6600 Bruceville Rd
Sacramento CA 95823
Medical School: University Of Illinois At Chicago Health Science Center - 2000
Accepts Medicare: Yes
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: A89881
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Association analysis of PDE4B polymorphisms with schizophrenia and smooth pursuit eye movement abnormality in a Korean population. - General physiology and biophysics
Schizophrenia is a debilitating mental disorder with a high heritability rate. Located on chromosome 1p31.3, the human cAMP-specific 3',5'-cyclic phosphodiesterase 4B (PDE4B) gene has been considered as an important candidate gene for the risk of schizophrenia. Several genetic association studies reported the association between PDE4B polymorphisms and the risk of schizophrenia in Caucasian, African American, Indian, and Japanese populations. The aim of this study is to examine the association of PDE4B variations with schizophrenia and smooth pursuit eye movement (SPEM) abnormality in a Korean population. A case-control association analysis was carried out by comparing the genotype distribution of eight PDE4B polymorphisms between 457 schizophrenia patients and 386 normal healthy subjects. Differences in the frequency distribution of PDE4B single nucleotide polymorphisms (SNPs) and haplotypes were analyzed by logistic regression analyses controlling for age as a covariate. Statistical analyses revealed nominal significant associations of rs1040716, rs472952, rs1321177, and rs2144719 with the risk of schizophrenia (p = 0.02~0.05). The rs11208756 polymorphism showed a nominal significant association with SPEM abnormality (p = 0.05). In a meta-analysis with Japanese and Korean populations, three SNPs (rs472952, rs1040716, and rs2180335) revealed significant associations with schizophrenia (meta-p value = 0.0038~0.019). Our results support previously reported association of PDE4B variations with schizophrenia in other populations. The findings in this study add a new evidence for the involvement of PDE4B gene in schizophrenia etiology.
Inducible deletion of protein kinase Map4k4 in obese mice improves insulin sensitivity in liver and adipose tissues. - Molecular and cellular biology
Studies in vitro suggest that mitogen-activated protein kinase kinase kinase kinase 4 (Map4k4) attenuates insulin signaling, but confirmation in vivo is lacking since Map4k4 knockout is lethal during embryogenesis. We thus generated mice with floxed Map4k4 alleles and a tamoxifen-inducible Cre/ERT(2) recombinase under the control of the Ubiquitin C promoter to induce whole-body Map4k4 deletion after these animals reach maturity. Tamoxifen administration to these mice induced Map4k4 deletion in all tissues examined, causing decreased fasting blood glucose concentrations and enhanced insulin signaling to AKT in adipose tissue and liver, but not skeletal muscle. Surprisingly, however, mice generated with conditional Map4k4 deletion in adiponectin-positive adipocytes or in albumin-positive hepatocytes displayed no detectable metabolic phenotypes. Instead, mice with Map4k4 deleted in Myf5-positive tissues, including all skeletal muscles tested, were protected from obesity-induced glucose intolerance and insulin resistance. Remarkably, these mice also showed increased insulin sensitivity in adipose tissue but not skeletal muscle, similar to the metabolic phenotypes observed in inducible whole-body knockout mice. Taken together, these results indicate that, 1.) Map4k4 controls a pathway in Myf5-positive cells that suppresses whole-body insulin sensitivity and 2.) Map4k4 is a potential therapeutic target for improving glucose tolerance and insulin sensitivity in type-2 diabetes.Copyright Â© 2015, American Society for Microbiology. All Rights Reserved.
