Liquidity Risk Management of Agricultural Cooperatives in Isabela, Philippines

Purpose: The aim of this study is to examinethe liquidity risks the cooperative is exposed to, the effectiveness of liquidity risk management activities and the challenges faced by these selected agricultural cooperatives in Isabela in managing its liquidity risks.   Theoretical framework:  Cooperative development encompasses a wide range of individual and economic development issues. It is challenging for cooperatives of all sizes to control liquidity risk and assess the degree of uncertainty in their liquidity position. Since strategies for risk management are costly, cooperatives have had difficulties in reducing these liquidity risks, which might result in an increased rate of insolvency and pose problems for the financial condition of cooperatives.   Design/Methodology/Approach: Data were gathered from 25 agricultural cooperatives located in the province of Isabela, Philippines through a four-point likert scale survey questionnaire, open and close-ended interview questionnaire and information from annual reports and financial statements. Quantitative data were analyzed using descriptive statistics.   Findings:  The results of the study revealed that agricultural cooperatives in Isabela are exposed to liquidity risk at low level. Numerous activities were implemented to minimize liquidity risk through liquidity risk identification, liquidity risk evaluation and liquidity risk mitigation. Moreover, cooperatives face various challenges in the implementation of risk management activities even though most of the cooperatives practice an effective liquidity risk management.   Research, Practical & Social implications: The study will benefit the stakeholders of agricultural cooperatives in Isabela since cooperative operations are always evolving and liquidity risks are inherent in every organization.   Originality/Value: The research examines agicultural cooperatives which is one of the organizations that provide assistance to the community. By producing liquidity risk management assessment, cooperatives will impove its operations and provide more support to its members

Dysregulation of System Xc- and Its Impact on Cocaine Seeking

Abnormal glutamate signaling in the brain, particularly in the nucleus accumbens core, contributes to compulsive cocaine-seeking behavior. In the nucleus accumbens, two distinct pools of glutamate exist. The synaptic pool stimulates excitatory postsynaptic receptors, leading to cocaine seeking. Cystine-glutamate exchange by system xc- contributes to the extrasynaptic pool and regulates neurotransmission by activating extrasynaptic receptors including inhibitory Group II metabotropic glutamate receptors, positioning this as an important mechanism for regulating nucleus accumbens activity. We and others have found decreased levels of cystine-glutamate exchange in animals withdrawn from chronic cocaine administration. In chapter 1, we describe studies directly implicating diminished system xc- activity in abnormal glutamate signaling necessary for promoting drug seeking. Given that altered system xc- activity is essential to drug seeking, understanding the cellular basis of reduced cystine-glutamate exchange would advance our knowledge of the neural basis of addiction. Unfortunately, little is known about how the system is regulated. To address this, we sought to define conditions that permit the study of system xc- (chapter 2). In chapter 3, we examined potential regulation of xc- by dopamine, nonspecific dopamine agonists, D1-liked dopamine receptor agonists, and D2-like dopamine receptor agonists. While we found D1-like receptor regulation of cystine-glutamate exchange in mixed cortical culture, we did not observe this effect in tissue punches; thus, it is unlikely that abnormal regulation of system xc- by dopamine underlies reduced cystine-glutamate exchange in cocaine-withdrawn animals. In chapter 4, we examined pituitary adenylyl cyclase activating polypeptide (PACAP) because it has been recently shown to regulate extracellular glutamate homeostasis. We found acute and tonic regulation of cystine-glutamate exchange by PACAP-induced stimulation of Ca2+-dependent protein kinase (PKC) activity. More importantly, we also determined that PACAP regulation of system xc- is diminished in animals withdrawn from cocaine self-administration. These findings suggest dysregulated PACAP neurotransmission in cocaine-withdrawn animals contributes to the neural basis of addiction. By revealing novel mechanisms contributing to addiction, scientists can identify novel targets for therapeutic treatment

Drug-Induced Plasticity Contributing to Heightened Relapse Susceptibility: Neurochemical Changes and Augmented Reinstatement in High-Intake Rats

