A Case Study Examining High-Achieving Black and Latinx Students’ Reasons for Using or Not Using Academic Support Services

Black and Latinx students are completing college at lower rates compared to White and Asian students. Many studies have documented the role of academic support services in helping students successfully complete college. Yet, many of the support services are built into students’ course schedules during freshman year to help transition to college. During the sophomore year, many of those supports are no longer built in, and students must seek them out themselves. Therefore, the purpose of this qualitative case study was to examine the reasons high-achieving Black and Latinx students opt in or opt out of using academic support services and whether their reasons are related to cultural wealth, stereotype threat, and/or the culture of a predominantly White institution (PWI). Interviews were conducted with 14 students and 5 administrators. Students who used the tutoring or writing center found it helpful to pass a course or improve their writing. Other students noted they participated in an academic support program because they wanted to make friends with students of color on campus. The reasons students opted out of using support services included the availability of tutors, seeking help from family and peers, and wanting to figure things out on their own. Some students reported negative racial experiences at the PWI, which impacted their decision to use academic support services. Both students and administrators overwhelmingly indicated the need for an increase in diversity. Administrators believed Black and Latinx students opt out of using services due to not knowing how to access the services, the extent of the services available, and the location of the services—this contradicts what the students said. The administrators had many stereotypes about Black and Latinx, first-generation students accessing cultural wealth instead of the formal support services available at the college, showing that they are not well informed about students of color on campus. Results of this study can inform administrators on the perceptions and experiences of students as well as Black and Latinx College Students and Academic Support Services how academic support services are offered and received so that more students in need of these services feel comfortable accessing them and succeed in completing their college degree

The challenges of exploring the impact of genogram construction on an Appalachian family\u27s health consciousness

Abstract Purpose Appalachians exhibit high rates of chronic disease-related behaviors which might improve with heightened health consciousness. Knowing one\u27s family history can be an important health maintenance tool. Appalachians\u27 health attitudes are shaped in large, closely knit extended families in which matriarchs play central roles. We sought assistance from West Virginian grandmothers in a family medicine practice in engaging their extended families with their genogram to assess the impact on family members\u27 level of health consciousness. Methods The family physician identified West Virginian grandmothers in his practice. We sent each of them invitations to participate, along with their extended family, in constructing a genogram,. However, none of the thirty-four women contacted agreed to participate. We explored the reasons for their non-participation. We mailed a follow-up survey to all the potential participants. We made follow-up phone calls after sending a reminder letter. Twenty-seven women responded. We collated and arranged in order of frequency their reasons for non-participation. Results The most frequently cited reason for non-participation was that the respondent perceived her extended family to be too busy or to live too far from one another to participate. Her own sense of not feeling up to what was being asked of her was the second most frequently expressed reason, almost as often as the first. Conclusions The hypothesis that family physicians might improve health consciousness of Appalachian extended families by engaging them with their genogram remains untested. Testing it will require being mindful of several methodological lessons regarding recruitment of subjects, use of written materials and inclusion criteria. The researcher will be wise to adopt a collaborative, collegial approach such as employed in participatory research

Regenerative medicine : a promising approach in overcoming diabetes as an increasing economic health burden / Nafeeza Mohd Ismail and Renu Agarwal

Diabetes mellitus is a serious public health issue, particularly in developing nations due to the cost associated with its management and its debilitating complications. Patients with diabetes mellitus type 1 are insulin-dependent due to complete loss of insulin producing beta cells in the pancreas and require a well-balanced regimen of insulin injections for life-time. The patients with diabetes mellitus type 2 also require insulin therapy in later stages of disease. In these patients insulin helps by correcting the insulin deficiency, however, the root cause of the disease still persists. Regenerative therapy is now offering solutions and hope to people with insulin-dependent diabetes. This paper gives an outline of the currently used methods in regenerative medicine that aim to re-establish the functional beta cells and restore the body’s original ability to regulate blood glucose levels

Retinal ganglion cell protection against endothelin-1-induced injury by magnesium acetyl taurinate in rats / Dr. Sabrilhakim Sidek … [et al.]

