Publications by authors named "Shaonin Ji"

This study describes clinical characteristics of poor and uninsured patients living with hepatitis C virus (HCV) who received care from a multidisciplinary HCV clinic, reports treatment completion and cure rates, and estimates the cost of HCV medications provided at no cost to uninsured patients. A retrospective chart review was performed and identified 69 uninsured HCV patients who received medical care at Mercy Health Center, a small non-profit community clinic, between January 2008 and March 2015. Three-fourths of the patients were unemployed, a third had multiple HCV exposures, nearly half acquired HCV due to illicit drug use, and more than half had active psychiatric disorders.

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The purpose of this study was to compare African American and non-African American hepatitis C virus (HCV) patients on self-reported symptoms of HCV liver disease and psychosocial characteristics commonly affected by it in a sample of 309 patients enrolled in a randomized controlled trial. African Americans (n = 196) rated a higher reliance on religion/spirituality for coping with HCV compared to non-African Americans. This study's findings are a basis for encouragement of public health efforts and programs to seek partnerships with African American faith and religious communities to identify and treat undiagnosed cases of HCV and promote HCV awareness.

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Associations of perceived health and social and physical activities with end-of-life (EOL) issues have been rarely studied, not to mention racial disparities in such associations. To address this gap, this study examined racial differences in the associations of perceived health and levels of social and physical activities with advance care planning, EOL concerns, and knowledge of hospice care among community-dwelling older adults in Alabama. Data from a statewide survey of 1044 community-dwelling older adults on their long-term care needs were analyzed using descriptive statistics and logistic and linear regressions.

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Epidemiological studies have established the role of cigarette smoking as a risk factor in the progression of chronic kidney disease, including diabetic nephropathy. We have previously reported that nicotine promotes mesangial cell proliferation and hypertrophy via activation of nonneuronal nicotinic acetylcholine receptors and that nicotine worsens renal injury in a model of acute glomerulonephritis (Jaimes E, Tian RX, Raij L. Am J Physiol Heart Circ Physiol 292: H76-H82, 2007; Jaimes EA, Tian RX, Joshi M, Raij L.

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The fat-1 gene, derived from Caenorhabditis elegans, encodes for a fatty acid n-3 desaturase. In order to study the potential metabolic benefits of n-3 fatty acids, independent of dietary fatty acids, we developed seven lines of fat-1 transgenic mice (C57/BL6) controlled by the regulatory sequences of the adipocyte protein-2 (aP2) gene for adipocyte-specific expression (AP-lines). We were unable to obtain homozygous fat-1 transgenic offspring from the two highest expressing lines, suggesting that excessive expression of this enzyme may be lethal during gestation.

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The mechanism(s) of insulin's effects on growth hormone receptor (GHR) gene expression are poorly understood. Using rat hepatoma cells, we have previously shown that insulin treatment reduces GHR mRNA and protein in a time- and concentration-dependent manner, at least in part via down-regulation of GHR transcription. The present study determines whether the phosphatidylinositol-3 kinase (PI-3 kinase) and mitogen activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathways are involved in mediating these effects of insulin.

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Carnitine palmitoyltransferase-1 (CPT-1) catalyzes the rate-limiting step of mitochondrial beta-oxidation of long chain fatty acids (LCFA), the most abundant fatty acids in mammalian membranes and in energy metabolism. Human deficiency of the muscle isoform CPT-1b is poorly understood. In the current study, embryos with a homozygous knockout of Cpt-1b were lost before embryonic day 9.

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Conventional cancer treatments are not adequate for the majority of most patients stricken with squamous cell carcinomas of the head and neck (SCCHN). Conditionally replicating adenoviruses (CRAds) represent a promising new modality for treating of neoplastic diseases, including SCCHN. Specifically, CRAd agents infect tumor cells and selectively replicate within them, thus causing their death while sparing surrounding normal cells in the host.

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The role of insulin in regulating responsiveness to growth hormone (GH) remains unclear. Continuous insulin treatment reduces GH binding, which suggests that insulin may effect growth hormone receptor (GHR) levels. The present study used rat hepatoma cells to examine the effects of insulin and GH on GHR gene expression.

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Muscular dystrophies include a diverse group of genetically heterogeneous disorders that together affect 1 in 2000 births worldwide. The diseases are characterized by progressive muscle weakness and wasting that lead to severe disability and often premature death. Rostrocaudal muscular dystrophy (rmd) is a new recessive mouse mutation that causes a rapidly progressive muscular dystrophy and a neonatal forelimb bone deformity.

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Growth hormone (GH) and insulin are important regulators of cellular and whole body metabolism as well as somatic growth and body composition. Studies have indicated complex feedback effects of GH on insulin action and of insulin on GH signaling pathways. Previous studies in our laboratory have shown that GH induction of signal transducers and activators of transcription (STAT)5B tyrosine phosphorylation is inhibited by prolonged insulin treatment, probably via downregulation of GHR.

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Secretion of growth hormone (GH) in adult male rats is characterized by high peak and undetectable trough levels, both of which are required for male-specific pattern of liver gene expression and GH-induced phosphorylation of STAT5. The present study suggests that regulation of GH receptor (GHR) levels in rat hepatoma cells by repeated GH stimulation determines GH responsiveness via the JAK2/STAT5 pathway. A short exposure to GH rapidly reduced GHR levels which resulted in an equal desensitization of the JAK2/STAT5 pathway.

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