Transient receptor potential vanilloid type-1 channel regulates diet-induced obesity, insulin resistance, and leptin resistance. - FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Insulin resistance is a major characteristic of obesity and type 2 diabetes, but the underlying mechanism is unclear. Recent studies have shown a metabolic role of capsaicin that may be mediated via the transient receptor potential vanilloid type (TRPV)-1 channel. In this study, TRPV1 knockout (KO) and wild-type (WT) mice (as controls) were fed a high-fat diet (HFD), and metabolic studies were performed to measure insulin and leptin action. The TRPV1 KO mice became more obese than the WT mice after HFD, partly attributed to altered energy balance and leptin resistance in the KO mice. The hyperinsulinemic-euglycemic clamp experiment showed that the TRPV1 KO mice were more insulin resistant after HFD because of the âˆ¼40% reduction in glucose metabolism in the white and brown adipose tissue, compared with that in the WT mice. Leptin treatment failed to suppress food intake, and leptin-mediated hypothalamic signal transducer and activator of transcription (STAT)-3 activity was blunted in the TRPV1 KO mice. We also found that the TRPV1 KO mice were more obese and insulin resistant than the WT mice at 9 mo of age. Taken together, these results indicate that lacking TRPV1 exacerbates the obesity and insulin resistance associated with an HFD and aging, and our findings further suggest that TRPV1 has a major role in regulating glucose metabolism and hypothalamic leptin's effects in obesity.-Lee, E., Jung, D. Y., Kim, J. H., Patel, P. R., Hu, X., Lee, Y., Azuma, Y., Wang, H.-F., Tsitsilianos, N., Shafiq, U., Kwon, J. Y., Lee, H. J., Lee, K. W., Kim, J. K. Transient receptor potential vanilloid type-1 channel regulates diet-induced obesity, insulin resistance, and leptin resistance.Â© FASEB.
The role of information technology (apps) in FPMRS. - Current urology reports
The objective of this study is to provide a comprehensive overview of the use of smartphone "apps" within the field of female pelvic medicine and reconstructive surgery (FPMRS) and the role they play in improving patient education. The authors conducted a keyword search using the search tab in the Apple App Store. The apps selected were ones that specifically pertained to female pelvic medicine. A total of 13 apps were found. The apps were separated into three categories: patient education (five apps), wellness (four apps), and reference (four apps). The majority of the patient education apps consisted of anatomical diagrams of the pelvis and anatomy videos to help explain the pathophysiology behind different pelvic and voiding disorders. Female pelvic medicine apps have a large focus on patient education, which can help patients achieve a greater understanding of female pelvic disorders and the treatment options that are available.
Topical Cyclosporine A 1% for the Treatment of Chronic Follicular Conjunctivitis. - Eye & contact lens
To evaluate the use of topical cyclosporine A (CSA) 1% in the treatment of chronic follicular conjunctivitis (CFC).Retrospective chart review from 2001 to 2012 identified 12 patients (22 eyes) with CFC (meanÂ±standard deviation [SD] age, 50.2Â±15.4 years; 75% female; 92% white) treated with CSA. Main outcome measures included inflammation grade, visual acuity, concurrent corticosteroid (CS) therapy, effect on CS taper, and adverse effects.MeanÂ±SD follow-up time was 11.7Â±9.7 months. MeanÂ±SD time from diagnosis to CSA treatment initiation was 2.4Â±3.2 months. MeanÂ±SD duration of CSA treatment was 5.8Â±2.8 months. Four patients (33%) complained of irritation (n=2), redness (n=1), itching (n=1), and burning (n=1) but none discontinued treatment. Concurrent CSs were tapered off in all patients after a meanÂ±SD of 5.0Â±2.5 weeks. MeanÂ±SD initial vision was 0.078Â±0.093 logMAR, whereas vision at final examination was 0.056Â±0.081 logMAR (P=0.02). MeanÂ±SD initial inflammation grade of 1.9Â±1.0 was significantly reduced to final grade of 0.7Â±0.9 (P=0.0002). MeanÂ±SD time to initial inflammation control in 9 patients (75%) was 33.2Â±24.5 days. Two patients (17%) switched to oral CSA because of lack of inflammation control.Topical CSA 1% is an effective and well-tolerated therapy that decreased chronic inflammation and tapered topical CS in patients with CFC. The use of CSA in such patients warrants further investigation.
