11 resultados para Brain - Sampling studies
em Digital Commons at Florida International University
Resumo:
From 8/95 to 2/01, we investigated the ecological effects of intra- and inter-annual variability in freshwater flow through Taylor Creek in southeastern Everglades National Park. Continuous monitoring and intensive sampling studies overlapped with an array of pulsed weather events that impacted physical, chemical, and biological attributes of this region. We quantified the effects of three events representing a range of characteristics (duration, amount of precipitation, storm intensity, wind direction) on the hydraulic connectivity, nutrient and sediment dynamics, and vegetation structure of the SE Everglades estuarine ecotone. These events included a strong winter storm in November 1996, Tropical Storm Harvey in September 1999, and Hurricane Irene in October 1999. Continuous hydrologic and daily water sample data were used to examine the effects of these events on the physical forcing and quality of water in Taylor Creek. A high resolution, flow-through sampling and mapping approach was used to characterize water quality in the adjacent bay. To understand the effects of these events on vegetation communities, we measured mangrove litter production and estimated seagrass cover in the bay at monthly intervals. We also quantified sediment deposition associated with Hurricane Irene's flood surge along the Buttonwood Ridge. These three events resulted in dramatic changes in surface water movement and chemistry in Taylor Creek and adjacent regions of Florida Bay as well as increased mangrove litterfall and flood surge scouring of seagrass beds. Up to 5 cm of bay-derived mud was deposited along the ridge adjacent to the creek in this single pulsed event. These short-term events can account for a substantial proportion of the annual flux of freshwater and materials between the mangrove zone and Florida Bay. Our findings shed light on the capacity of these storm events, especially when in succession, to have far reaching and long lasting effects on coastal ecosystems such as the estuarine ecotone of the SE Everglades.
Resumo:
A method to estimate speed of free-ranging fishes using a passive sampling device is described and illustrated with data from the Everglades, U.S.A. Catch per unit effort (CPUE) from minnow traps embedded in drift fences was treated as an encounter rate and used to estimate speed, when combined with an independent estimate of density obtained by use of throw traps that enclose 1 m2 of marsh habitat. Underwater video was used to evaluate capture efficiency and species-specific bias of minnow traps and two sampling studies were used to estimate trap saturation and diel-movement patterns; these results were used to optimize sampling and derive correction factors to adjust species-specific encounter rates for bias and capture efficiency. Sailfin mollies Poecilia latipinna displayed a high frequency of escape from traps, whereas eastern mosquitofish Gambusia holbrooki were most likely to avoid a trap once they encountered it; dollar sunfish Lepomis marginatus were least likely to avoid the trap once they encountered it or to escape once they were captured. Length of sampling and time of day affected CPUE; fishes generally had a very low retention rate over a 24 h sample time and only the Everglades pygmy sunfish Elassoma evergladei were commonly captured at night. Dispersal speed of fishes in the Florida Everglades, U.S.A., was shown to vary seasonally and among species, ranging from 0· 05 to 0· 15 m s−1 for small poeciliids and fundulids to 0· 1 to 1· 8 m s−1 for L. marginatus. Speed was generally highest late in the wet season and lowest in the dry season, possibly tied to dispersal behaviours linked to finding and remaining in dry-season refuges. These speed estimates can be used to estimate the diffusive movement rate, which is commonly employed in spatial ecological models.
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The paper examines the nature of qualitative empirical studies published in the AHRD proceedings from 1999-2003 and discusses findings on method, rationale for method, data collection, sampling strategies, and integrity measures.
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This material is based upon work supported by the National Science Foundation through the Florida Coastal Everglades Long-Term Ecological Research program under Cooperative Agreements #DBI-0620409 and #DEB-9910514. This image is made available for non-commercial or educational use only.
Resumo:
Learning and memory in adult females decline during menopause and estrogen replacement therapy is commonly prescribed during menopause. Post-menopausal women tend to suffer from depression and are prescribed antidepressants – in addition to hormone therapy. Estrogen replacement therapy is a topic that engenders debate since several studies contradict its efficacy as a palliative therapy for cognitive decline and neurodegenerative diseases. Signaling transduction pathways can alter brain cell activity, survival, and morphology by facilitating transcription factor DNA binding and protein production. The steroidal hormone estrogen and the anti-depressant drug lithium interact through these signaling transduction pathways facilitating transcription factor activation. The paucity of data on how combined hormones and antidepressants interact in regulating gene expression led me to hypothesize that in primary mixed brain cell cultures, combined 17β-estradiol (E2) and lithium chloride (LiCl) (E2/LiCl) will alter genetic expression of markers involved in synaptic plasticity and neuroprotection. Results from these studies indicated that a 48 h treatment of E2/LiCl reduced glutamate receptor subunit genetic expression, but increased neurotrophic factor and estrogen receptor genetic expression. Combined treatment also failed to protect brain cell cultures from glutamate excitotoxicity. If lithium facilitates protein signaling pathways mediated by estrogen, can lithium alone serve as a palliative treatment for post-menopause? This question led me to hypothesize that in estrogen-deficient mice, lithium alone will increase episodic memory (tested via object recognition), and enhance expression in the brain of factors involved in anti-apoptosis, learning and memory. I used bilaterally ovariectomized (bOVX) C57BL/6J mice treated with LiCl for one month. Results indicated that LiCl-treated bOVX mice increased performance in object recognition compared with non-treated bOVX. Increased performance in LiCl-treated bOVX mice coincided with augmented genetic and protein expression in the brain. Understanding the molecular pathways of estrogen will assist in identifying a palliative therapy for menopause-related dementia, and lithium may serve this purpose by acting as a selective estrogen-mediated signaling modulator.
