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Biomedical subjects

R Y Liu

Publications and source records attributed to R Y Liu.

At least 19 recordsLinked to original sources
PubMed2006

Origin and phylogeographical structure of Chinese cattle.

Complete mitochondrial D-loop sequences of 231 samples were used to explore the origin and genetic diversity of Chinese cattle. Phylogenetical analysis of these sequences revealed both Bos taurus and Bos indicus mitochondrial types in Chinese cattle. Four of the previously identified mitochondrial DNA lineages (T1-T4) were identified in the Bos taurus type, including lineage T1, which was found for the first time in Chinese cattle. Two lineages (I1 and I2) were identified in the Bos indicus type. Our results support the suggestion that the Yunnan-Guizhou Plateau is the domestication site of Chinese zebu. We also found evidence that Tibetan cattle originated from taurine and zebu cattle. The distribution pattern of Chinese cattle breeds was closely related to the geographical and climatic background. It was possible to divide Chinese cattle in this study into two major groups: northern and southern cattle.

Animals↗
PubMed2001

Different signaling pathways mediate regenerative versus developmental sensory axon growth.

Recent advances in defining neurotrophin signaling mediators have provided insights into the signal transduction mechanisms that underlie axon growth. Evidence is accumulating that major Trk effectors regulate the morphological development of embryonic peripheral neurons. Less is known about signaling related to the robust axon extension that follows peripheral axotomy of adult neurons. Regenerative axon growth can be mimicked in vitro by a "conditioning" lesion performed 2 weeks before culture (Smith and Skene, 1997). Previous work has implicated both neurotrophins and cytokines in this response. Because signal transduction mediators of both of these families of growth factors are well characterized, we have compared the role of neurotrophin and cytokine signaling in developmental versus regenerative sensory axon growth. Chemical inhibitors were administrated to embryonic and axotomized sensory neurons in vitro to block the activation of Erk kinase (MEK)-extracellular signal-regulated kinase (ERK), phosphatidylinositol-3 kinase (PI3-K), and janus kinase (JAK) signaling. As expected, both MEK and PI3-K inhibition blocked axon growth from both naive and NGF-stimulated embryonic day 13 sensory neurons, whereas inhibition of JAK phosphorylation had no effect. In contrast, neither MEK nor PI3-K inhibitors blocked elongation of adult sensory neurons after a conditioning lesion. However, the addition of a JAK2 inhibitor prevented the regenerative axon response. Consistent with these pharmacological results, the percentage of neurons showing intense nuclear signal transducers and activators of transcription 3 phosphorylation after a conditioning lesion was markedly increased compared with controls. These observations demonstrate that the signaling mediators that underlie regenerative axon growth are distinct from those used during development and suggest that cytokine signaling may be critical to peripheral nervous system regeneration.

Animals↗
PubMed2001

The effects of diet and supplements on a male world champion lightweight rower.

A world-class lightweight rower who came to the Hong Kong Sports Institute was evaluated over a two-month period of training. He was preparing for the 1995 World Rowing Championships. The subjects trained for approximately 70 minutes per day at different levels of intensity, to simulate race conditions. Caloric expenditures (based upon heart rate response and estimation from specific activity) were estimated to be approximately 4125 kcal/day. A three day dietary survey revealed that the subject was able to maintain caloric balance (caloric intake = 4088 kcal/day). Body weight was maintained at a constant level, another indication that the subject was able to meet energy needs. A breakdown of his food intake revealed protein, carbohydrate, and fat, made up 19%, 51%, and 30% of his caloric intake, respectively. This was somewhat surprising since recommendations for endurance athletes are for higher carbohydrate contribution. During and after the training bouts the subject consumed two separate carbohydrate supplements. A total of 218 g of carbohydrate were consumed daily. This level of supplementation was able to maintain the subject's blood glucose concentration at normal levels following recovery from exercise. Comparisons of recovery heart rates when either water or carbohydrate was consumed indicate a beneficial effect of the supplement. Despite consuming carbohydrates at lower than recommended levels, this athlete went on to win this third gold medal in rowing.

Adult↗
PubMed2000

Multi-lipofection efficiently transfected genes into astrocytes in primary culture.

