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Biomedical subjects

J Yeh

Publications and source records attributed to J Yeh.

At least 19 recordsLinked to original sources
PubMed2006

Nature of signals that initiate the immune response during Wallerian degeneration of peripheral nerves.

Monocyte chemoattractant protein-1 is produced by Schwann cells during Wallerian degeneration of a peripheral nerve and contributes to a selective accumulation of macrophages in the degenerating segment. An in vitro preparation has been developed to analyze the molecules from axons and non-neuronal cells in nerves that stimulate an increased production of monocyte chemoattractant protein-1 mRNA by Schwann cells. For this purpose, Schwann cells obtained from neonatal rats were maintained in culture, exposed to putative molecular stimuli and analyzed for their content of monocyte chemoattractant protein-1 mRNA. Under basal conditions, the concentration of monocyte chemoattractant protein-1 in Schwann cells was low. Freeze-killed fragments or homogenates of nerve (or brain) but not viable nerve or freeze-killed muscle were effective in inducing monocyte chemoattractant protein-1 mRNA. The inductive activity was abolished by heating. Results of dialysis of supernatants of nerve homogenates indicate that a protein or proteins of 1-10 kDa were capable of stimulating synthesis of monocyte chemoattractant protein-1 by Schwann cells. Also, the activity in nerve homogenates was partially inhibited by antibodies to Toll-like receptor-4. The observations suggest that a non-secreted protein is released from disintegrating axons to initiate the innate immune response that characterizes Wallerian degeneration.

Animals↗
PubMed2005

COX-2 is necessary for venous ligation-mediated bone adaptation in mice.

In osteoblasts, cyclooxygenase 2 (COX-2) is the major isozyme responsible for production of prostaglandins. Prostaglandins are local mediators of bone resorption and formation and are known to be involved in bone's adaptive response to fluid shear stress (FSS). We have previously described a model of trabecular bone loss in hindlimb-suspended mice and rats and demonstrated partial protection from osteopenia by ligation of the femoral vein. The increased FSS resulting from this ligation drove bone adaptation in the absence of mechanical loading. In this study, we investigated the role of COX-2 in this adaptive response to FSS by use of COX-2 knockout mice. COX-2 knockout ("KO"), COX-2 heterozygote ("HET"), and COX-2 wild-type ("WT") animals all lost comparable amounts of trabecular bone from sham-operated limbs as a result of suspension. In WT mice, loss of trabecular BMD in the venous-ligated limb was significantly less than that of the sham-operated limb; this effect, however, was not seen in KO or HET mice. Percentage gain in femoral periosteal circumference was greater in the ligated limb than the sham-operated limb for WT mice. KO and HET mice already possess femora of larger periosteal circumference than their WT littermates and ligation in these bones did not result in an increase in perimeter relative to sham. Histomorphometry on embedded bones revealed thinner cortices and less mineralizing perimeter in KO femora than controls. In conclusion, this is the first in vivo study to show that fluid-flow-mediated bone adaptation, independent of mechanical strain, is COX-2 dependent.

Animals↗
PubMed2004

PECAM-1 interacts with nitric oxide synthase in human endothelial cells: implication for flow-induced nitric oxide synthase activation.

OBJECTIVE: We have previously shown that fluid shear stress (FSS) triggers endothelial nitric oxide synthase (eNOS) activity in endothelial cells and that the mechanotransduction mechanisms responsible for activation discriminate between rapid changes in FSS and FSS per se. We hypothesized that the particular sublocalization of eNOS at the cell-cell junction would render it responsive to activation by FSS temporal gradients. METHODS AND RESULTS: In human umbilical vein endothelial cells (HUVECs), immunofluorescence revealed strong eNOS membrane staining at the cell-cell junction colocalizing with platelet/endothelial cell adhesion molecule-1 (PECAM-1). In PECAM-1-/- mouse aorta, eNOS junctional localization seen in the wild type was absent. Similarly, junctional staining was lost in wild-type aorta near intercostal artery branches. eNOS/PECAM-1 association in HUVECs was confirmed by coimmunoprecipitation. When HUVECs were subjected to a 0.5s impulse of 12 dynes/cm2, a transient disruption of the eNOS/PECAM-1 complex was observed, accompanied by an increase in eNOS activity (cGMP production). Ramped flow did not trigger complex dissociation or an increase in cGMP production. In a cell-free system, a direct inhibition of eNOS activity by PECAM-1 is shown. CONCLUSIONS: These results suggest that eNOS is complexed with PECAM-1 at the cell-cell junction and is likely involved in the modulation of eNOS activity by FSS temporal gradients but not by FSS itself.