Resumo:
This dissertation evaluated the feasibility of using commercially available immortalized cell lines in building a tissue engineered in vitro blood-brain barrier (BBB) co-culture model for preliminary drug development studies. Mouse endothelial cell line and rat astrocyte cell lines purchased from American Type Culture Collections (ATCC) were the building blocks of the co-culture model. An astrocyte derived acellular extracellular matrix (aECM) was introduced in the co-culture model to provide a novel in vitro biomimetic basement membrane for the endothelial cells to form endothelial tight junctions. Trans-endothelial electrical resistance (TEER) and solute mass transport studies were engaged to quantitatively evaluate the tight junction formation on the in-vitro BBB models. Immuno-fluorescence microscopy and Western Blot analysis were used to qualitatively verify the in vitro expression of occludin, one of the earliest discovered tight junction proteins. Experimental data from a total of 12 experiments conclusively showed that the novel BBB in vitro co-culture model with the astrocyte derived aECM (CO+aECM) was promising in terms of establishing tight junction formation represented by TEER values, transport profiles and tight junction protein expression when compared with traditional co-culture (CO) model setups and endothelial cells cultured alone. Experimental data were also found to be comparable with several existing in vitro BBB models built from various methods. In vitro colorimetric sulforhodamine B (SRB) assay revealed that the co-cultured samples with aECM resulted in less cell loss on the basal sides of the insert membranes than that from traditional co-culture samples. The novel tissue engineering approach using immortalized cell lines with the addition of aECM was proven to be a relevant alternative to the traditional BBB in vitro modeling.
Resumo:
Parenteral use of drugs; such as opiates exert immunomodulatory effects and serve as a cofactor in the progression of HIV-1 infection, thereby potentiating HIV related neurotoxicity ultimately leading to progression of NeuroAIDS. Morphine exposure is known to induce apoptosis, down regulate cAMP response element-binding (CREB) expression and decrease in dendritic branching and spine density in cultured cells. Use of neuroprotective agent; brain derived neurotropic factor (BDNF), which protects neurons against these effects, could be of therapeutic benefit in the treatment of opiate addiction. Previous studies have shown that BDNF was not transported through the blood brain barrier (BBB) in-vivo.; and hence it is not effectivein-vivo. Therefore development of a drug delivery system that can cross BBB may have significant therapeutic advantage. In the present study, we hypothesized that magnetically guided nanocarrier may provide a viable approach for targeting BDNF across the BBB. We developed a magnetic nanoparticle (MNP) based carrier bound to BDNF and evaluated its efficacy and ability to transmigrate across the BBB using an in-vitro BBB model. The end point determinations of BDNF that crossed BBB were apoptosis, CREB expression and dendritic spine density measurement. We found that transmigrated BDNF was effective in suppressing the morphine induced apoptosis, inducing CREB expression and restoring the spine density. Our results suggest that the developed nanocarrier will provide a potential therapeutic approach to treat opiate addiction, protect neurotoxicity and synaptic density degeneration.