This study demonstrated that liposome-mediated transfection - lipofection - is suitable for delivering genes into astrocytes. By repeatedly lipofecting the same astrocyte cultures, a process we call multi-lipofection, the transfection efficiency of the beta-galactosidase (beta-gal) gene was improved from 2.6+/-0.6 to 17. 4+/-1.1%. This is the highest efficiency ever reported in gene-transfer with Lipofectin(R) in a primary culture of mouse cerebral cortical astrocytes. Furthermore, multi-lipofection did not cause observable disturbance to astrocytes as indicated by insignificant changes in the glial fibrillary acidic protein content in the cultures. In order to demonstrate that the transfected gene achieved a physiologically relevant expression level, a plasmid containing the pEF-hsp70 protein gene was lipofected into astrocytes. This produced colonies of astrocytes showing an increased resistance to heat-induced cell death. A similar experiment was performed with the glial-derived neurotrophic factor (GDNF) gene. Control astrocytes had no detectable GDNF. In the transfected astrocytes, the GDNF protein could be identified intracellularly by immunocytochemistry. Western blot analysis revealed, as compared to astrocytes with one lipofection, a 2.9-fold increase of GDNF with four lipofections. GDNF remained detectable in astrocytes 2 weeks after four lipofections. Thus, multi-lipofection provides a mild and efficient means of delivering foreign genes into astrocytes in a primary culture, making astrocytes good candidate vehicle cells for gene/cell therapy in the CNS.

Animals↗
PubMed2000

Activation of p38 mitogen-activated protein kinase is required for tumor necrosis factor-alpha -supported proliferation of leukemia and lymphoma cell lines.

To elucidate mechanisms of tumor necrosis factor alpha (TNF-alpha)-induced proliferation of a number of human leukemia and lymphoma cell lines, we examined the role of p38 mitogen-activated protein kinase (MAPK) in TNF-alpha signaling in Mo7e and Hut-78 cells. TNF-alpha-dependent p38 MAPK activation was detected in both Mo7e and Hut-78 cells and was blocked by the p38 MAPK inhibitor, SB203580. Ablation of p38 MAPK activity by SB203580 abrogated TNF-alpha-induced Mo7e cell proliferation and TNF-alpha-dependent autocrine growth of Hut-78. As we have shown previously that activation of the nuclear factor kappaB (NF-kappaB) is also required for TNF-alpha-induced Mo7e cell proliferation, the involvement of p38 MAPK in NF-kappaB activation was assessed. SB203580 did not affect TNF-alpha-signaled nuclear translocation and DNA-binding activity of NF-kappaB, and inhibition of NF-kappaB function did not affect TNF-alpha-induced p38 MAPK activation, indicating that these events are not dependent on each other. However, SB203580 depressed the expression of NF-kappaB-dependent genes, as monitored by a kappaB-driven reporter gene. Our findings demonstrate that activation of both p38 MAPK and NF-kappaB plays a critical role in TNF-alpha-mediated survival and proliferation of human leukemia and lymphoma cells, and p38 MAPK acts at least in part by facilitating the transcriptional activation function of NF-kappaB.

Cell Division↗
PubMed2000

Decreased vasopressin gene expression in the biological clock of Alzheimer disease patients with and without depression.

Circadian rhythm disturbances are frequently present in Alzheimer disease (AD). In the present study, we investigated the expression of vasopressin (AVP) mRNA in the human suprachiasmatic nucleus (SCN). The in situ hybridization procedure on formalin-fixed paraffin-embedded material was improved to such a degree that we could, for the first time, visualize AVP mRNA expressing neurons in the human SCN and carry out quantitative measurements. The total amount of AVP mRNA expressed as masked silver grains in the SCN was 3 times lower in AD patients (n = 14; 2,135 +/- 597 microm2) than in age- and time-of-death-matched controls (n = 11; 6,667 +/- 1466 microm2) (p = 0.003). No significant difference was found in the amount of AVP mRNA between AD patients with depression (n = 7) and without depression (n = 7) (2,985 +/-1103 microm2 and 1,285 +/- 298 microm2, respectively; p = 0.38). In addition, the human SCN AVP mRNA expressing neurons showed a marked day-night difference in controls under 80 years of age. The amount of AVP mRNA was more than 3 times higher during the daytime (9,028 +/- 1709 microm2, n = 7) than at night (2,536 +/- 740 microm2, n = 4; p = 0.02), whereas no clear diurnal rhythm of AVP mRNA in the SCN was observed in AD patients. There was no relationship between the amount of AVP mRNA in the SCN and age at onset of dementia, duration of AD and the neuropathological changes in the cerebral cortex. These findings suggest that the neurobiological basis of the circadian rhythm disturbances that are responsible for behavioral rhythm disorders is located in the SCN. It also explains the beneficial effects of light therapy on nightly restlessness in AD patients.