Investigating the potential genetic association between RANBP9 polymorphisms and the risk of schizophrenia. - Molecular medicine reports
Schizophrenia is a serious mental disorder that is affected by genetic and environmental factors. As the disease has a high heritability rate, genetic studies identifying candidate genes for schizophrenia have been conducted in various populations. The gene for human Ranâ€‘binding protein 9 (RANBP9) is a newly discovered candidate gene for schizophrenia. As RANBP9 is a small guanosineâ€‘5'â€‘triphosphateâ€‘binding protein that interacts with the disrupted in schizophrenia 1 protein, it is considered to be an important molecule in the pathogenesis of schizophrenia. However, to date, no study has examined the possible association between the genetic variations of RANBP9 and the risk of schizophrenia. In the present study, it was hypothesized that RANBP9 variations may influence the risk of schizophrenia. In order to investigate the association between RANBP9 polymorphisms and the risk of schizophrenia and smooth pursuit eye movement (SPEM) abnormalities, a caseâ€‘control association analysis was performed. Using a TaqMan assay, five singleâ€‘nucleotide polymorphisms and an insertion/deletion variation within the start codon region of RANBP9 were genotyped. Five major haplotypes were identified in 449 patients with schizophrenia and 393 unrelated healthy individuals as controls (total, n=842). However, the association analyses revealed no associations between all genetic variants and schizophrenia and SPEM abnormality. To the best of our knowledge, this is the first study to investigate an association between RANBP9 polymorphisms and schizophrenia and SPEM abnormality. The findings of allele frequencies and association results in this study may aid in further genetic etiological studies in schizophrenia in various populations.
Functional Study of Haplotypes in UGT1A1 Promoter to find a novel genetic variant leading to reduced gene expression. - Therapeutic drug monitoring
Uridine diphosphate glucuronyltransferase 1 family, A1 (UGT1A1) encodes for an enzyme which is a part of glucuronidation pathway, and a number of studies have shown that the promoter polymorphisms of UGT1A1 are associated with various diseases and drug response. In this study, we examined a possible association between UGT1A1 promoter haplotypes and the gene expression level.In order to identify promoter haplotype structure population, we directly sequenced the promoter region of UGT1A1 in 192 healthy Korean to identify 10 UGT1A1 promoter SNPs. Then, we genotyped the 10 SNPs in additional 192 non-Korean samples comprised of Chinese, Japanese, European American, and African American and constructed haplotype structures. Furthermore, we conducted luciferase assay for the promoter single nucleotide polymorphism (SNP) haplotypes to examine a possible expression change.rs3755319C - rs2003569A - rs887829C - rs8175347(TA)6 (6.60Â±0.15) and rs3755319A - rs2003569G - rs887829C - rs8175347(TA)7 (2.79Â±0.97) led to significantly lower gene expression when compared with rs3755319C - rs2003569G - rs887829T - rs8175347(TA)6 (8.28Â±0.60).Our result suggests that the haplotypes in UGT1A1 promoter region can affect the expression level of the gene and drug metabolism associated with UGT1A1. Furthermore, in addition to rs8175347, rs3755319 was found to induce lower gene expression of UGT1A1.
The LXR-Idol axis differentially regulates plasma LDL levels in primates and mice. - Cell metabolism
The LXR-regulated E3 ubiquitin ligase IDOL controls LDLR receptor stability independent of SREBP and PCSK9, but its relevance to plasma lipid levels is unknown. Here we demonstrate that the effects of the LXR-IDOL axis are both tissue and species specific. In mice, LXR agonist induces Idol transcript levels inÂ peripheral tissues but not in liver, and does not change plasma LDL levels. Accordingly, Idol-deficient mice exhibit elevated LDLR protein levels in peripheral tissues, but not in the liver. By contrast, LXR activation in cynomolgus monkeys induces hepatic IDOL expression, reduces LDLR protein levels, and raises plasma LDL levels. Knockdown of IDOL in monkeys with an antisense oligonucleotide blunts the effect of LXR agonist on LDL levels. These results implicate IDOL as a modulator of plasma lipid levels in primates and support further investigation into IDOL inhibition as a potential strategy for LDL lowering in humans.Copyright Â© 2014 Elsevier Inc. All rights reserved.
