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PubMedDate not supplied

Robust image signal-to-noise ratio estimation using mixed Lagrange time delay estimation autoregressive model.

A new technique based on the statistical autoregressive (AR) model has recently been developed as a solution to signal-to-noise (SNR) estimation in scanning electron microscope (SEM) images. In the present study, we propose to cascade the Lagrange time delay (LTD) estimator with the AR model. We call this technique the mixed Lagrange time delay estimation autoregressive (MLTDEAR) model. In a few test cases involving different images, this model is found to present an optimum solution for SNR estimation problems under different noise environments. In addition, it requires only a small filter order and has no noticeable estimation bias. The performance of the proposed estimator is compared with three existing methods: simple method, first-order linear interpolator, and AR-based estimator over several images. The efficiency of the MLTDEAR estimator, being more robust with noise, is significantly greater than that of the other three methods.

Journal Article↗
PubMed1996

Current and future strategies to block tumor angiogenesis, invasion, and metastasis.

Progression of malignancy involves a series of sequential steps that ultimately lead to cancer-cell dissemination. In addition to the loss of growth control, an imbalanced regulation of motility and proteolysis is a prerequisite for invasion and metastasis. These factors are also necessary for angiogenesis-an integral process occurring at both the primary and the metastatic sites. Investigators have elucidated in detail many of the molecular mechanisms involved in the sequential steps of the metastatic cascade and have thereby provided new targets for therapeutic intervention. For each step, different model systems have been developed and various strategies for antimetastatic therapy have been tested in vitro as well as in murine systems. Difficulties in translating results obtained in preclinical models into the clinical setting have become apparent and have not been unexpected in light of the sometimes highly artificial interaction in the experimental setting. Nevertheless, continued development of model systems and further research into the genetic control of malignancy should lead to the identification of common signal-transduction pathways. Interference at such sites promises to be particularly effective in inhibiting proliferation and metastasis.

Animals↗
PubMed1995

Yolk sac concentration of prostaglandin E2 in diabetic pregnancy: further clues to the etiology of diabetic embryopathy.

Fetal malformation associated with maternal diabetes occurs before the seventh week of pregnancy. Current hypotheses suggest that the diabetic milieu causes a reduction in phosphatidylinositol turnover, leading to a disruption in the arachidonic acid cascade and resulting in a deficiency of prostaglandins, particularly prostaglandin E2. This in turn results in a wide variety of congenital anomalies. This hypothesis has not been tested experimentally in humans. The yolk sac is thought to be the most important source of nutrition in early pregnancy. We sought to compare yolk sac prostaglandin levels in normal and diabetic women. Under ultrasonographic guidance, yolk sacs were aspirated form 8 normal and 12 diabetic women ranging from 8 to 10 weeks gestational age prior to elective abortion. Prostaglandin E2 levels were determined using RIA. The mean prostaglandin E2 level in normal controls was 3605 pg/mL, and was undetected in all of the yolk sacs aspirated from diabetic women (P < 0.001). Yolk sac diameter in diabetic pregnancies was 1.2 mm larger than that of normal pregnancies. The functional and morphological changes demonstrated in this study may increase our understanding of the pathophysiology of diabetic embryopathy.

Blood Glucose↗
PubMed1996

Psychobiology of plasticity: effects of training and experience on brain and behavior.

Supporting Hebb's 1949 hypothesis of use-induced plasticity of the nervous system, our group found in the 1960s that training or differential experience induced neurochemical changes in cerebral cortex of the rat and regional changes in weight of cortex. Further studies revealed changes in cortical thickness, size of synaptic contacts, number of dendritic spines, and dendritic branching. Similar effects were found whether rats were assigned to differential experience at weaning (25 days of age), as young adults (105 days) or as adults (285 days). Enriched early experience improved performance on several tests of learning. Cerebral results of experience in an enriched environment are similar to results of formal training. Enriched experience and training appear to evoke the same cascade of neurochemical events in causing plastic changes in brain. Sufficiently rich experience may be necessary for full growth of species-specific brain characteristics and behavioral potential. Clayton and Krebs found in 1994 that birds that normally store food have larger hippocampi than related species that do not store. This difference develops only in birds given the opportunity to store and recover food. Research on use-induced plasticity is being applied to promote child development, successful aging, and recovery from brain damage; it is also being applied to benefit animals in laboratories, zoos and farms.