Aged↗
PubMed1999

Tumor necrosis factor-alpha-induced proliferation of human Mo7e leukemic cells occurs via activation of nuclear factor kappaB transcription factor.

Tumor necrosis factor-alpha (TNF-alpha) stimulates proliferation of Mo7e, CMK, HU-3, and M-MOK human leukemic cell lines. We report here the signal transduction pathway involved in TNF-alpha-induced Mo7e cell proliferation. Mo7e cells spontaneously die in the absence of growth factors, but treating the cells with interleukin (IL)-3, IL-6, thrombopoietin, granulocyte/macrophage colony-stimulating factor, or TNF-alpha promotes their survival and proliferation. Although most of these factors activate MAP kinase and Jun NH2-terminal kinase/signal transducer and activators of transcription signaling pathways, TNF-alpha fails to activate either pathway. When Mo7e cells were treated with TNF-alpha, nuclear factor kappaB (NF-kappaB) was activated transiently. The activated NF-kappaB consisted of heterodimers of p65 and p50 subunits. The degradation of IkappaBalpha coincided with activation of NF-kappaB in TNF-alpha-treated cells. To investigate the role of activated NF-kappaB in TNF-alpha-induced Mo7e proliferation, a cell-permeable peptide (SN50) carrying the nuclear localization sequence of p50 NF-kappaB was used to block nuclear translocation of activated NF-kappaB. Pretreating Mo7e cells with SN50 blocked TNF-alpha-induced nuclear translocation of NF-kappaB and inhibited TNF-alpha-induced Mo7e cell survival and proliferation. A mutant SN50 peptide did not affect TNF-alpha-induced Mo7e cell growth. SN50 had no effects on IL-3- or granulocyte/macrophage colony-stimulating factor-induced Mo7e cell proliferation. The results indicate that activation of NF-kappaB is involved in TNF-alpha-induced Mo7e cell survival and proliferation.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1999

Constitutive activation of the JAK2/STAT5 signal transduction pathway correlates with growth factor independence of megakaryocytic leukemic cell lines.

The factor-independent Dami/HEL and Meg-01 and factor-dependent Mo7e leukemic cell lines were used as models to investigate JAK/STAT signal transduction pathways in leukemic cell proliferation. Although Dami/HEL and Meg-01 cell proliferation in vitro was independent of and unresponsive to exogenous cytokines including granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), IL-6, thrombopoietin (TPO), and tumor necrosis factor-alpha (TNF-alpha), the growth of Mo7e cells was dependent on hematopoietic growth factors. When these cell lines were cultured in medium without cytokines, a constitutively activated STAT-like DNA-binding factor was detected in nuclear extracts from both Dami/HEL and Meg-01 cells. However, the STAT-like factor was not detectable in untreated Mo7e cells, but was activated transiently in Mo7e cells in response to cytokine treatments. The constitutively activated and cytokine-induced STAT-like DNA-binding factor in these three cell lines was identified as STAT5 by oligonucleotide competition gel mobility assays and by specific anti-STAT antibody gel supershift assays. Constitutive activation of JAK2 also was detected in the factor-independent cell lines, but not in Mo7e cells without cytokine exposure. Meg-01 cells express a p185 BCR/ABL oncogene, which may be responsible for the constitutive activation of STAT5. Dami/HEL cells do not express the BCR/ABL oncogene, but increased constitutive phosphorylation of Raf-1 oncoprotein was detected. In cytokine bioassays using growth factor-dependent Mo7e and TF-1 cells as targets, conditioned media from Dami/HEL and Meg-01 cells did not show stimulatory effects on cell proliferation. Our results indicate that the constitutive activation of JAK2/STAT5 correlates with the factor-independent growth of Dami/HEL and Meg-01 cells. The constitutive activation of JAK2/STAT5 in Dami/HEL cells is triggered by a mechanism other than autocrine cytokines or the BCR/ABL oncoprotein.

Cell Division↗
PubMed1999

Decreased melatonin levels in postmortem cerebrospinal fluid in relation to aging, Alzheimer's disease, and apolipoprotein E-epsilon4/4 genotype.