A key in understanding the neurobiology of addiction and developing effective pharmacotherapies is revealing drug-induced plasticity that results in heightened relapse susceptibility. Previous studies have demonstrated that increased extracellular glutamate, but not dopamine, in the nucleus accumbens core (NAcc) is necessary for cocaine-induced reinstatement. In this report, we examined whether drug-induced adaptations that are necessary to generate cocaine-induced reinstatement also determine relapse vulnerability. To do this, rats were assigned to self-administer cocaine under conditions resulting in low (2 h/d; 0.5 mg/kg/infusion, i.v.) or high (6 h/d; 1.0 mg/kg/infusion, i.v.) levels of drug intake since these manipulations produce groups of rats exhibiting differences in the magnitude of cocaine-induced reinstatement. Approximately 19 d after the last session, cocaine-induced drug seeking and extracellular levels of glutamate and dopamine in the NAcc were measured. Contrary to our hypothesis, high-intake rats exhibited a more robust cocaine-induced increase in extracellular levels of dopamine but not glutamate. Further, increased reinstatement in high-intake rats was no longer observed when the D1 receptor antagonist SCH-23390 was infused into the NAcc. The sensitized dopamine response to cocaine in high-intake rats may involve blunted cystine–glutamate exchange by system xc−. Reduced 14C-cystine uptake through system xc− was evident in NAcc tissue slices obtained from high-intake rats, and the augmented dopamine response in these rats was no longer observed when subjects received the cysteine prodrug N-acetyl cysteine. These data reveal a role for drug-induced NAcc dopamine in heightened relapse vulnerability observed in rats with a history of high levels of drug intake

Blunted Cystine–Glutamate Antiporter Function in the Nucleus Accumbens Promotes Cocaine-induced Drug Seeking

Repeated cocaine alters glutamate neurotransmission, in part, by reducing cystine–glutamate exchange via system xc−, which maintains glutamate levels and receptor stimulation in the extrasynaptic compartment. In the present study, we undertook two approaches to determine the significance of plasticity involving system xc−. First, we examined whether the cysteine prodrug N-acetylcysteine attenuates cocaine-primed reinstatement by targeting system xc−. Rats were trained to self-administer cocaine (1 mg/kg/200 μl, i.v.) under extended access conditions (6 h/day). After extinction training, cocaine (10 mg/kg, i.p.) primed reinstatement was assessed in rats pretreated with N-acetylcysteine (0–60 mg/kg, i.p.) in the presence or absence of the system xc− inhibitor (S)-4-carboxyphenylglycine (CPG; 0.5 μM; infused into the nucleus accumbens). N-acetylcysteine attenuated cocaine-primed reinstatement, and this effect was reversed by co-administration of CPG. Secondly, we examined whether reduced system xc− activity is necessary for cocaine-primed reinstatement. To do this, we administered N-acetylcysteine (0 or 90 mg/kg, i.p.) prior to 12 daily self-administration sessions (1 mg/kg/200 μl, i.v.; 6 h/day) since this procedure has previously been shown to prevent reduced activity of system xc−. On the reinstatement test day, we then acutely impaired system xc− in some of the rats by infusing CPG (0.5 μM) into the nucleus accumbens. Rats that had received N-acetylcysteine prior to daily self-administration sessions exhibited diminished cocaine-primed reinstatement; this effect was reversed by infusing the cystine–glutamate exchange inhibitor CPG into the nucleus accumbens. Collectively these data establish system xc− in the nucleus accumbens as a key mechanism contributing to cocaine-primed reinstatement

Repeated \u3cem\u3eN\u3c/em\u3e-Acetylcysteine Administration Alters Plasticity-Dependent Effects of Cocaine