Animals↗
PubMed2005

Selective downregulation of ubiquitin conjugation cascade mRNA occurs in the senescent rat soleus muscle.

Aging-related alterations of the ubiquitin proteasome pathway (UPP) have been reported in locomotor skeletal muscle. Specifically, declines in proteasome activity have been observed in the soleus of senescent animals compared to the soleus of young controls. However, the influence of aging on the mRNA levels of key components within the ubiquitin conjugation cascade (UCC) remains unknown. We hypothesized that aged soleus muscle would exhibit downregulated expression of select UCC mRNA and decreased levels of ubiquitin-protein conjugates. To test this postulate, we harvested soleus muscles from 6 and 24-26 month old Fisher 344 rats. Aging resulted in a decline in mRNA expression of two key UCC components in soleus muscle; ubiquitin conjugating enzyme E2(14k) (E2(14k)) and muscle ring finger-1 (MuRF1). Surprisingly, no age-related differences existed in the total content of endogenous ubiquitin-protein conjugates in the soleus muscle. Nonetheless, a selective decrease in the level of ubiquitin-protein conjugates ( approximately 30kDa) was detected in the soleus of senescent animals. These results indicate that the soleus muscle displays a differential mRNA response of select UCC components to aging. Furthermore, the decline in E2(14k) and MuRF1 mRNA levels may contribute to altered substrate degradation by the UCC in the soleus muscle of senescent rats.

Aging↗
PubMed1998

Protection against beta-amyloid toxicity in primary neurons by paclitaxel (Taxol).

Neurofibrillary tangles in Alzheimer's disease contain aggregates of abnormally phosphorylated microtubule-associated protein tau, indicating that microtubule breakdown is a primary event in the neurodegenerative cascade. Recent studies have shown that addition to neuronal cultures of amyloid peptides found in Alzheimer's leads to abnormal phosphorylation of tau and neurofibrillary pathology. We tested the possibility that the microtubule-stabilizing drug paclitaxel (Taxol) might protect primary neurons against amyloid-induced toxicity. Neurons exposed to aggregated amyloid peptides 25-35 and 1-42 became pyknotic with degenerating neurites within 24 h. Treatment of cultures with paclitaxel either 2 h before or 2 h after addition of the peptide prevented these morphological alterations. When numbers of viable cells were determined in cultures exposed to amyloid peptide with or without paclitaxel for 24 or 96 h, the percentage of surviving cells was significantly higher in paclitaxel-treated cultures, and activation of the apoptosis-associated protease CPP32 was significantly reduced. These observations indicate that microtubule-stabilizing drugs may help slow development of the neurofibrillary pathology that leads to the loss of neuronal integrity in Alzheimer's disease.

Amyloid beta-Peptides↗
PubMed1981

Phospholipase A2 stimulated release of prostanoids from the isolated, perfused rabbit liver: implications in regional cellular injury.

We have previously demonstrated a direct relationship between the activity of the arachidonic acid cascade in vivo and the extent of cellular damage following several types of experimental injury. Since phospholipase activity has been shown to regulate arachidonic acid availability, we tested the ability of circulating phospholipase A2 (PLA2) of pancreatic origin to stimulate prostanoid production or induce cellular injury in the isolated, perfused rabbit liver. Experimental conditions were similar to those present during pancreatitis or early splanchnic artery occlusion shock. The administration of PLA2 at a rate of 100 U/min for 10 min resulted in enhanced rates of thromboxane B2 and 6-ketoprostaglandin F1 alpha release between 1 and 5 min into the infusion period. No changes in hepatic perfusion pressure, vascular resistance, wet tissue weight, or release of lactic dehydrogenase or acid phosphatase into the effluent were observed in either vehicle or PLA2-treated livers. This indicates that cellular injury was not a factor in the prostanoid release. These data suggest that circulating PLA2 can directly stimulate de novo prostanoid synthesis in noninjured tissues. Thus, enhanced plasma prostanoid concentrations in intact animals during periods or regional cellular injury may be due in part to circulating PLA2 released from damaged tissues.

Animals↗
PubMed1993

Comparison of receptors for Escherichia coli heat-stable enterotoxin: novel receptor present in IEC-6 cells.

