuroinflammation. Here, we investigated whether activation of nAChRs by nicotine or α7 agonists improved the excessive inflammatory and behavioral phenotypes of a progranulin-deficient FTD mouse model. We found that treatment with selective α7 agonists, PHA-568487 or ABT-107, strongly suppressed the activation of NF-κB in progranulin-deficient cells. Treatment with ABT-107 also reduced microgliosis, decreased TNFα levels, and reduced compulsive behavior in progranulin-deficient mice. Collectively, these data suggest that targeting activation of the α7 nAChR pathway may be beneficial in decreasing neuroinflammation and reversing some of the behavioral deficits observed in progranulin-deficient FTD

Reducing inflammation and rescuing FTD-related behavioral deficits in progranulin-deficient mice with α7 nicotinic acetylcholine receptor agonists.

Mutations in the progranulin gene cause frontotemporal dementia (FTD), a debilitating neurodegenerative disease that involves atrophy of the frontal and temporal lobes and affects personality, behavior, and language. Progranulin-deficient mouse models of FTD exhibit deficits in compulsive and social behaviors reminiscent of patients with FTD, and develop excessive microgliosis and increased release of inflammatory cytokines. Activation of nicotinic acetylcholine receptors (nAChRs) by nicotine or specific α7 nAChR agonists reduces neuroinflammation. Here, we investigated whether activation of nAChRs by nicotine or α7 agonists improved the excessive inflammatory and behavioral phenotypes of a progranulin-deficient FTD mouse model. We found that treatment with selective α7 agonists, PHA-568487 or ABT-107, strongly suppressed the activation of NF-κB in progranulin-deficient cells. Treatment with ABT-107 also reduced microgliosis, decreased TNFα levels, and reduced compulsive behavior in progranulin-deficient mice. Collectively, these data suggest that targeting activation of the α7 nAChR pathway may be beneficial in decreasing neuroinflammation and reversing some of the behavioral deficits observed in progranulin-deficient FTD

A mini-invasive procedure for treating arthrofibrosis of the knee

The aim of this study was to introduce the results of a novel mini-invasive operative technique comprising mini-incision release, “pie-crusting” lengthening of the quadriceps extensor, and arthroscopic lysis in severe arthrofibrotic knees. From 2010 to 2014, 17 patients (12 males and 5 females with a mean age of 44 years (range, 19–62 years)) with severely arthrofibrotic knees were treated with this operative technique. The mean follow-up duration was 23 months. The knee range of motion (ROM) was assessed with a goniometer. The functional outcomes were evaluated according to the Hospital for Special Surgery (HSS) score and Judets criteria. The ROM significantly improved from 29.7° (range, 7°–56°) preoperatively to 127° (range, 120°–136°) at the final follow-up in all patients (p 100°). The HSS score was improved from 70 points (range, 60–85 points) preoperatively to 91 points (range, 84–98 points) (p < 0.001) at the final follow-up. No extension lag, skin necrosis, quadriceps weakness, wound dehiscence or quadriceps tendon rupture occurred. Mini-invasive quadricepsplasty-associated arthroscopic lysis and manipulation of the knee in flexion is simple and easy and should be considered as a legitimate treatment for arthrofibrosis of the knee

Discovery and Structure-Activity Relationships of Novel Template, Truncated 1 &apos;-Homologated Adenosine Derivatives as Pure Dual PPAR gamma/delta Modulators

Following our report that A(3) adenosine receptor (AR) antagonist 1 exhibited a polypharmacological profile as a dual modulator of peroxisome proliferator-activated receptor (PPAR)gamma/delta, we discovered a new template, 1&apos;-homologated adenosine analogues 4a-4t, as dual PPARy/delta modulators without AR binding. Removal of binding affinity to A(3)AR was achieved by 1&apos;-homologation, and PPAR gamma/delta dual modulation was derived from the structural similarity between the target nucleosides and PPAR modulator drug, rosiglitazone. All the final nucleosides were devoid of AR-binding affinity and exhibited high binding affinities to PPAR gamma/delta but lacked PPAR alpha binding. 2-Cl derivatives exhibited dual receptor-binding affinity to PPAR gamma/delta, which was absent for the corresponding 2-H derivatives. 2-Propynyl substitution prevented PPAR delta-binding affinity but preserved PPAR gamma affinity, indicating that the C2 position defines a pharmacophore for selective PPAR gamma ligand designs. PPAR gamma/delta dual modulators functioning as both PPAR gamma partial agonists and PPAR delta antagonists promoted adiponectin production, potential against hypoadiponectinemia-associated cancer and metabolic diseases.N

Reducing inflammation and rescuing FTD-related behavioral deficits in progranulin-deficient mice with α7 nicotinic acetylcholine receptor agonists

Mutations in the progranulin gene cause frontotemporal dementia (FTD), a debilitating neurodegenerative disease that involves atrophy of the frontal and temporal lobes and affects personality, behavior, and language. Progranulin-deficient mouse models of FTD exhibit deficits in compulsive and social behaviors reminiscent of patients with FTD, and develop excessive microgliosis and increased release of inflammatory cytokines. Activation of nicotinic acetylcholine receptors (nAChRs) by nicotine or specific α7 nAChR agonists reduces neuroinflammation. Here, we investigated whether activation of nAChRs by nicotine or α7 agonists improved the excessive inflammatory and behavioral phenotypes of a progranulin-deficient FTD mouse model. We found that treatment with selective α7 agonists, PHA-568487 or ABT-107, strongly suppressed the activation of NF-κB in progranulin-deficient cells. Treatment with ABT-107 also reduced microgliosis, decreased TNFα levels, and reduced compulsive behavior in progranulin-deficient mice. Collectively, these data suggest that targeting activation of the α7 nAChR pathway may be beneficial in decreasing neuroinflammation and reversing some of the behavioral deficits observed in progranulin-deficient FTD