Animals↗
PubMed2004

Non-traumatic compression fractures of the thoracic spine following a seizure -- treatment by percutaneous kyphoplasty.

A 26-year-old male presented with acute mid-thoracic back pain following a witnessed grand mal seizure. There was no trauma and the patient was on steroids for systemic lupus erythematosus. X-rays and CT scans of the thoracic spine revealed compression fractures at T5 and T6, with 50 % loss of vertebral height and kyphosis. He underwent percutaneous kyphoplasty of both vertebrae, with symptomatic improvement. Non-traumatic compression fractures of the thoracic spine following seizures are a rare injury. This may be related to the compressive forces exerted on the vertebral column by the contractions of the truncal muscles, during a seizure. These compression fractures are suitable for treatment by minimally invasive techniques, such as kyphoplasty.

Adult↗
PubMed2001

Precision measurement of the spin-dependent asymmetry in the threshold region of 3He(e, e').

We present the first precision measurement of the spin-dependent asymmetry in the threshold region of 3He(e,e') at Q2 values of 0.1 and 0.2 (GeV/c)2. The agreement between the data and nonrelativistic Faddeev calculations which include both final-state interactions and meson-exchange current effects is very good at Q2 = 0.1 (GeV/c)2, while a small discrepancy at Q2 = 0.2 (GeV/c)2 is observed.

Journal Article↗
PubMed2001

Relations of stroke volume and cardiac output to body composition: the strong heart study.

BACKGROUND: Although cardiac output (CO) plays the vital role of delivering nutrients to body tissues, few data are available concerning the relations of stroke volume (SV) and CO to body composition in large population samples. METHODS AND RESULTS: Doppler and 2D echocardiography and bioelectric impedance in 2744 Strong Heart Study participants were used to calculate SV and CO and to relate them to fat-free body mass (FFM), adipose mass, and demographic variables. Both SV and CO were higher in men than women and in overweight than normal-weight individuals, but these differences were diminished or even reversed by normalization for FFM or body surface area. In both sexes, SV and CO were more strongly related to FFM than adipose mass, other body habitus measures, arterial pressure, diabetes, or age. In multivariate analyses using the average of Doppler and left ventricular SV to minimize measurement variability, FFM was the strongest correlate of SV and CO; other independent correlates were adipose mass, systolic pressure, diabetes, age, and use of digoxin and calcium channel and beta-blockers. CONCLUSIONS: In a population-based sample, SV and CO are more strongly related to FFM than other variables; increased FFM may be the primary determinant of increased SV and CO in obesity.

Adipose Tissue↗
PubMed2001

Axotomy and nerve growth factor regulate levels of neuronal nicotinic acetylcholine receptor alpha3 subunit protein in the rat superior cervical ganglion.