Enterotoxigenic Escherichia coli elaborate a heat-stable enterotoxin that causes diarrhea in humans and animals. The primary event in the diarrheal cascade is the binding of this enterotoxin to specific receptors on enterocytes and activation of guanylyl cyclase. Two intestinal cell lines, Caco-2 and IEC-6, were tested for the presence of these receptors. Although both cell lines exhibited specific binding, only the Caco-2 cell line responded to heat-stable enterotoxin with increased guanylyl cyclase activity. Cloning and expression studies confirmed that the receptor present in Caco-2 cells is a homologue of guanylyl cyclase C, a known transmembrane heat-stable enterotoxin receptor. Expression of the receptor in differentiating Caco-2 cells increases with cell maturation, indicating that these cells are a suitable model for future studies. However, Northern and polymerase chain reaction analyses demonstrated that guanylyl cyclase C is not expressed in IEC-6 cells, strongly suggesting the presence of a novel heat-stable enterotoxin receptor that is not coupled to guanylyl cyclase activity.

Amino Acid Sequence↗
PubMed2005

Macrophage differentiation to foam cells.

Foam cell formation from macrophages with subsequent fatty streak formation plays a key role in early atherogenesis. Foam cell formation is thought to be induced by Low Density Lipoproteins (LDL), including oxidized LDL (OxLDL) or minimally modified LDL (mmLDL). Understanding the molecular mechanisms involved in OxLDL- and mmLDL-induced foam cell formation is of fundamental importance for atherosclerosis and cardiovascular disease. The expression of many genes is likely modulated during macrophage transformation into a foam cell. In this mini-review we describe functional consequences of modulation of three groups of genes: Scavenger Receptors (SR-A, CLA-1/SR-BI, CD36, CD68, LOX-1, and SR-PSOX), the PPAR family of nuclear receptors, and a number of genes involved in eicosanoid biosynthesis, including lipoxygenases and leukotriene receptors. Scavenger receptors appear to play a key role in uptake of OxLDL, while mmLDL appears to interact with CD14/TLR4. The regulation of scavenger receptors is, in part, mediated by the PPAR family of nuclear receptors. PPARalpha and PPARgamma agonists, such as thiazolidinediones and fibrates, and PPARdelta agonists were tested as atheroprotective drugs and showed some beneficial effects. Eicosanoids are naturally occuring agonists for PPARs. Recent observations indicate a role of the components of the eicosanoid cascade, such as 5-lipoxygenase, 15-lipoxygenase and the leukotriene receptors in foam cell formation. Selective inhibitors of lipoxygenases and leukotriene receptors could be useful in the treatment of atherosclerosis by preventing or reducing foam cell formation.

Animals↗
PubMed1989

The contractile effects of porcine tetradecapeptide renin substrate in human resistance vessels: evidence of activation by vascular wall renin and serine proteases.

In order to test the hypothesis that the contraction induced in human resistance arterioles by porcine tetradecapeptide renin substrate (TDP) is mediated by enzymes specific to the renin-angiotensin cascade, human resistance vessels from skin and subcutaneous fat were mounted in a myograph and exposed to TDP in the presence and absence of the human renin inhibitor H261, the serine protease inhibitor aprotinin, a polyclonal anti-human renin antibody and captopril. TDP induced a dose-dependent contraction that could be abolished by saralasin. The sensitivity to TDP was significantly attenuated by H261, aprotinin and combinations of captopril with aprotinin and captopril plus aprotinin and H261, as indicated by a significant reduction in pD2 (-log10ED50 [mmol/l]) for TDP. However, captopril alone was ineffective. It was concluded that at physiological pH, porcine TDP induces contraction in human resistance vessels by the action of enzymes not specific to the renin-angiotensin cascade. Whilst a clear inhibitory effect of H261 was demonstrated, a significant comparable inhibition by captopril and a polyclonal renin antibody was not observed. This may reflect the difficulty with which these inhibitors gain access to their intracellularly located substrates.

Electric Stimulation↗
PubMed1993

Detection of glucose intolerance in pregnancy.