Sleep disruption, nightly restlessness, sundowning, and other circadian disturbances are frequently seen in Alzheimer's disease (AD) patients. Changes in the suprachiasmatic nucleus and pineal gland are thought to be the biological basis for these behavioral disturbances. Melatonin is the main endocrine message for circadian rhythmicity from the pineal. To determine whether melatonin production was affected in AD, melatonin levels were determined in the cerebrospinal fluid (CSF) of 85 patients with AD (mean age, 75 +/- 1.1 yr) and in 82 age-matched controls (mean age, 76 +/- 1.4 yr). Ventricular postmortem CSF was collected from clinically and neuropathologically well defined AD patients and from control subjects without primary neurological or psychiatric disease. In old control subjects (>80 yr of age), CSF melatonin levels were half of those in control subjects of 41-80 yr of age [176 +/- 58 (n = 29) and 330 +/- 66 (n = 53) pg/mL, respectively; P = 0.016]. We did not find a diurnal rhythm in CSF melatonin levels in control subjects. In AD patients the CSF melatonin levels were only one fifth (55 +/- 7 pg/mL) of those in control subjects (273 +/- 47 pg/mL; P = 0.0001). There was no difference in the CSF melatonin levels between the presenile (42 +/- 11 pg/mL; n = 21) and the senile (59 +/- 8 pg/mL; n = 64; P = 0.35) AD patients. The melatonin level in AD patients expressing apolipoprotein E-epsilon3/4 (71 +/- 11 pg/mL) was significantly higher than that in patients expressing apolipoprotein E-epsilon4/4 (32 +/- 8 pg/ml; P = 0.02). In the AD patients no significant correlation was observed between age of onset or duration of AD and CSF melatonin levels. In the present study, a dramatic decrease in the CSF melatonin levels was found in old control subjects and even more so in AD patients. Whether supplementation of melatonin may indeed improve behavioral disturbances in AD patients should be investigated.

Aged↗
PubMed1998

The role of type I and type II tumor necrosis factor (TNF) receptors in the ability of TNF-alpha to transduce a proliferative signal in the human megakaryoblastic leukemic cell line Mo7e.

We investigated the effects of tumor necrosis factor (TNF) alpha on the human megakaryocytic leukemic cell lines Mo7e, Meg-01, and Dami/HEL. Our data show that both type I and type II TNF receptors (TNF-RI and TNF-RII) are expressed on all of these cells, and TNF-alpha significantly stimulates the proliferation of growth factor-dependent Mo7e cells but not of Meg-01 or Dami/HEL cells, which grow in a factor-independent manner. TNF-alpha serves predominantly as a mitogen for Mo7e cell proliferation and does not induce Mo7e cell differentiation. Coincubation with both TNF-alpha and anti-TNF-alpha neutralizing antibody completely abolishes the TNF-alpha-induced proliferation of Mo7e cells. In bioassays, there is no detectable level of other stimulatory cytokines in conditioned medium from Mo7e cells previously stimulated by TNF-alpha, implying that the stimulatory effect of TNF-alpha on Mo7e cells is derived from the direct action of TNF-alpha rather than via the induction of secondary cytokines by TNF-alpha. Flow cytometric studies demonstrated that TNF-alpha binds to Mo7e cells that have been pretreated with either anti-TNF-RI or anti-TNF-RII neutralizing antibody, but TNF-alpha does not bind to cells pre-exposed to both receptor antibodies. However, the incubation of Mo7e cells with either TNF-RI or TNF-RII neutralizing antibodies or with either soluble TNF-RI or TNF-RII inhibits TNF-alpha-induced cell proliferation, indicating the requirement of interactions with both TNF receptors for the mitogenic activity of TNF-alpha. Furthermore, our data suggest that an alternative signaling pathway may be involved in TNF-alpha-induced Mo7e cell proliferation, because the common mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription (STAT) signaling pathways activated by other cytokines that induce Mo7e cell proliferation are not activated by TNF-alpha.

Cell Division↗
PubMed1998

Proliferative potential and apoptosis in rat glioma cell lines after hyperthermia.

The proliferative potential of cultured rat glioma cells (C6 and 9L) was evaluated after hyperthermia using immunohistochemical staining with bromodeoxyuridine (BrdU) and Ki-67 monoclonal antibodies. Apoptosis was assessed by in situ end-labeling of deoxyribonucleic acid breaks. Both BrdU and Ki-67 labeling indexes decreased with increasing hyperthermia time. The decrease of the Ki-67 labeling index was not as great as that of the BrdU labeling index. The number of apoptotic cells increased with time after hyperthermia. These results indicate that the antitumor effect of hyperthermia may reflect the induction of apoptosis in the cells within the cell cycle, and the resultant reduction of the proliferative potential of surviving cells, especially in the S phase.