Neuronal nicotinic acetylcholine receptors (nAChRs) play a significant role in sympathetic transmission in the superior cervical ganglia (SCG), with most of the signal carried by a nAChR containing an alpha3 subunit. Work has shown that transection of the postganglionic nerves (axotomy) of the SCG results in a decrease in mRNA transcripts for alpha3, alpha5, alpha7 and beta4 and in protein expression of alpha7 and beta4. To evaluate effects of axotomy on alpha3 protein in the SCG, quantitative immunoblotting was used to demonstrate a dramatic decrease (> 80%) in the levels of this subunit 4 days after axotomy. Similarly, immunocytochemistry showed a marked decline in the number and the intensity of stained neurons for the alpha3 subunit as well as tyrosine hydroxylase. Ganglia explanted into culture for 4 days also showed a substantial decrease in alpha3 subunit protein. This decrease was partially prevented by the addition of nerve growth factor (NGF) to the culture medium at the time of explantation. Additionally, this decrease was reversed by the addition of NGF to the culture medium following 4 days in culture in the absence of NGF. These findings suggest that the loss of alpha3 subunit contributes to the reported decrease in ganglionic synaptic transmission that follows axotomy, and that NGF plays an important role in regulating the expression of alpha3-containing nAChRs in the SCG.

Animals↗
PubMed2000

Mitochondria and caspases in induced apoptosis in human luteinized granulosa cells.

Apoptosis occurs as a physiologic process in the ovarian life cycle. Staurosporine, a protein kinase inhibitor, is reported to induce apoptosis. Here, we hypothesize that staurosporine will induce apoptosis in human luteinized granulosa cells and that mitochondria and the caspase cascade participate in this process. Luteinized granulosa cells isolated from in vitro fertilization patients were treated with staurosporine. Microscopy revealed that staurosporine treatment resulted in cells exhibiting evidence of apoptosis, including cell detachment, loss of cell processes, membrane shrinkage, and formation of apoptotic bodies. In the staurosporine-treated cells, flow cytometry and confocal microscopy showed a decrease in the mitochondrial cardiolipin levels. Western analysis showed cleavage of caspase-9, an initiator caspase, of caspase-3, an executioner caspase, and of a caspase substrate, poly-(ADP-ribose)-polymerase (PARP) in staurosporine-treated cells. These data support our hypothesis and that this is the first demonstration of the involvement of mitochondria and of cleavage of caspases in human luteinized granulosa cell apoptosis. This may serve as a useful model to delineate the mechanism of apoptosis in the ovary, such as corpus luteum regression.

Apoptosis↗
PubMed2000

Neu differentiation factor/heregulin induction by hepatocyte and keratinocyte growth factors.

Hepatocyte growth-factor (HGF) is a potent, widely produced, pleiotropic mediator of mesenchymal-epithelial interaction. In a study of changes in gene expression initiated by HGF in Balb/MK keratinocytes, we observed the induction of Neu-differentiation factor (NDF) mRNA (also known as heregulin, or HRG). Further characterization of the regulation of NDF expression in Balb/MK keratinocytes revealed potent induction by keratinocyte growth factor (KGF) and epidermal growth factor (EGF), but not by HGF/NK2, an alternative HGF isoform with motogenic but not mitogenic or morphogenic activities. Sustained treatment (8 h) of Balb/MK cells with KGF stimulated secretion of mature NDF protein into the culture medium, and Balb/ MK cells treated with purified recombinant NDF protein showed increased DNA synthesis. We also found evidence of NDF induction in two models of tissue repair in mice: in full-thickness skin wounds, following locally increased KGF production, and in kidney after partial hepatectomy, following elevation of circulating HGF levels. These results reveal that mesenchymally-derived HGF and KGF can activate autocrine NDF signaling in their epithelial targets, and suggest that this mechanism contributes to the coordination of stages of wound repair, and possibly development, where these growth factors act in concert to direct epithelial proliferation, morphogenesis and differentiation.

Amino Acid Sequence↗
PubMed2000

Depletion of Raf-1 protooncogene by geldanamycin causes apoptosis in human luteinized granulosa cells.