Glaucoma, the leading cause of irreversible blindness, is characterized by apoptotic death of retinal ganglion cells (RGCs). Elevated levels of endothelin1 (ET1), a potent vasoconstrictor, have been detected in the eyes and plasma of glaucoma patients. Increased endothelin 1 causes retinal ischemia increased expression of nitric oxide synthase (NOS) isoforms and oxidative stress, which culminate into RGC apoptosis. Considering the vasodilating, and antioxidant properties of magnesium acetyltaurinate (MgAT) we hypothesized that it can prevent endothelin 1-induced vasospasm, improve retinal perfusion and reduce retinal oxidative stress by altering expression of 3 isoforms of NOS. Rats received single intravitreal injection of vehicle/ET1/ET1 with MgAT. Subsequently, histopathological examination of optic nerve were done to detect the extent of optic nerve damage. Immunochemical detection of NOS isoforms and estimation of NO and antioxidants was done in retina. It was observed that MgAT reduces retinal and optic nerve damage. This neuroprotective effect of MgAT was associated with reduced expression of NOS1 and 2, increased expression of NOS3 and reduced retinal oxidative stress. The results of this study were published in a Q1 journal and were presented in 2 national and 3 international conferences. One student has completed her Master's research work and has been promoted to PhD

Expressions of endothelial cells adhesion molecules are significantly reduced in the presence of minute amount of tocotrienols

Comparative effects of palm tocotrienol rich fractions (TRF) and α–tocopherol on the expression of adhesion molecules by human umbilical vein endothelial cells (HUVECs) were investigated in the present study. Cell based ELISA technique using a monospecific, monoclonal antibodies was employed to measure expression of intracellular cell adhesion molecules–1 (ICAM–1) and vascular cell adhesion molecules–1 (VCAM–1). Primary HUVECs, cultured on a96 wells microtiter plate was incubated for 4 hours with different concentration (ng⁄ml) of TRF or α–tocopherol before subjected to inflammatory stimulation by incubating it with 2 ng⁄ml tumour necrosis factor-α (??F-α) and further incubated for 4 hours. MTS assay was carried out to ascertain the effects of the different dosages on the cells viability. VCAM–1 expression was significantly decreased when HUVECs were incubated with palm TRF between 10–50ng⁄ ml concentrations. Similar effects of the palm TRF were also observed on the expression of ICAM–1. The effect of α–tocopherol however was found to be less consistent. At 10ng⁄ml and 20ng⁄ml, α–tocopherol increased VCAM–1 expression. Higher concentration (30–50ng⁄ml) returned the expression to normal. On the other hand, ICAM–1 was significantly decreased when incubated with 10ng⁄ml of α–tocopherol but gradually increased with increased dosage of α–tocopherol. Our findings suggest that TRF are more potent adhesion molecules expression inhibitor compared to α–tocopherol in–vitro

Retinal ganglion cell protection against endothelin-1-induced injury by magnesium acetyl taurinate in rats / Dr. Sabrilhakim Sidek … [et al.]

Glaucoma, the leading cause of irreversible blindness, is characterized by apoptotic death of retinal ganglion cells (RGCs). Elevated levels of endothelin1 (ET1), a potent vasoconstrictor, have been detected in the eyes and plasma of glaucoma patients. Increased endothelin 1 causes retinal ischemia increased expression of nitric oxide synthase (NOS) isoforms and oxidative stress, which culminate into RGC apoptosis. Considering the vasodilating, and antioxidant properties of magnesium acetyltaurinate (MgAT) we hypothesized that it can prevent endothelin 1-induced vasospasm, improve retinal perfusion and reduce retinal oxidative stress by altering expression of 3 isoforms of NOS. Rats received single intravitreal injection of vehicle/ET1/ET1 with MgAT. Subsequently, histopathological examination of optic nerve were done to detect the extent of optic nerve damage. Immunochemical detection of NOS isoforms and estimation of NO and antioxidants was done in retina. It was observed that MgAT reduces retinal and optic nerve damage. This neuroprotective effect of MgAT was associated with reduced expression of NOS1 and 2, increased expression of NOS3 and reduced retinal oxidative stress. The results of this study were published in a Q1 journal and were presented in 2 national and 3 international conferences. One student has completed her Master's research work and has been promoted to PhD

X-linked Angelman-like syndrome caused by Slc9a6 knockout in mice exhibits evidence of endosomal–lysosomal dysfunction

