What Factors Influence the Academic Success of Somali Graduate Students?

As Somali refugees arrive in the United States, their unique culture and religion has become a challenge for academic institutions unaware of how to accommodate these new students with unique academic needs and social status. This study aims to identify the factors influencing the academic success of Somali graduate students and explore ways the Somali graduate students overcome the academic challenges. This phenomenological study analyzed the experiences and perceptions of ten Somali graduate students in the Midwest universities. Participants were either foreign born or second-generation born Americans. Data was collected through semi-structured interviews aimed at identifying challenges in the academic environment, and the ways the participants overcame their unique academic challenges. This study revealed that the primary factors affecting their academic success are in the presence of/or absence of inclusions academic environments, socioeconomic status, level of family obligation, levels of resilience, and encountering racism. These students overcame academic challenges by taking un-Islamic financial assistance, prioritizing English language learning, relying on family/spousal support, making connections with faculty, and forming ethnically homogenous academic support groups. Somali students have a plethora of academic factors affecting their success, most of which are common to more minority students in America. The ways these students deal with those academic challenges are unique to first-generation Somalis, especially concerning the paramount cultural and religious values around the importance of education which was the main source of academic motivation. Future research for Somali graduate students should be focused on what separates them from others in their same ethnic group who do not go to college. Keywords: academic, achievement, challenges, integration, retention, economic integratio

Role of dopamine in pilocarpine induced motor seizures.

Secondarily generalised motor seizures of limbic origin (hereafter referred to as "limbic" motor seizures) were induced in rats by injecting a high dose of the muscarinic agonist pilocarpine intraperitoneally. This model was used to investigate the involvement of central dopaminergic systems in the development and spread of these seizures. Pilocarpine was found to induce motor seizures in rats in a dose dependent manner. From this study 200 mg/kg and 600 mg/kg pilocarpine i.p. were taken to be threshold convulsant and convulsant doses respectively. Pretreatment with the D1 partial agonist SKF 38393 (30 mg/kg i.p.) caused 100 % of animals tested to convulse in response to 200 mg/kg pilocarpine, and this effect was blocked by the D, antagonist SCH 23390 (0.25 mg/kg i.p.). By contrast, the Dj agonist LY 171555 (0.5 mg/kg s.c.) protected rats against a convulsant dose of pilocarpine, and this action was abolished by the D2 receptor blocker metoclopramide (1.25 mg/kg i.p.). Neither SCH 23390 nor metoclopramide on their own affected seizures induced by 600 mg/kg and 200 mg/kg pilocarpine respectively. These results clearly demonstrated that D, and D2 dopamine receptors function in opposition to regulate seizure activity in this model. Stereotaxic injection of drugs via chronically implanted guide cannulae demonstrated that the proconvulsant action of SKF 38393 could be duplicated by injecting the drug into the substantia nigra (2.5 ?g in 0.5 ?1 bilaterally), and that this action was blocked by pretreatment with SCH 23390 (0.25 mg/kg i.p.). Intranigral injection of the D1 antagonist SCH 23390 (1 ?g in 0.5 ?l bilaterally) protected rats against a convulsant dose of pilocarpine. Intranigral injection of the D2 agonist LY 171555 (1 fig in 0.5 ?1) had no effect on seizures induced by a convulsant dose of pilocarpine. In the striatum, it was confirmed that injection of LY 171555 (1 ?g in 1 ?l bilaterally) into the rostral parts of the caudate is anticonvulsant. However, another I D2 agonist, RU 24213 (1 ?g in 1 ?l bilaterally), failed to protect rats against a convulsant dose of pilocarpine. Systemically injected RU 24213 (4.5 mg/kg s.c.) had no effect on the convulsant action of 600 mg/kg pilocarpine. These data suggest a subpopulation of D2 receptors is responsible for mediating the anticonvulsant response. With regards to D1 receptors in the striatum, the antagonist SCH 23390 (1 ?g in 1 ?l bilaterally) protected rats from a convulsant dose of pilocarpine when injected throughout the rostro-caudal axis of the caudate and into the nucleus accumbens. By contrast, both SKF 38393 (0.1, 1 and 2.5 ?g in 1 ?l bilaterally) and another D1 partial agonist CY 208-243 (0.1 and 1 ?g in 1 ?l bilaterally) had no effect on seizure threshold when injected into the caudate. Both drugs were similarly ineffective when injected into the nucleus accumbens (1 ?g in 1 ?l bilaterally). Early studies indicated that excessive mechanical damage to the cortex may be associated with a lack of seizure protection of intrastriatal LY 171555. This was confirmed when intrastriatal injection of LY 171555, into animals with kainic acid- induced cortical lesions, was found not to be anticonvulsant, as compared with unlesioned controls. Thus it appeared that intact corticostriatal connections were essential for intrastriatal LY 171555 to be anticonvulsant. In vivo microdialysis studies were conducted in conscious, freely moving rats, to investigate changes in striatal dopaminergic transmission associated with seizures induced by pilocarpine. A highly disorganised pattern of dopamine release coincided with the onset of convulsions, with the magnitude of the disruption parallelling the severity of the seizures. It was unclear however whether this phenomenon was part of the mechanism underlying seizure propagation, or whether it was an adaptive response. By contrast, the metabolite homovanillic acid significantly increased, but only did so after seizures had developed, suggesting this might be a compensatory mechanism to contain the seizure. Similar microdialysis studies were done to measure striatal aspartate and glutamate releases during pilocarpine induced seizures, although it is questionable whether the method used necessarily measures amino acid release from a transmitter pool, since it was not always stimulated by high K+; what was apparent was that SKF 38393 significantly decreased aspartate release, with a more modest reduction in glutamate output. In view of the fact that excitatory activity in the striatum is anticonvulsant, a reduction in this activity is consistent with a lowering of seizure threshold