OBJECTIVE: To investigate the hypothesis that epidermal growth factor (EGF) signaling in luteinized granulosa cells works through Raf-1 and mitogen-activated protein (MAP) kinases and that depletion of Raf-1 by geldanamycin will inhibit the signaling pathway and cause apoptosis. DESIGN: Laboratory study. SETTING: University of Minnesota. PATIENT(S): Human luteinized granulosa cells from IVF patients. INTERVENTION(S): The cells were treated with vehicle (DMSO), 0.5 microM of geldanamycin, 10 ng/mL of EGF, and geldanamycin + EGF. MAIN OUTCOME MEASURE(S): Radiochemical MAP kinase assay, Western blotting, confocal microscopy, and flow cytometry. RESULT(S): Geldanamycin treatment depleted Raf-1 and lowered MAP kinase activity in luteinized granulosa cells. EGF treatment increased MAP kinase phosphorylation and translocation of the phosphorylated MAP kinase to the nucleus. Geldanamycin blocked this effect. Cleavage of caspase-3, the executioner protein in apoptosis, into an active 17 kD fragment was observed by Western blotting in geldanamycin-treated cells. Finally, by flow cytometry we observed significantly increased percentages of subdiploid apoptotic nuclei in geldanamycin-treated cells. CONCLUSION(S): In human luteinized granulosa cells, EGF works through Raf-1, and MAP kinase and depletion of Raf-1 by geldanamycin resulted in decreased MAP kinase activity, increased activated caspase-3, and, ultimately, apoptosis.

Apoptosis↗
PubMed2000

Porous carriers for biomedical applications based on alginate hydrogels.

Macroporous scaffolds are typically utilized in tissue engineering applications to allow for the migration of cells throughout the scaffold and integration of the engineered tissue with the surrounding host tissue. A method to form macroporous beads with an interconnected pore structure from alginate has been developed by incorporating gas pockets within alginate beads, stabilizing the gas bubbles with surfactants, and subsequently removing the gas. Macroporous scaffolds could be formed from alginate with different average molecular weights (5-200 kDa) and various surfactants. The gross morphology, amount of interconnected pores, and total void volume was investigated both qualitatively and quantitatively. Importantly, macroporous alginate beads supported cell invasion in vitro and in vivo.

Alginates↗
PubMed2000

Transforming growth factor-beta(1), -beta(2), -beta(3) and their type I and II receptors in human term placenta.

Expression of transforming growth factor (TGF)-beta(3) as well as cellular localization of TGF-beta receptors has not been demonstrated in placenta. TGF-beta receptor type I (RI) and type II (RII) are required to transmit TGF-beta signals, therefore the determination of cells expressing both receptors in concert is necessary to identify target cells for TGF-beta. We investigated presence and localization of TGF-betas and their receptors (RI, RII) in human term placenta using reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. RT-PCR showed that messenger RNA for TGF-beta(1), -beta(2), -beta(3), and RI and RII is present in human term placenta. We found intense staining for all TGF-beta isoform and receptor proteins in the syncytiotrophoblastic layer, chorionic plate, and in cells of the extravillous trophoblasts using immunohistochemistry. The simultaneous expression of ligands and their receptors support the hypothesis that TGF-beta may play an important role in regulating growth, differentiation, and function of the human placenta.

Amnion↗
PubMed2000

Apoptosis in human term placenta. A morphological and gene expression study.

The objective of this study was to examine placentas after delivery from normal, healthy patients at term gestation. The placentas were from elective cesarean sections (n = 10, prior to the onset of labor) and spontaneous vaginal delivery (n = 10, after labor). We found that deoxyribonucleic acid laddering was present in all placentas and consistent with the pattern found in tissues that undergo apoptosis. Paraffin-embedded sections of placental villi stained by the in situ terminal deoxynucleotidyl transferase mediated biotinylated dUTP nick end labeling method revealed positive apoptotic nuclei in the placental villi. Reverse-transcriptase polymerase chain reaction demonstrated expression of messenger RNA for testosterone-repressed prostate message 2 and B cell lymphoma/leukemia-2 in the placenta. Our data demonstrate that apoptosis occurs in human term placenta.

Apoptosis↗