An Analysis of the Achille Lauro Affair: Towards an Effective and Legal Method of Bringing International Terrorists to Justice

This Note will propose five steps towards establishing an effective method of bringing terrorists to justice. Part I of this Note will detail the facts surrounding the Achille Lauro incident. Part II will discuss the laws governing extradition, including the obligations of Egypt and the United States arising under the United States-Egypt Extradition Treaty, the Convention Against the Taking of Hostages, and the doctrine of mala captus bene delentus. Part III will also discuss the international community\u27s historical inability to define terrorism. Part III will examine the legal precedent for acts of abduction. Part IV details the criticism of the use of abduction as an alternative to extradition, and examines the threat abduction poses to the international legal system, which depends upon voluntary compliance to be effective

An Analysis of the Achille Lauro Affair: Towards an Effective and Legal Method of Bringing International Terrorists to Justice

This Note will propose five steps towards establishing an effective method of bringing terrorists to justice. Part I of this Note will detail the facts surrounding the Achille Lauro incident. Part II will discuss the laws governing extradition, including the obligations of Egypt and the United States arising under the United States-Egypt Extradition Treaty, the Convention Against the Taking of Hostages, and the doctrine of mala captus bene delentus. Part III will also discuss the international community\u27s historical inability to define terrorism. Part III will examine the legal precedent for acts of abduction. Part IV details the criticism of the use of abduction as an alternative to extradition, and examines the threat abduction poses to the international legal system, which depends upon voluntary compliance to be effective

PRECLINICAL DEVELOPMENT OF PHYTOCANNABINOID- AND ENDOCANNABINOID- BASED PHARMACOTHERAPIES FOR THE TREATMENT OF ETHANOL-INDUCED NEURODEGENERATION

Excessive ethanol consumption, characteristic of alcohol use disorders (AUDs), is associated with widespread neurodegeneration and cognitive and behavioral impairments that may contribute to the chronic and relapsing nature of alcoholism. Therefore, identifying novel targets that can afford neuroprotection will undoubtedly aid current treatment strategies for AUDs. The cannabinoids have been shown to provide neuroprotection in a variety of preclinical models of neurodegeneration; however minimal data is available regarding the use of cannabinoid-based pharmacotherapies for treating ethanol-induced neurodegeneration. Therefore, the current dissertation examined the overarching hypothesis: the cannabinoids are a therapeutic strategy to afford neuroprotection in the context of ethanol-induced neurodegeneration. Importantly, this overarching hypothesis was approached with translational considerations in mind. Specifically, the use of many cannabinoids in the clinic is hindered due to multiple unfavorable pharmacokinetic/pharmacodynamic profiles, including high first pass metabolism and untoward psychoactivity. Therefore, the studies herein were designed to circumvent these PK/PD obstacles. The first set of studies examined whether transdermal delivery of the phytocannabinoid, cannabidiol (CBD), could attenuate binge ethanol induced neurodegeneration. Transdermal CBD afforded neuroprotection in the entorhinal cortex and neuroprotection was similar in magnitude as intraperitoneal administration. The second set of studies found that binge ethanol treatment transiently down-regulated the main CNS cannabinoid receptor, CB1R. Interestingly, these changes were not accompanied by alterations in one of the major endogenous ligands, anandamide (AEA), or other related n-acylethanolamides (NAEs). The latter finding is in contrast to other literature reports demonstrating that endocannabinoid content is substantially elevated in response to a CNS insult. Nevertheless, studies were carried out to determine if administration of the AEA and NAE catabolism inhibitor, URB597, could attenuate binge ethanol induced neurodegeneration. URB597 failed to produce neuroprotection in the entorhinal cortex and dentate gyrus of the hippocampus. However, additional studies found that URB597 failed to elevate AEA in the entorhinal cortex, and in general the biological activity of URB597 was impaired by ethanol exposure. Therefore, with further drug discovery/development efforts, it may be feasible to optimize such treatment strategies. In conclusion, the studies within the current dissertation demonstrated the feasibility of using some cannabinoid-based agents to prevent ethanol-induced neurodegeneration