Current methods for the screening and diagnosis of glucose intolerance first discovered in pregnancy are reviewed and innovative approaches to the detection of metabolic disturbances in pregnancy are presented. Glucose intolerance first detected in pregnancy, termed gestational diabetes mellitus (GDM), is amongst the most significant risks of adverse fetal and maternal outcome. Normal pregnancy is characterized by both insulin resistance and pancreatic B cell compensation. In those pregnancies complicated by glucose intolerance reflected in hyperglycemia, insulin resistance appears to be heightened, both blood flow and transcapillary transport of insulin are compromised and insulin receptor and post receptor defects are exacerbated. The resulting hyperinsulinemia and hyperglycemia have, in turn, been associated with accumulated maternal fat deposition and fetal macrosomia. This cascade of events constitutes GDM or impaired glucose tolerance. The discovery of GDM is made through a process of screening and diagnosis, employing standardized oral glucose challenge tests. These tests were designed to identify those women at risk for subsequent development of non-insulin dependent diabetes mellitus. The current efficacy of glucose challenge tests has been questioned in light of increasing concern over their usefulness in detecting those women at risk for maternal and fetal complications of pregnancy. Alternative methods, including both the modification of the standardized tests, as well as the introduction of newer methodologies, such as capillary blood glucose monitoring, have been proposed. The implementation of newer approaches may result in improved detection of those women whose infants are at high risk for both metabolic and morphologic complications of persistent hyperglycemia in pregnancy.

Diabetes, Gestational↗
PubMed1997

Sequestration of p56(lck) by gp120, a model for TCR desensitization.

Ligation of the CD4 receptor by HIV envelope glycoprotein gp120 inhibits T cell activation and signaling through the TCR complex. Recent reports suggest CD4 ligation by gp120 + anti-gp120 Abs uncouples protein tyrosine kinases (PTKs) from the TCR signal-transduction cascade. This finding and other observations led us to hypothesize that the effects of gp120 are mediated through p56(lck), a PTK noncovalently associated with CD4. To test this hypothesis, we first examined the kinetics of gp120/anti-gp120-induced TCR signaling defects in the Jurkat T cell line. Pretreating cells with gp120/anti-gp120 for 1 to 4 h before stimulation prevented TCR-directed PTK activation. Coincident with TCR desensitization, pretreatment with gp120/anti-gp120 also decreased the amount of p56(lck) that could be immunoprecipitated from the Nonidet P-40 detergent-soluble fraction of cellular lysates, while simultaneously increasing the recovery of p56(lck) from the Nonidet P-40 detergent-insoluble fraction (or cytoskeleton). To assess the potential role of the actin in this process, experiments were conducted in the presence of cytochalasin D. Cytochalasin D restored TCR signaling in cells previously desensitized with gp120/anti-gp120 and prevented translocation of p56lck from the Nonidet P-40 detergent-soluble fraction of cell lysates. Furthermore, p56(lck) was found to coimmunoprecipitate with anti-actin. These data suggest that gp120/anti-gp120 may inhibit TCR signaling by sequestering p56(lck) to the cytoskeleton.

Actins↗
PubMed2006

Violet laser diodes in flow cytometry: an update.

INTRODUCTION: In previous studies we and others have demonstrated the usefulness of violet laser diodes (VLDs) as replacement laser sources for krypton-ion lasers on stream-in-air cytometers. Previously available VLDs had a maximum available power of less than 25 mW; this was sufficient for excitation of densely labeled cell surface antigens using fluorochromes such as Cascade Blue or Pacific Blue, but may have been insufficient for applications requiring higher levels of photon saturation, such as low-level expression of Cyan Fluorescent Protein (ECFP) in CFP-YFP FRET applications. In this follow-up study, we have tested more powerful VLDs emitting at 55 mW, and a beam-merged dual module VLD with 100 mW combined output, for their ability to excite a variety of violet-excited fluorochromes, including CFP. METHODS: A dual module VLD (two linear polarized VLDs with their beams merged by a polarized beam combiner) emitting at 404 nm was mounted on a BD FACSVantage DiVa stream-in-air cytometer. The individual polarized 55 mW beams or the 100 mW combined beams were used to analyze PBMCs labeled with the violet-excited probes Cascade Blue, Alexa Fluor 405, Cascade Yellow and Pacific Orange dyes. Violet-excited fluorescent microsphere mixtures with decreasing fluorescence levels were also used to detect the minimum sensitivity threshold and precision of these lasers. VLD excitation on a gel-coupled cuvette flow cytometer was used as a sensitivity baseline. RESULTS: The dual module 100 mW VLD gave both sensitivity and precision levels approaching that observed for lower-power sources on a cuvette cytometer. Single polarized VLD modules at 55 mW gave slightly decreased sensitivity for the microspheres standards and all the tested fluorochromes compared to the 100 mW source. CONCLUSIONS: While 55 mW laser sources performed adequately in the stream-in-air format, increasing the power to 100 mW did give a small but detectable increase in instrument sensitivity. This sensitivity level approached that of cuvette systems.

