Caecidae (Mollusca: Gastropoda) in Broward County, Florida

Caecidae is a widespread family of minute gastropod snails. Although a few species have previously been found in abundance in a few localized studies in Broward County waters, little is known about their richness, diversity, abundance and distribution in different habitats throughout local waters. This project examined species assemblages both qualitatively and quantitatively in a range of benthic habitats across Broward County. Samples were collected from five different habitat types from northern and southern Broward Country, and included two of each of the following five sites: mangrove, Intracoastal Waterway, creek, reef and rubble. Caecid specimens were removed from general samples, separated by species or developmental stage and preserved in 95% ethanol. Also, as artificial substrates have become an increasingly important resource enhancement technique, this project also compared Caecidae assemblages on artificial vs. natural substrates using a large dataset previously used primarily to examine amphipod crustacean assemblages. Species recorded in Broward County include Caecum pulchellum, C. imbricatum, C. floridanum, C. textile and Meioceras nitidum. Published records exist for 14 additional species collected elsewhere in South Florida (e.g., Palm Beach County). Descriptions, distributional data and synonymies summarizing available information are given for all 19 species. Nearly 97% of the specimens, including Caecum pulchellum, Caecum floridanum and Meioceras nitidum, were found on the reef and rubble habitats; approximately 2.5% percent were found in the Intracoastal; approximately 0.5% were found in the creek, and all taxa were absent in both mangrove habitats. A repeated measures MANOVA indicated no significant differences among any of the factors (reef type, substrate or genus) over time; (RM MANOVA, F=0.112, 2.596, 0.018, 4.604), p values = 0.769, 0.248, 0.906, 0.141) suggesting that there were no preferences in substrate material among the species investigated

Prognostic relevance of a T-type calcium channels gene signature in solid tumours: A correlation ready for clinical validation

BackgroundT-type calcium channels (TTCCs) mediate calcium influx across the cell membrane. TTCCs regulate numerous physiological processes including cardiac pacemaking and neuronal activity. In addition, they have been implicated in the proliferation, migration and differentiation of tumour tissues. Although the signalling events downstream of TTCC-mediated calcium influx are not fully elucidated, it is clear that variations in the expression of TTCCs promote tumour formation and hinder response to treatment.MethodsWe examined the expression of TTCC genes (all three subtypes; CACNA-1G, CACNA-1H and CACNA-1I) and their prognostic value in three major solid tumours (i.e. gastric, lung and ovarian cancers) via a publicly accessible database.ResultsIn gastric cancer, expression of all the CACNA genes was associated with overall survival (OS) among stage I-IV patients (all pConclusionsAlterations in CACNA gene expression are linked to tumour prognosis. Gastric cancer represents the most promising setting for further evaluation

Drugs developed to treat diabetes, liraglutide and lixisenatide, cross the blood brain barrier and enhance neurogenesis

<p>Abstract</p> <p>Background</p> <p>Type 2 diabetes is a risk factor for Alzheimer's disease (AD), most likely linked to an impairment of insulin signalling in the brain. Therefore, drugs that enhance insulin signalling may have therapeutic potential for AD. Liraglutide (Victoza) and exenatide (Byetta) are novel long-lasting analogues of the GLP-1 incretin hormone and are currently available to treat diabetes. They facilitate insulin signalling via the GLP-1 receptor (GLP-1R). Numerous <it>in vitro </it>and <it>in vivo </it>studies have shown that GLP-1 analogues have a range of neuroprotective properties. GLP-1Rs are expressed in the hippocampal area of the brain an important site of adult neurogenesis and maintenance of cognition and memory formation. Therefore, if GLP-1 analogues can cross the blood brain barrier, diffuse through the brain to reach the receptors and most importantly activate them, their neuroprotective effects may be realized.</p> <p>Results</p> <p>In the present study we profiled the GLP-1 receptor agonists liraglutide (Victoza) and lixisenatide (Lyxumia). We measured the kinetics of crossing the blood brain barrier (BBB), activation of the GLP-1R by measuring cAMP levels, and physiological effects in the brain on neuronal stem cell proliferation and neurogenesis. Both drugs were able to cross the BBB. Lixisenatide crossed the BBB at all doses tested (2.5, 25, or 250 nmol/kg bw ip.) when measured 30 min post-injection and at 2.5-25 nmol/kg bw ip. 3 h post-injection. Lixisenatide also enhanced neurogenesis in the brain. Liraglutide crossed the BBB at 25 and 250 nmol/kg ip. but no increase was detectable at 2.5 nmol/kg ip. 30 min post-injection, and at 250 nmol/kg ip. at 3 h post-injection. Liraglutide and lixisenatide enhanced cAMP levels in the brain, with lixisenatide being more effective.</p> <p>Conclusions</p> <p>Our results suggest that these novel incretin analogues cross the BBB and show physiological activity and neurogenesis in the brain, which may be of use as a treatment of neurodegenerative diseases.</p