Occurrence and degree of iliopsoas muscle contracture in regular male squash players

Introduction: Sprints combined with changes in direction and repeated lunges are the most frequent movements during a squash game. These motions overload the iliopsoas muscle which may cause a lot of microinjuries. Accumulating microinjuries combined with a lack of stretching exercises may lead to iliopsoas contracture. Aim of the study: Assessment of the frequency and degree of iliopsoas contracture in regular squash players. Material and methods: The experimental group comprised 25 regular squash players (minimum 2 years of playing at least twice a week) and 21 non-players (control group). A modified Thomas Test was used to assess iliopsoas contracture using goniometric and linear measurements. Results: Iliopsoas contracture was observed in 96% of the squash players and 66.7% of the non-players (p = 0.0089). The degree of muscle contracture in the goniometric measurement was greater in squash players than in the non-players in both the left (p = 0.0303) and right (p = 0.0007) iliopsoas muscles. There were no statistically significant differences in the linear measurement. Conclusions: There is a positive relationship between regularly playing squash and the frequency of iliopsoas contracture occurrence being significantly greater in squash players than in non-players

Binge Alcohol Exposure Transiently Changes the Endocannabinoid System: A Potential Target to Prevent Alcohol-Induced Neurodegeneration

Excessive alcohol consumption leads to neurodegeneration, which contributes to cognitive decline that is associated with alcohol use disorders (AUDs). The endocannabinoid system has been implicated in the development of AUDs, but little is known about how the neurotoxic effects of alcohol impact the endocannabinoid system. Therefore, the current study investigated the effects of neurotoxic, binge-like alcohol exposure on components of the endocannabinoid system and related N-acylethanolamines (NAEs), and then evaluated the efficacy of fatty acid amide hydrolase (FAAH) inhibition on attenuating alcohol-induced neurodegeneration. Male rats were administered alcohol according to a binge model, which resulted in a transient decrease in [3H]-CP-55,940 binding in the entorhinal cortex and hippocampus following two days, but not four days, of treatment. Furthermore, binge alcohol treatment did not change the tissue content of the three NAEs quantified, including the endocannabinoid and anandamide. In a separate study, the FAAH inhibitor, URB597 was administered to rats during alcohol treatment and neuroprotection was assessed by FluoroJade B (FJB) staining. The administration of URB597 during binge treatment did not significantly reduce FJB+ cells in the entorhinal cortex or hippocampus, however, a follow up “target engagement” study found that NAE augmentation by URB597 was impaired in alcohol intoxicated rats. Thus, potential alcohol induced alterations in URB597 pharmacodynamics may have contributed to the lack of neuroprotection by FAAH inhibition

Quantification of anandamide, oleoylethanolamide and palmitoylethanolamide in rodent brain tissue using high performance liquid chromatography–electrospray mass spectroscopy

AbstractReported concentrations for endocannabinoids and related lipids in biological tissues can vary greatly; therefore, methods used to quantify these compounds need to be validated. This report describes a method to quantify anandamide (AEA), oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) from rodent brain tissue. Analytes were extracted using acetonitrile without further sample clean up, resolved on a C18 reverse-phase column using a gradient mobile phase and detected using electrospray ionization in positive selected ion monitoring mode on a single quadrupole mass spectrometer. The method produced high recovery rates for AEA, OEA and PEA, ranging from 98.1% to 106.2%, 98.5% to 102.2% and 85.4% to 89.5%, respectively. The method resulted in adequate sensitivity with a lower limit of quantification for AEA, OEA and PEA of 1.4ng/mL, 0.6ng/mL and 0.5ng/mL, respectively. The method was reproducible as intraday and interday accuracies and precisions were under 15%. This method was suitable for quantifying AEA, OEA and PEA from rat brain following pharmacological inhibition of fatty acid amide hydrolase