Britain, the Shaikh and the administration of Bahrain, 1920-1945.

This thesis is concerned with the history of Bahrain in the period 1920-45. It is based primarily on archival material in the India Office Records. The earlier chapters in the thesis deal with the Administration of Shaikh Isa bin Ali Alkhalifah, whose active rule of Bahrain encompassed 55 years, from 1869 to May 1923 when the British Government retired him, against his will, in the long-term interests of the ruling family of Bahrain and those of the country as a whole. Under his period in office, both the ruling family and their tribal associates had acquired immense power, privileges and autonomy. After the First World War, the serious faults which the Shaikh's administration had manifested over the years became a much publicized affair and a source of great embarrassment to the British Government. In Bahrain, the Shaikh's Shiah Arab subjects, who were the victims of discriminatory policies, rebelled in February 1922 and brought the country's administration to a halt. The thesis assesses the role played by the Foreign Office, the Government of India which maintained direct links with the Shaikh and the British Political Authorities in the Gulf, before and during the adoption of a policy of reforms in Bahrain. Also included in the discussion are: the actual reforms carried out under Shaikh Hamad, the Heir Apparent and Shaikh Isa's deputy, the struggle conducted by the ruling family and their tribal supporters against the reforms, and the support given by the Shi ah Arabs to Shaikh Hamad's Administration over their introduction. The modernization process during the years 1923-26 was supervized by the British Agent in Bahrain and it produced an organized government structure formed of specialized, secular departments and offices. This was the first time such a modern administration had been created in the Arab Shaikhdoms. Other chapters examine the politics of education and educational reform, reform of the pearling industry and the causes for the decline of the pearl-trade of Bahrain. The advent of oil is also studied and the new industry is seen to have saved the country from economic disaster in the aftermath of the recession of the early 1930s. The thesis concludes that the Government of India vacillated over the initiation of the reforms in Baihrain and that even when it agreed to them it was goaded into action by the Foreign Office whose officials acted in response to Tehran's criticisms that the Government of India shared responsibility for Shaikh Isa's misrule. The reforms curbed the power of the ruling family and at the same time they enhanced British influence over the administration of Bahrain. More penetrating than the administrative reforms were the far-reaching socio-economic changes induced by the establishment of the oil industry in Bahrain. Greater communication and travel became possible after Bahrain's entry into the age of oil. Wider co-operation between Sunnis and Shi ahs, such as Bahrain witnessed in the second half of the 1930s was due chiefly to the subjection of Bahraini schoolboys of both sects to a unified system of education and to their sharing of jobs as employees of the Oil Company, and also to the increased political awareness of the people and their leaders. It should be noted also that the influx of oil revenues gave greater wealth to the ruling family and thereby helped to strengthen their position and powers