Mutations in solute carrier family 9 isoform 6 on chromosome Xq26.3 encoding sodium–hydrogen exchanger 6, a protein mainly expressed in early and recycling endosomes are known to cause a complex and slowly progressive degenerative human neurological disease. Three resulting phenotypes have so far been reported: an X-linked Angelman syndrome-like condition, Christianson syndrome and corticobasal degeneration with tau deposition, with each characterized by severe intellectual disability, epilepsy, autistic behaviour and ataxia. Hypothesizing that a sodium–hydrogen exchanger 6 deficiency would most likely disrupt the endosomal–lysosomal system of neurons, we examined Slc9a6 knockout mice with tissue staining and related techniques commonly used to study lysosomal storage disorders. As a result, we found that sodium–hydrogen exchanger 6 depletion leads to abnormal accumulation of GM2 ganglioside and unesterified cholesterol within late endosomes and lysosomes of neurons in selective brain regions, most notably the basolateral nuclei of the amygdala, the CA3 and CA4 regions and dentate gyrus of the hippocampus and some areas of cerebral cortex. In these select neuronal populations, histochemical staining for β-hexosaminidase activity, a lysosomal enzyme involved in the degradation of GM2 ganglioside, was undetectable. Neuroaxonal dystrophy similar to that observed in lysosomal disease was observed in the cerebellum and was accompanied by a marked and progressive loss of Purkinje cells, particularly in those lacking the expression of Zebrin II. On behavioural testing, Slc9a6 knockout mice displayed a discrete clinical phenotype attributable to motor hyperactivity and cerebellar dysfunction. Importantly, these findings show that sodium–hydrogen exchanger 6 loss of function in the Slc9a6-targeted mouse model leads to compromise of endosomal–lysosomal function similar to lysosomal disease and to conspicuous neuronal abnormalities in specific brain regions, which in concert could provide a unified explanation for the cellular and clinical phenotypes in humans with SLC9A6 mutations

Chronic Cyclodextrin Treatment of Murine Niemann-Pick C Disease Ameliorates Neuronal Cholesterol and Glycosphingolipid Storage and Disease Progression

BACKGROUND:Niemann-Pick type C (NPC) disease is a fatal neurodegenerative disorder caused most commonly by a defect in the NPC1 protein and characterized by widespread intracellular accumulation of unesterified cholesterol and glycosphingolipids (GSLs). While current treatment therapies are limited, a few drugs tested in Npc1(-/-) mice have shown partial benefit. During a combination treatment trial using two such compounds, N-butyldeoxynojirimycin (NB-DNJ) and allopregnanolone, we noted increased lifespan for Npc1(-/-) mice receiving only 2-hydroxypropyl-beta-cyclodextrin (CD), the vehicle for allopregnanolone. This finding suggested that administration of CD alone, but with greater frequency, might provide additional benefit. METHODOLOGY/PRINCIPAL FINDINGS:Administration of CD to Npc1(-/-) mice beginning at either P7 or P21 and continuing every other day delayed clinical onset, reduced intraneuronal cholesterol and GSL storage as well as free sphingosine accumulation, reduced markers of neurodegeneration, and led to longer survival than any previous treatment regime. We reasoned that other lysosomal diseases characterized by cholesterol and GSL accumulation, including NPC disease due to NPC2 deficiency, GM1 gangliosidosis and mucopolysaccharidosis (MPS) type IIIA, might likewise benefit from CD treatment. Treated Npc2(-/-) mice showed benefits similar to NPC1 disease, however, mice with GM1 gangliosidosis or MPS IIIA failed to show reduction in storage. CONCLUSIONS/SIGNIFICANCE:Treatment with CD delayed clinical disease onset, reduced intraneuronal storage and secondary markers of neurodegeneration, and significantly increased lifespan of both Npc1(-/-) and Npc2(-/-) mice. In contrast, CD failed to ameliorate cholesterol or glycosphingolipid storage in GM1 gangliosidosis and MPS IIIA disease. Understanding the mechanism(s) by which CD leads to reduced neuronal storage may provide important new opportunities for treatment of NPC and related neurodegenerative diseases characterized by cholesterol dyshomeostasis