Animals↗
PubMed2005

Apolipoprotein A-IV attenuates oxidant-induced apoptosis in mitotic competent, undifferentiated cells by modulating intracellular glutathione redox balance.

Oxidant-mediated modulation of the intracellular redox state affects the apoptotic cascade by altering the balance between cellular signals for survival and suicide. Apolipoprotein A-IV (Apo A-IV) is known to possess antioxidant-like activity. In the present study, we tested 1) whether Apo A-IV could influence redox-dependent apoptosis and, if so, 2) whether such an effect could be mediated by modulation of intracellular redox balance. Mitotic competent, undifferentiated PC-12 cells were incubated with either tert-butyl hydroperoxide (TBH) or diamide with or without preincubation with human Apo A-IV. Apo A-IV significantly decreased apoptosis produced by both TBH and diamide, and washout of A-IV before incubation with TBH and diamide did not eliminate its protective effect. Apo A-I had no such protective effect. The Apo A-IV effect was not blocked by D,L-buthionine-[S,R]-sulfoximine, but it was reversed by both dehydroisoandrosterone and transfection with an antisense oligodeoxynucleotide to glucose-6-phosphate dehydrogenase (G6PD). Apo A-IV abolished the transient, oxidant-induced rise in glutathione disulfide (GSSG) and cellular redox imbalance previously shown to initiate the apoptotic cascade. Apo A-IV had no effect on GSSG reductase activity, but it stimulated G6PD activity 10-fold. These results suggest a novel role for Apo A-IV in the regulation of intracellular glutathione redox balance and the modulation of redox-dependent apoptosis via stimulation of G6PD activity.

Animals↗
PubMed1998

Immunohistochemical analysis of the functional status of estrogen receptor cascade in breast cancer.

Hormone receptor expression in human breast cancer cells does not always reflect tumor response to therapy. Thus, relations between hormone receptor status and other parameters need further examination. The aim of this study was to test the ability of estrogen receptors (ER) to induce progesterone receptor (PR) synthesis as well as to test their role in the regulation of cell proliferation. Measurement of the relation between expressions of ER and the estrogen receptor related protein p29 (ERRP) was a further goal. The results show that some hormone receptor phenotypes are closely related to tumor proliferative activity: in the ER-group, especially ER-PR-phenotype, proliferative activity shows no obvious relationship to phenotype status, suggesting that proliferation in this group probably is not under estrogen control, while in the ER+ group, PR expression was related to reduced proliferation. There was no clear association between ERRP and nuclear ER but the highest ERRP expression was most closely related to ER negative (ER-) or slightly positive (ER +/-) hormone receptor statuses. Tumors with these phenotypes are known to have a poorer prognosis. The conclusion drawn is that simultaneous estimation of proliferative activity, ERRP p29 expression and a comparison with ER/PR hormone receptor phenotype, could provide pathologist with a valuable tool for predicting hormone response and prognosis in breast cancer patients.

Adult↗
PubMed1983

Protein phosphorylation as a regulatory device.

Phosphorylation-dephosphorylation cascade systems represent a major mechanism of cellular regulation. A theoretical analysis of such systems (Stadtman & Chock 1977) revealed that they are endowed with extraordinary regulatory capacities; they may exhibit smooth, flexible responses to changes in single and multiple metabolite levels, signal amplification, and apparent positive cooperativity. To test the theories and equations involved in this analysis, an in vitro phosphorylation-dephosphorylation model system was developed. The system consists of a cyclic-AMP-dependent protein kinase and a phosphoprotein phosphatase, both isolated to near-homogeneity from bovine heart, and a nanopeptide that serves as the interconvertible substrate. Experiments with the model system confirm the predictions about the behaviour of a monocyclic cascade. They also reveal that when the concentration of enzyme-substrate complex is not negligible, cyclic cascades are potentially more sensitive to variations in effector concentrations and can achieve even greater signal amplification than previously predicted.

Animals↗
PubMed1988

Abnormal cathepsin B activity in Batten disease.