Cocaine produces a persistent reduction in cystine–glutamate exchange via system xc− in the nucleus accumbens that may contribute to pathological glutamate signaling linked to addiction. System xc− influences glutamate neurotransmission by maintaining basal, extracellular glutamate in the nucleus accumbens, which, in turn, shapes synaptic activity by stimulating group II metabotropic glutamate autoreceptors. In the present study, we tested the hypothesis that a long-term reduction in system xc− activity is part of the plasticity produced by repeated cocaine that results in the establishment of compulsive drug seeking. To test this, the cysteine prodrug N-acetylcysteine was administered before daily cocaine to determine the impact of increased cystine–glutamate exchange on the development of plasticity-dependent cocaine seeking. Although N-acetylcysteine administered before cocaine did not alter the acute effects of cocaine on self-administration or locomotor activity, it prevented behaviors produced by repeated cocaine including escalation of drug intake, behavioral sensitization, and cocaine-primed reinstatement. Because sensitization or reinstatement was not evident even 2–3 weeks after the last injection of N-acetylcysteine, we examined whether N-acetylcysteine administered before daily cocaine also prevented the persistent reduction in system xc− activity produced by repeated cocaine. Interestingly, N-acetylcysteine pretreatment prevented cocaine-induced changes in [35S]cystine transport via system xc−, basal glutamate, and cocaine-evoked glutamate in the nucleus accumbens when assessed at least 3 weeks after the last N-acetylcysteine pretreatment. These findings indicate that N-acetylcysteine selectively alters plasticity-dependent behaviors and that normal system xc− activity prevents pathological changes in extracellular glutamate that may be necessary for compulsive drug seeking

Pituitary Adenylate Cyclase-Activating Polypeptide Orchestrates Neuronal Regulation Of The Astrocytic Glutamate-Releasing Mechanism System x\u3csub\u3ec\u3c/sub\u3e\u3csup\u3e−\u3c/sup\u3e

Glutamate signaling is achieved by an elaborate network involving neurons and astrocytes. Hence, it is critical to better understand how neurons and astrocytes interact to coordinate the cellular regulation of glutamate signaling. In these studies, we used rat cortical cell cultures to examine whether neurons or releasable neuronal factors were capable of regulating system xc-(Sxc), a glutamate-releasing mechanism that is expressed primarily by astrocytes and has been shown to regulate synaptic transmission. We found that astrocytes cultured with neurons or exposed to neuronal-conditioned media displayed significantly higher levels of Sxc activity. Next, we demonstrated that the pituitary adenylate cyclase-activating polypeptide (PACAP) may be a neuronal factor capable of regulating astrocytes. In support, we found that PACAP expression was restricted to neurons, and that PACAP receptors were expressed in astro-cytes. Interestingly, blockade of PACAP receptors in cultures comprised of astrocytes and neurons significantly decreased Sxc activity to the level observed in purified astrocytes, whereas application of PACAP to purified astrocytes increased Sxc activity to the level observed in cultures comprised of neurons and astrocytes. Collectively, these data reveal that neurons coordinate the actions of glutamate-related mechanisms expressed by astrocytes, such as Sxc, a process that likely involves PACAP

Resisting Erasure: Forging Our Own Space and Histories

The idea that queer communities, due to their marginalized state, are inherently accepting of all identities regardless of race, gender, culture, and religion is extremely flawed. Racism and discrimination based off one’s identities are commonly experienced within LGBTQ2IA+ community, placing queer and trans, Black, Indigenous, and more people of colour (QTBIPOC) in a vulnerable position forcing them to seek out and forge spaces where their identities feel welcomed and valued. This major paper and the accompanying film contributes to these discussions by exploring the spatial accounts of queer racialized people who are living, working, playing or participating in activism in Toronto’s Church-Wellesley area, also known as The Village. This major paper and film also includes an analysis looking at the impacts of planners and the field of planning on how queer racialized people experience queer space; putting forth a perspective that is absent from the practice, including the curriculum. This major paper therefore provides an argument for the need to reconstruct how spaces are formed, whilst beginning to underscore the inadequacies of the system(s) which planning and adjacent city-building professions operate under

Ur Next GF: Urine as Next Generation Fertilizer with Meat and Bone Meal Applied on Vigna radiata (Monggo plant)