Diurnal changes of polysome loading track sucrose content in the rosette of wildtype Arabidopsis and the starchless pgm mutant

Growth is driven by newly fixed carbon in the light, but depends at night on reserves, like starch, that are laid down in the light. Unless plants coordinate their growth with diurnal changes in the carbon supply, they will experience acute carbon starvation during the night. Protein synthesis represents a major component of cellular growth. Polysome loading was investigated during the diurnal cycle, an extended night and low CO2 in Arabidopsis Col-0 and in the starchless pgm mutant. In Col-0, polysome loading was 60-70% in the light, 40-45% for much of the night and <20% in an extended night, whilst in pgm it fell to <25% early in the night. Quantification of rRNA species using qRT-PCR revealed that polysome loading remained high for much of the night in the cytosol, was strongly light-dependent in the plastid, and was always high in mitochondria. The rosette sucrose content correlated with overall and with cytosolic polysome loading. Ribosome abundance did not show significant diurnal changes. However, compared to Col-0, pgm had decreased and increased abundance of plastidic and mitochondrial ribosomes, respectively. Incorporation of label from 13CO2 into protein confirmed that protein synthesis continues at a diminished rate in the dark. Modelling revealed that a decrease in polysome loading at night is required to balance protein synthesis with the availability of carbon from starch breakdown. Costs are also reduced by using amino acids that accumulated in previous light period. These results uncover a tight coordination of protein synthesis with the momentary supply of carbon

Rem2, a member of the RGK family of small GTPases, is enriched in nuclei of the basal ganglia.

Rem2 is a member of the RGK subfamily of RAS small GTPases. Rem2 inhibits high voltage activated calcium channels, is involved in synaptogenesis, and regulates dendritic morphology. Rem2 is the primary RGK protein expressed in the nervous system, but to date, the precise expression patterns of this protein are unknown. In this study, we characterized Rem2 expression in the mouse nervous system. In the CNS, Rem2 mRNA was detected in all regions examined, but was enriched in the striatum. An antibody specific for Rem2 was validated using a Rem2 knockout mouse model and used to show abundant expression in striatonigral and striatopallidal medium spiny neurons but not in several interneuron populations. In the PNS, Rem2 was abundant in a subpopulation of neurons in the trigeminal and dorsal root ganglia, but was absent in sympathetic neurons of superior cervical ganglia. Under basal conditions, Rem2 was subject to post-translational phosphorylation, likely at multiple residues. Further, Rem2 mRNA and protein expression peaked at postnatal week two, which corresponds to the period of robust neuronal maturation in rodents. This study will be useful for elucidating the functions of Rem2 in basal ganglia physiology

Rem2, a member of the RGK family of small GTPases, is enriched in nuclei of the basal ganglia.

Rem2 is a member of the RGK subfamily of RAS small GTPases. Rem2 inhibits high voltage activated calcium channels, is involved in synaptogenesis, and regulates dendritic morphology. Rem2 is the primary RGK protein expressed in the nervous system, but to date, the precise expression patterns of this protein are unknown. In this study, we characterized Rem2 expression in the mouse nervous system. In the CNS, Rem2 mRNA was detected in all regions examined, but was enriched in the striatum. An antibody specific for Rem2 was validated using a Rem2 knockout mouse model and used to show abundant expression in striatonigral and striatopallidal medium spiny neurons but not in several interneuron populations. In the PNS, Rem2 was abundant in a subpopulation of neurons in the trigeminal and dorsal root ganglia, but was absent in sympathetic neurons of superior cervical ganglia. Under basal conditions, Rem2 was subject to post-translational phosphorylation, likely at multiple residues. Further, Rem2 mRNA and protein expression peaked at postnatal week two, which corresponds to the period of robust neuronal maturation in rodents. This study will be useful for elucidating the functions of Rem2 in basal ganglia physiology