Fibroblasts cultured from patients with various forms of neuronal ceroid-lipofuscinosis (NCL; Batten disease) showed variably decreasing cathepsin B activity with increasing passage number and months in culture in the presence of fetal calf serum. Cathepsin H activity and that of a wide range of lysosomal hydrolases was unaffected by these conditions. Cathepsin B activity was assayed either colorimetrically (N alpha-benzoyl-DL-Arg-beta-naphthylamide; BANA), fluorimetrically (Z-Arg-Arg-methylcoumarin), or autoradiographically, following NaDodSO4-12.5% polyacrylamide gel electrophoresis ([125]Tyr-Ala-Lys-Arg-CH2Cl) and was found to be lysosomal in localization. Fractionation of disrupted fibroblasts on a Percoll gradient showed evidence of abnormally buoyant lysosomes in some NCL patients, and these tended to be low in cathepsin B but rich in other lysosomal hydrolases. Our data do not support a primary defect in cathepsin B as the basic defect in NCL. However, a possible explanation for various studies implicating a protease defect in NCL is that cathepsin B was highly sensitive to inactivation by peroxides and aldehydes. Thus hydrogen peroxide (0.3 mM) or 4-hydroxynonenal (1 nM) inactivated cathepsin B without inhibiting cathepsin H or lysosomal hydrolases such as alpha-L-fucosidase. Since peroxides and 4-hydroxynonenal have been shown to accumulate in NCL tissue (despite apparently normal peroxidase activity), we tested the possibility of a defect in the removal of peroxidized lipids from phospholipids as the primary defect in NCL. The nociceptive peptide bradykinin (BK) normally initiates a cascade involving receptor-mediated phospholipase C activation and release of arachidonate and prostanoids from cultured skin fibroblasts. Release of [3H]arachidonate by BK was deficient in NCL fibroblasts, suggesting that the primary defect in NCL could involve the deficiency of a specific phospholipase A2 activity.

Acid Phosphatase↗
PubMed2006

Liver X receptor agonists ameliorate TNFalpha-induced insulin resistance in murine brown adipocytes by downregulating protein tyrosine phosphatase-1B gene expression.

AIMS/HYPOTHESIS: The nuclear receptors, including nuclear receptor subfamily 1, group H, member 3 (NR1HR, also known as liver X receptor [LXR]), are sensors of cholesterol metabolism and lipid biosynthesis that have recently been proposed as insulin sensitisers. TNFalpha has been described as a link between obesity and the development of insulin resistance, an important contributor to the pathogenesis of type 2 diabetes. Therefore, we decided to investigate the ability of NR1HR agonists to ameliorate TNFalpha-induced insulin resistance in brown adipocytes. METHODS: Primary brown adipocytes from rat fetuses, and from wild-type neonate mice and neonate mice deficient in the gene encoding protein tyrosine phosphatase-1B (Ptpn1, also known as Ptp1b) were cultured in the absence or presence of TNFalpha and different nuclear receptor agonists. Among them, the unrelated NR1HR ligands T0901317, GW3965 and (22R)-hydroxycholesterol were tested. After insulin stimulation, glucose uptake and solute carrier family 2 (facilitated glucose transporter), member 4 (SLC2A4, formerly known as GLUT4) translocation were measured. Next the insulin signalling cascade was determined by submitting cells to lysis, immunoprecipitation and immunoblotting. RESULTS: NR1HR agonists ameliorate TNFalpha-induced insulin resistance restoring completely insulin-stimulated glucose uptake and SLC2A4 translocation to plasma membrane. This effect is parallel to the recovery of the insulin cascade insulin receptor/IRS-2/phosphatidylinositol 3-kinase/protein kinase B, and could be due to the fact that T0901317 prevents the increase of PTPN1 production and phosphatase activity produced by TNFalpha. In this regard, Ptpn1-deficient brown adipocytes showed protection against insulin resistance by TNFalpha. Moreover, we observed that T0901317 produced in itself a significant increase over basal glucose uptake consistent with an increase of SLC2A4 protein content in plasma membrane, attributable to the activation of protein kinase zeta and/or the increase of Slc2a4 expression. CONCLUSIONS/INTERPRETATION: Nuclear receptors NR1HR are interesting potential targets for drug treatment of insulin resistance.

Adipocytes↗