Macrophage polarization phenotype regulates adiponectin receptor expression and adiponectin anti-inflammatory response. - FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Adiponectin (APN), a pleiotropic adipokine that exerts anti-inflammatory, antidiabetic, and antiatherogenic effects through its receptors (AdipoRs), AdipoR1 and AdipoR2, is an important therapeutic target. Factors regulating AdipoR expression in monocyte/macrophages are poorly understood, and the significance of polarized macrophage activation in controlling AdipoR expression and the APN-mediated inflammatory response has not been investigated. The aim of this study was to investigate whether the macrophage polarization phenotype controls the AdipoR expression and APN-mediated inflammatory response. With the use of mouse bone marrow and peritoneal macrophages, we demonstrate that classical activation (M1) of macrophages suppressed (40-60% of control) AdipoR expression, whereas alternative activation (M2) preserved it. Remarkably, the macrophage polarization phenotypes produced contrasting inflammatory responses to APN (EC50 5 Âµg/ml). In M1 macrophages, APN induced proinflammatory cytokines, TNF-Î±, IL-6, and IL-12 (>10-fold of control) and AdipoR levels. In contrast, in M2 macrophages, APN induced the anti-inflammatory cytokine IL-10 without altering AdipoR expression. Furthermore, M1 macrophages adapt to a cytokine environment by reversing AdipoR expression. APN induced AdipoR mRNA and protein expression by up-regulating liver X receptor-Î± (LXRÎ±) in macrophages. These results provide the first evidence that macrophage polarization is a key determinant regulating AdipoR expression and differential APN-mediated macrophage inflammatory responses, which can profoundly influence their pathogenic role in inflammatory and metabolic disorders.Â© FASEB.
Deficiency of the tumor promoter gene wip1 induces insulin resistance. - Molecular endocrinology (Baltimore, Md.)
Diabetes is a growing health care issue, and prediabetes has been established as a risk factor for type 2 diabetes. Prediabetes is characterized by deregulated glucose control, and elucidating pathways which govern this process is critical. We have identified the wild-type (WT) p53-inducible phosphatase (WIP1) phosphatase as a regulator of glucose homeostasis. Initial characterization of insulin signaling in WIP1 knockout (WIP1(KO)) murine embryo fibroblasts demonstrated reduced insulin-mediated Ak mouse transforming activation. In order to assess the role of WIP1 in glucose homeostasis, we performed metabolic analysis on mice on a low-fat chow diet (LFD) and high fat diet (HFD). We observed increased expression of proinflammatory cytokines in WIP1(KO) murine embryo fibroblasts, and WIP1(KO) mice fed a LFD and a HFD. WIP1(KO) mice exhibited glucose intolerance and insulin intolerance on a LFD and HFD. However, the effects of WIP1 deficiency cause different metabolic defects in mice on a LFD and a HFD. WIP1(KO) mice on a LFD develop hepatic insulin resistance, whereas this is not observed in HFD-fed mice. Mouse body weights and food consumption increase slightly over time in LFD-fed WT and WIP1(KO) mice. Leptin levels are increased in LFD-fed WIP1(KO) mice, compared with WT. In contrast, HFD-fed WIP1(KO) mice are resistant to HFD-induced obesity, have decreased levels of food consumption, and decreased leptin levels compared with HFD-WT mice. WIP1 has been shown to regulate the nuclear factor kappa-light-chain-enhancer of activated B cells pathway, loss of which leads to increased inflammation. We propose that this increased inflammation triggers insulin resistance in WIP1(KO) mice on LFD and HFD.
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6600 Bruceville Rd Sacramento, CA 95823
7601 Hospital Dr Suite 220
6600 Bruceville Rd