Fertilizers play an important role in providing crops with essential nutrients such as nitrogen (N), phosphorus (P), and potassium (K), which supplements plant growth. Compared to synthetically composed commercial fertilizers, next generation fertilizers are manufactured from low-energy mechanisms and are composed of nutrients from repurposed wastes which make them cost-efficient and sustainable. With the objective of determining which would deem to be an effective next generation fertilizer, we focus on human urine and meat and bone meal, to which its processing included solar drying, freezing, grinding, and utilizing additives to prevent fungal growth as well as improve efficacy. Three iterations, each with four set ups: plain urine, urine and meat and bone meal, control, and meat and bone meal only; were used to examine which content would prove more beneficial to the growth and quality of the chosen plant, Vigna radiata. The study adapted a quantitative analysis that aimed to measure the plant height, leaf area index, and dark green color index through the conduction of statistical tests and the use of ImageJ. As a result, the paper was able to conclude that the combination of urine and meat and bone meal poses a great potential for future fertilizer use

Mineralization, alteration assemblages and stable isotopes of the intermediate-sulfidation epithermal Strauss Deposit, Drake Goldfield, North-Eastern NSW, Australia

The intermediate-sulfidation epithermal Strauss deposit is part of the Drake Goldfield of north-eastern NSW, Australia. The mineralization is gold dominant with minor silver and significant zinc, copper and lead. Strauss has a combined total resource of 2.66 Mt @ 1.5 g/T Au and 1.9 g/T Ag. Petrographic analysis has shown the deposit to be hosted by varying layers of dacitic ash flow tuffs and a cross-cutting lamprophyre dyke though previous authors classified some of the tuffs as intrusive andesites. Mineralization mainly occurs in the form of vein stockworks of three main orientations. Structural analysis indicates that these resulted from two fault system events and one conjugate fault system. Petrographic and SEM analysis shows that there are two different mineralization styles, a pyrite dominant and chalcopyrite dominant assemblage, with three main mineralization events. Correlation analysis for the assay data indicates that Au has a strong relationship with Ag and a moderate correlation with Pb. XRD analysis indicates widespread argillic-phyllic and propylitic alteration. Silver tellurides have been found as late-stage grains associated with the chalcopyrite mineralization assemblage. Sr shows a significant depletion due to the intense and pervasive alteration at Strauss. The carbon and oxygen isotopes of the vein carbonates suggests that the carbon from the late-stage carbonates was derived from a magmatic source with a significant input of low temperature meteoric water, while the sulfur isotopes indicate a magmatic sulfur source

The Effects of Cocaine on Different Redox Forms of Cysteine and Homocysteine, and on Labile, Reduced Sulfur in the Rat Plasma Following Active versus Passive Drug Injections

Received: 28 November 2012 / Revised: 19 April 2013 / Accepted: 6 May 2013 / Published online: 16 May 2013 The Author(s) 2013. This article is published with open access at Springerlink.comThe aim of the present studies was to evaluate cocaine-induced changes in the concentrations of different redox forms of cysteine (Cys) and homocysteine (Hcy), and products of anaerobic Cys metabolism, i.e., labile, reduced sulfur (LS) in the rat plasma. The above-mentioned parameters were determined after i.p. acute and subchronic cocaine treatment as well as following i.v. cocaine self-administration using the yoked procedure. Additionally, Cys, Hcy, and LS levels were measured during the 10-day extinction training in rats that underwent i.v. cocaine administration. Acute i.p. cocaine treatment increased the total and protein-bound Hcy contents, decreased LS, and did not change the concentrations of Cys fractions in the rat plasma. In turn, subchronic i.p. cocaine administration significantly increased free Hcy and lowered the total and protein-bound Cys concentrations while LS level was unchanged. Cocaine self-administration enhanced the total and protein-bound Hcy levels, decreased LS content, and did not affect the Cys fractions. On the other hand, yoked cocaine infusions did not alter the concentration of Hcy fractions while decreased the total and protein-bound Cys and LS content. This extinction training resulted in the lack of changes in the examined parameters in rats with a history of cocaine self-administration while in the yoked cocaine group an increase in the plasma free Cys fraction and LS was seen. Our results demonstrate for the first time that cocaine does evoke significant changes in homeostasis of thiol amino acids Cys and Hcy, and in some products of anaerobic Cys metabolism, which are dependent on the way of cocaine administration