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In the 1980s, government agencies sought to utilize research on drug use prevention to design media campaigns. Enlisting the assistance of the national media, several campaigns were designed and initiated to bring anti-drug use messages to adolescents in the form of public service advertising. This research explores the sources of information selected by adolescents in grades 7 through 12 and how the selection of media and other sources of information relate to drug use behavior and attitudes and perceptions related to risk/harm and disapproval of friends' drug-using activities.^ Data collected from 1989 to 1992 in the Miami Coalition School Survey provided a random selection of secondary school studies. The responses of these students were analyzed using multivariate statistical techniques.^ Although many of the students selected media as the source for most of their information on the effects of drugs on the people who use them, the selection of media was found to be positively related to alcohol use and negatively related to marijuana use. The selection of friends, brothers, or sisters was a statistically significant source for adolescents who smoke cigarettes, use alcohol or marijuana.^ The results indicate that the anti-drug use messages received by students may be canceled out by media messages perceived to advocate substance use and that a more persuasive source of information for adolescents may be friends and siblings. As federal reports suggest that the economic costs of drug abuse will reach an estimated $150 billion by 1997 if current trends continue, prevention policy that addresses the glamorization of substance use remains a national priority. Additionally, programs that advocate prevention within the peer cluster must be supported, as peers are an influential source for both inspiring and possibly preventing drug use behavior. ^
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Persistence of HIV-1 reservoirs within the Central Nervous System (CNS) remains a significant challenge to the efficacy of potent anti-HIV-1 drugs. The primary human Brain Microvascular Endothelial Cells (HBMVEC) constitutes the Blood Brain Barrier (BBB) which interferes with anti-HIV drug delivery into the CNS. The ATP binding cassette (ABC) transporters expressed on HBMVEC can efflux HIV-1 protease inhibitors (HPI), enabling the persistence of HIV-1 in CNS. Constitutive low level expression of several ABC-transporters, such as MDR1 (a.k.a. P-gp) and MRPs are documented in HBMVEC. Although it is recognized that inflammatory cytokines and exposure to xenobiotic drug substrates (e.g HPI) can augment the expression of these transporters, it is not known whether concomitant exposure to virus and anti-retroviral drugs can increase drug-efflux functions in HBMVEC. Our in vitro studies showed that exposure of HBMVEC to HIV-1 significantly up-regulates both MDR1 gene expression and protein levels; however, no significant increases in either MRP-1 or MRP-2 were observed. Furthermore, calcein-AM dye-efflux assays using HBMVEC showed that, compared to virus exposure alone, the MDR1 mediated drug-efflux function was significantly induced following concomitant exposure to both HIV-1 and saquinavir (SQV). This increase in MDR1 mediated drug-efflux was further substantiated via increased intracellular retention of radiolabeled [3H-] SQV. The crucial role of MDR1 in 3H-SQV efflux from HBMVEC was further confirmed by using both a MDR1 specific blocker (PSC-833) and MDR1 specific siRNAs. Therefore, MDR1 specific drug-efflux function increases in HBMVEC following co-exposure to HIV-1 and SQV which can reduce the penetration of HPIs into the infected brain reservoirs of HIV-1. A targeted suppression of MDR1 in the BBB may thus provide a novel strategy to suppress residual viral replication in the CNS, by augmenting the therapeutic efficacy of HAART drugs.
Resumo:
Learning and memory in adult females decline during menopause and estrogen replacement therapy is commonly prescribed during menopause. Post-menopausal women tend to suffer from depression and are prescribed antidepressants – in addition to hormone therapy. Estrogen replacement therapy is a topic that engenders debate since several studies contradict its efficacy as a palliative therapy for cognitive decline and neurodegenerative diseases. Signaling transduction pathways can alter brain cell activity, survival, and morphology by facilitating transcription factor DNA binding and protein production. The steroidal hormone estrogen and the anti-depressant drug lithium interact through these signaling transduction pathways facilitating transcription factor activation. The paucity of data on how combined hormones and antidepressants interact in regulating gene expression led me to hypothesize that in primary mixed brain cell cultures, combined 17beta-estradiol (E2) and lithium chloride (LiCl) (E2/LiCl) will alter genetic expression of markers involved in synaptic plasticity and neuroprotection. Results from these studies indicated that a 48 h treatment of E2/LiCl reduced glutamate receptor subunit genetic expression, but increased neurotrophic factor and estrogen receptor genetic expression. Combined treatment also failed to protect brain cell cultures from glutamate excitotoxicity. If lithium facilitates protein signaling pathways mediated by estrogen, can lithium alone serve as a palliative treatment for post-menopause? This question led me to hypothesize that in estrogen-deficient mice, lithium alone will increase episodic memory (tested via object recognition), and enhance expression in the brain of factors involved in anti-apoptosis, learning and memory. I used bilaterally ovariectomized (bOVX) C57BL/6J mice treated with LiCl for one month. Results indicated that LiCl-treated bOVX mice increased performance in object recognition compared with non-treated bOVX. Increased performance in LiCl-treated bOVX mice coincided with augmented genetic and protein expression in the brain. Understanding the molecular pathways of estrogen will assist in identifying a palliative therapy for menopause-related dementia, and lithium may serve this purpose by acting as a selective estrogen-mediated signaling modulator.
Resumo:
To demonstrate the extent of elder malnutrition risk in this country, a meta analysis of 30 studies that used the Nutrition Screening Initiative's "DETERMINE Your Nutritional Health Checklist" was conducted. The studies were divided into three categories: Elder Populations in Healthcare Related Systems (HS), Elder Meal Program Participants (MP), and General Community Residing Elder Population (GC). HS was sub-divided into Hospital Inpatient/Clinic Outpatient and Long Term Care/Home Care. The MP population were identified as Congregate or Home Delivered meal participants. Overall, results indicate that 63% of elders are at moderate (32%) or high (31 %) risk of malnutrition. Home Delivered Meal Participants and Hospital Inpatient/Clinic Outpatients are most likely to be at high risk of malnutrition (49.5% and 49.1%, respectively). Individuals least likely to be at high malnutrition risk are the General Community Residing Elder Population (17.5%) and Congregate Meal Participants (22.5%).