Exercise and cognitive function: a hypothesis for the association of type II diabetes mellitus and Alzheimer's disease from an evolutionary perspective

The association of type II diabetes mellitus (DM2) with Alzheimer's disease (AD) has received considerable attention in recent years. In the present paper, a hypothesis for this association from an evolutionary perspective, with emphasis on the close interplay between exercise and cognitive function, will be advanced in order to provide a biological rationale for the notion that the fundamental metabolic features of DM2 act in the brain over a protracted time span to induce the neuropathological characteristics of Alzheimer's disease thereby producing cognitive impairment. It is hoped that this hypothesis puts the association of DM2 and AD on firm conceptual grounds from a biological perspective and offers directions for further research

Internet-based interventions for the secondary prevention of coronary heart disease

Background The Internet could provide a means of delivering secondary prevention programmes to people with coronary heart disease (CHD). Objectives To determine the effectiveness of Internet-based interventions targeting lifestyle changes and medicines management for the secondary prevention of CHD. Search methods We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, in December 2014. We also searched six other databases in October 2014, and three trials registers in January 2015 together with reference checking and handsearching to identify additional studies. Selection criteria Randomised controlled trials (RCTs) evaluating Internet-delivered secondary prevention interventions aimed at people with CHD. Data collection and analysis Two review authors independently assessed risk of bias and extracted data according to the Cochrane Handbook for Systematic Reviews of Interventions. We assessed evidence quality using the GRADE approach and presented this in a 'Summary of findings' table

The ε3 and ε4 Alleles of Human APOE Differentially Affect Tau Phosphorylation in Hyperinsulinemic and Pioglitazone Treated Mice

Impaired insulin signalling is increasingly thought to contribute to Alzheimer's disease (AD). The ε4 isoform of the APOE gene is the greatest genetic risk factor for sporadic, late onset AD, and is also associated with risk for type 2 diabetes mellitus (T2DM). Neuropathological studies reported the highest number of AD lesions in brain tissue of ε4 diabetic patients. However other studies assessing AD pathology amongst the diabetic population have produced conflicting reports and have failed to show an increase in AD-related pathology in diabetic brain. The thiazolidinediones (TZDs), peroxisome proliferator-activated receptor gamma agonists, are peripheral insulin sensitisers used to treat T2DM. The TZD, pioglitazone, improved memory and cognitive functions in mild to moderate AD patients. Since it is not yet clear how apoE isoforms influence the development of T2DM and its progression to AD, we investigated amyloid beta and tau pathology in APOE knockout mice, carrying human APOEε3 or ε4 transgenes after diet-induced insulin resistance with and without pioglitazone treatment.Male APOE knockout, APOEε3-transgenic and APOEε4-transgenic mice, together with background strain C57BL6 mice were kept on a high fat diet (HFD) or low fat diet (LFD) for 32 weeks, or were all fed HFD for 32 weeks and during the final 3 weeks animals were treated with pioglitazone or vehicle.All HFD animals developed hyperglycaemia with elevated plasma insulin. Tau phosphorylation was reduced at 3 epitopes (Ser396, Ser202/Thr205 and Thr231) in all HFD, compared to LFD, animals independent of APOE genotype. The introduction of pioglitazone to HFD animals led to a significant reduction in tau phosphorylation at the Ser202/Thr205 epitope in APOEε3 animals only. We found no changes in APP processing however the levels of soluble amyloid beta 40 was reduced in APOE knockout animals treated with pioglitazone

Protective Effects of a Rhodiola Crenulata Extract and Salidroside on Hippocampal Neurogenesis against Streptozotocin-Induced Neural Injury in the Rat

Previously we have demonstrated that a Rhodiola crenulata extract (RCE), containing a potent antioxidant salidroside, promotes neurogenesis in the hippocampus of depressive rats. The current study was designed to further investigate the protective effect of the RCE on neurogenesis in a rat model of Alzheimer's disease (AD) induced by an intracerebroventricular injection of streptozotocin (STZ), and to determine whether this neuroprotective effect is induced by the antioxidative activity of salidroside. Our results showed that pretreatment with the RCE significantly improved the impaired neurogenesis and simultaneously reduced the oxidative stress in the hippocampus of AD rats. In vitro studies revealed that (1) exposure of neural stem cells (NSCs) from the hippocampus to STZ strikingly increased intracellular reactive oxygen species (ROS) levels, induced cell death and perturbed cell proliferation and differentiation, (2) hydrogen peroxide induced similar cellular activities as STZ, (3) pre-incubation of STZ-treated NSCs with catalase, an antioxidant, suppressed all these cellular activities induced by STZ, and (4) likewise, pre-incubation of STZ-treated NSCs with salidroside, also an antioxidant, suppressed all these activities as catalase: reduction of ROS levels and NSC death with simultaneous increases in proliferation and differentiation. Our findings indicated that the RCE improved the impaired hippocampal neurogenesis in the rat model of AD through protecting NSCs by its main ingredient salidroside which scavenged intracellular ROS