Animals↗
PubMed1997

Intraparenchymal metastatic tumor with periventricular dissemination--case report.

A 50-year-old male presented with a rare intraparenchymal metastatic tumor spreading through the periventricular tissue. Magnetic resonance (MR) imaging demonstrated the tumor as a heterogeneous low-intensity area on T1-weighted images with enhancement by gadolinium-diethylenetriaminepenta-acetic acid, and as a heterogeneous high- or isointensity area on T2-weighted images. Histological examination of a biopsy sample showed adenocarcinoma. This MR imaging appearance is typical of malignant glioma. The differential diagnosis of tumor in the cerebral parenchyma with ventricular dissemination should include both primary and secondary intracranial malignant tumors. MR imaging is useful in the diagnosis of such tumors, but the final diagnosis should be based on either tissue biopsy or cytological examination of the cerebrospinal fluid.

Brain Neoplasms↗
PubMed1995

Potential involvement of a constitutive heat shock element binding factor in the regulation of chemical stress-induced hsp70 gene expression.

It was reported that chemical stresses such as arsenite, cadmium or salicylate fail to induce synthesis of the inducible form of HSP70 (HSP70i). We report here that exposure of cells to higher doses of these chemical treatments induced significant synthesis of HSP70i in CHO cells as well as other cell lines. The synthesis of HSP70i is primarily regulated at the transcriptional level. Although all tested chemical treatments induced heat shock factor (HSF) binding to the heat shock element (HSE), HSP70i synthesis appears to be regulated by an alternative factor (CHBF) which constitutively binds to the HSE at 37 degrees C. The treatments, which dissociate the HSE-CHBF complex, induced significant HSP70i synthesis. The treatments, which failed to induce HSP70i synthesis, still activated HSF binding to HSE but the HSE-CHBF complex remained as that of untreated control cells.

Animals↗
PubMed1994

Regulation of chemical stress-induced hsp70 gene expression in murine L929 cells.

We have investigated the regulation mechanism of chemical stress-induced hsp70 gene expression in murine L929 cells. Our data show that chemical treatments including sodium arsenite, cadmium chloride and sodium salicylate, induced significant synthesis of hsp70 and its mRNA. The induced hsp70 gene expression appears to be regulated at the transcriptional level. A factor (CHBF), which constitutively binds to the heat shock element (HSE) at 37 degrees C, functions like a negative regulator and the heat-induced heat shock factor (HSF) acts as an activator. The chemical treatments that induce significant hsp70 synthesis activate HSF binding to HSE but also dissociate the HSE-CHBF complex. Some chemical treatments, e.g. IPTG, which fail to activate hsp70 gene transcription, still activate HSF binding to HSE. However, in this case, the HSE-CHBF complex remained like that of untreated control cells.

Adaptation, Biological↗
PubMed1993

Dual control of heat shock response: involvement of a constitutive heat shock element-binding factor.

Heat shock factor (HSF) has been implicated as the key regulatory protein in the heat shock response. Our studies on the response of rodent cells to heat shock or sodium arsenite indicate that a high level of HSF-DNA-binding activity, by itself, is not sufficient for the induction of hsp70 mRNA synthesis; furthermore, a high level of HSF binding is also not necessary for this induction. Analysis of the binding of protein factors to the heat shock element (HSE) in extracts of stressed rodent cells indicates that the regulation of heat shock response involves the heat-inducible HSF and a constitutive HSE-binding factor. Our results also suggest that overexpression of human hsp70 may decrease the level of heat-induced HSF-HSE-binding activity in rat cells.

Animals↗
PubMed1993

Inhibition of formalin-induced responses of spinal dorsal horn neurons by stimulation of lateral reticular nucleus in rats.

The effects of stimulation of the lateral reticular nucleus (LRN) on responses of spinal dorsal horn neurons produced by formalin (5%, 50 microliters, sc) were investigated. In 12 out of 19 neurons tested, formalin induced 2 distinct phases of response. The first phase was initiated immediately after the injection of formalin and lasted for 3-8 min. The second phase started gradually 20-35 min after administration of formalin and lasted 30-65 min. Both phases of the response were inhibited by LRN stimulation.

Animals↗