ADMET Prediction of synthesized Heterocyclic derivatives to treat renal cancer

A library of 121 potent, synthesized, and characterized compounds from different heterocyclic derivatives such as pyrimidine, phthalazine, benzothiazole, benzpyrazoline, indoline, benzimidazole, phthalazine, indole, quinoline, quinazoline were selected based on their anti-renal cancer activity. The Drug likeness, Bioactivity, Absorption, Distribution, Metabolism, Excretion, and Toxicity of all the screened compounds were predicted through Molinspiration, PreADMET, and Osiris software. After screening 121 compounds, 19 compounds showed drug-like properties and an absorption percentage better than the standard drug Sorafenib. These compounds were further assessed based on their distribution parameter and the compounds that showed plasma protein binding equal to or below 90% and blood-brain barrier penetration below 1.000 were selected, i.e., compounds 3, 23, 64, 65 were then further assessed for the toxicity. Osiris property explorer was used to predict drug relevance and toxicity of the synthesized compounds. Compounds 3 and 23 were non-toxic similar to the standard drug Sorafenib. Compounds 3 and 23 were found to be active as Kinase Inhibitors, with a bioactivity score of 0.2 and 0.6 compared to standard drug sorafenib, which scored 0.44. Therefore Compound 3 N-(4-fluoro-2-methoxyphenyl)-7-methyl-5,6,7,8-tetrahydropyrido [4',3':4,5] thieno[2,3-d] pyrimidin-4-amine and compound 23 1-(4-fluorophenyl)-3-methyl-N-phenyl-3a,7a-dihydro-1H-pyrazolo[3,4-d] pyrimidin-4-amine belonging to pyrimidine derivatives were considered as best and suggested to be taken further for preclinical and clinical trials. The pyrimidine derivatives with anti-renal cancer activity can serve as a scaffold for the design of renal cancer targeting agents and motivates the further development of effective and safer compounds

Clinical description and mutational profile of a moroccan series of patients with rubinstein taybi syndrome

Background: Rubinstein-Taybi syndrome (RSTS; OMIM 180849) is a rare autosomal dominant developmental disorder with an estimated prevalence of one case per 125,000 live births. RSTS is characterized by typical face, broad thumbs and halluces, short stature, and intellectual disability. Facial dysmorphy is characteristic with microcephaly, low frontal hairline, arched eyebrows, long eyelashes, convex profile of nose, narrow palate, and micrognathia. RSTS is mainly due to mutations or microdeletions of the CREBBP gene (about 60%) and more rarely of the EP300 gene (8%). Objective: Clinical description and identification of mutations of patients with Rubinstein Taybi syndrome Methods: PCR and direct sequencing of CREBBP gene. Results: We report here, the clinical and molecular data of a series of six Moroccan patients with a phenotype of RSTS. The molecular study of the major gene CREBBP (by Sanger Sequencing followed by CGH array, if sequence normal) revealed point mutations in five patients. For the sixth patient, CGH array revealed a microdeletion carrying the CREBBP gene. Through this work, we emphasize the importance of clinical expertise in the diagnosis, management and genetic counseling in Rubinstein Taybi syndrome

Systematic review of the safety of medication use in inpatient, outpatient and primary care settings in the Gulf Cooperation Council countries

Background Errors in medication use are a patient safety concern globally, with different regions reporting differing error rates, causes of errors and proposed solutions. The objectives of this review were to identify, summarise, review and evaluate published studies on medication errors, drug related problems and adverse drug events in the Gulf Cooperation Council (GCC) countries. Methods A systematic review was carried out using six databases, searching for literature published between January 1990 and August 2016. Research articles focussing on medication errors, drug related problems or adverse drug events within different healthcare settings in the GCC were included. Results Of 2094 records screened, 54 studies met our inclusion criteria. Kuwait was the only GCC country with no studies included. Prescribing errors were reported to be as high as 91% of a sample of primary care prescriptions analysed in one study. Of drug-related admissions evaluated in the emergency department the most common reason was patient non-compliance. In the inpatient care setting, a study of review of patient charts and medication orders identified prescribing errors in 7% of medication orders, another reported prescribing errors present in 56% of medication orders. The majority of drug related problems identified in inpatient paediatric wards were judged to be preventable. Adverse drug events were reported to occur in 8.5–16.9 per 100 admissions with up to 30% judged preventable, with occurrence being highest in the intensive care unit. Dosing errors were common in inpatient, outpatient and primary care settings. Omission of the administered dose as well as omission of prescribed medication at medication reconciliation were common. Studies of pharmacists’ interventions in clinical practice reported a varying level of acceptance, ranging from 53% to 98% of pharmacists’ recommendations. Conclusions Studies of medication errors, drug related problems and adverse drug events are increasing in the GCC. However, variation in methods, definitions and denominators preclude calculation of an overall error rate. Research with more robust methodologies and longer follow up periods is now required.Peer reviewe

Timing, rates and spectra of human germline mutation.

Germline mutations are a driving force behind genome evolution and genetic disease. We investigated genome-wide mutation rates and spectra in multi-sibling families. The mutation rate increased with paternal age in all families, but the number of additional mutations per year differed by more than twofold between families. Meta-analysis of 6,570 mutations showed that germline methylation influences mutation rates. In contrast to somatic mutations, we found remarkable consistency in germline mutation spectra between the sexes and at different paternal ages. In parental germ line, 3.8% of mutations were mosaic, resulting in 1.3% of mutations being shared by siblings. The number of these shared mutations varied significantly between families. Our data suggest that the mutation rate per cell division is higher during both early embryogenesis and differentiation of primordial germ cells but is reduced substantially during post-pubertal spermatogenesis. These findings have important consequences for the recurrence risks of disorders caused by de novo mutations

Human genetics and clinical aspects of neurodevelopmental disorders

This chapter traverses contemporary understandings of the genetic architecture of human disease, and explores the clinical implications of the current state of knowledge. Many different classes of genetic mutations have been implicated as being involved in predisposition to certain diseases, and researchers are continually uncovering other means by which genetics plays an important role in human disease, such as with somatic genetic mosaicism. Putative “de novo” mutations can represent cases of parental mosaicism (including in the germline), which could be revealed by careful genotyping of parental tissues other than peripheral blood lymphocytes. There is an increasingly rich literature regarding rare mutations with seemingly large phenotypic effects. Privacy concerns have added to the difficulties of implementing genomics-guided medicine. With the advent of exome and whole genome sequencing (WGS), one needs to focus again on families over several generations, so as to attempt to minimize genetic differences, locus heterogeneity and environmental influences

Adverse Drug Reactions in Children—A Systematic Review

Adverse drug reactions in children are an important public health problem. We have undertaken a systematic review of observational studies in children in three settings: causing admission to hospital, occurring during hospital stay and occurring in the community. We were particularly interested in understanding how ADRs might be better detected, assessed and avoided