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Biomedical subjects

H Peng

Publications and source records attributed to H Peng.

At least 19 recordsLinked to original sources
PubMed2006

Social, economic, and ecological impacts of the "Grain for Green" project in China: a preliminary case in Zhangye, Northwest China.

This paper provides applications of the integrated assessment (IA) approach in a case study in the Heihe River Basin of Northwest China. Some socio-economic and ecological impact results of forestry land use scenarios are presented in the paper. While seven types of land use scenarios for carbon sequestration purposes were considered for the IA applications, this paper mainly presents impacts of land use scenarios within the Grain for Green (GFG) category [see Yin et al., this volume]. China's national Grain for Green Project was implemented in order to protect and improve ecosystems, while allowing an evolution of agricultural management practices compatible with raising peasants' incomes. Zhangye Prefecture, located in the Heihe River Basin of an arid area in Northwest China, was chosen as the investigation site of the IA case study. Based on fundamental orientation theory, the social sustainability impacts of GFG land use options were assessed. Between 2002 and 2004, the GFG project brought US$23.56 million yuan in net income to the prefecture's peasants. Project implementation resulted in a 1.71 Gg increase in net primary productivity (NPP), as well as a 44.36 Gg rise in net ecosystem productivity (NEP). This suggested that, in Zhangye Prefecture, the Grain for Green Project could enhance the sustainability and stability of the local society, increase peasants' net income, as well as protect and remediate local ecosystems.

Agriculture↗
PubMed2006

Gender differences in long-term beneficial effects of erythropoietin given after neonatal stroke in postnatal day-7 rats.

Recently, we reported that erythropoietin attenuates neonatal brain injury caused by focal cerebral ischemia. The long-term effects of erythropoietin on focal cerebral ischemia-induced injury to the developing brain and the potential gender differences in these long-term effects have not been studied in detail. The current study demonstrated a similarity in the mean infarct volume in both the vehicle-treated male and female rats at 6 and 12 weeks after focal cerebral ischemia. On the other hand, erythropoietin treatment (1000 U/kg x three doses after focal cerebral ischemia) caused a significant reduction in the mean infarct volume in both males and females at 6 weeks after focal cerebral ischemia when compared with the corresponding vehicle-treated animals (males: 141.4+/-48.2 mm3 vs. 194.0+/-59.2 mm3, P<0.05; females: 85.4+/-31.6 mm3 vs. 183.4+/-46.3 mm3, P<0.05). Interestingly, the reduction in the mean infarct volume in the erythropoietin-treated males was significantly less than that in the erythropoietin-treated females at 6 weeks after focal cerebral ischemia (141.4+/-48.2 mm3 vs. 85.4+/-31.6 mm3, P<0.05). At 12 weeks after focal cerebral ischemia, the mean infarct volume in the erythropoietin-treated males significantly increased to 181.0+/-50.4 mm3 (P<0.05). In contrast, the mean infarct volume in the erythropoietin-treated females remained stable (87.0+/-41.7 mm3). Additionally, erythropoietin treatment significantly improved sensorimotor function recovery with a misstep number similar to the sham-operation group at 6 and 12 weeks after focal cerebral ischemia. Moreover, the mean number of missteps in the erythropoietin-treated females was less than that in males at 6 (13.5+/-2.0 vs. 24.5+/-2.5, P<0.05) and 12 (12.5+/-2.0 vs. 20.0+/-2.0, P<0.05) weeks after focal cerebral ischemia. These results indicate that erythropoietin administration after focal cerebral ischemia produces a significant long-term neuroprotective benefit on the developing brain, and that this effect is more beneficial in the female rats.

Animals↗
PubMed2006

E2F-HDAC complexes negatively regulate the tumor suppressor gene ARHI in breast cancer.

ARHI is a maternally imprinted tumor suppressor gene whose expression is markedly downregulated in breast cancer. Reactivation of ARHI expression in breast cancer cells is associated with increased histone H3 acetylation and decreased lysine 9 methylation of histone H3. An ARHI promoter segment that spanned bases -420 to +58 (designated the P2 region) exhibits significantly higher promoter activity in normal cells than in cancer cells. To better understand the molecular mechanisms contributing to this differential transcriptional activity, we sought to identify transcription factors that bind to the P2 region of the ARHI promoter and regulate its activity. Sequence analysis and oligonucleotide competition in electrophoretic mobility shift assays identified an A2 fragment containing an E2F-binding site. Using specific antibodies in supershift assays, we have shown that anti-E2F1 and 4 antibodies can supershift the A2-protein complexes, whereas anti-E2F2 and 6 antibodies cannot, demonstrating that the A2 fragment interacts with specific members of the E2F family proteins. When compared with normal breast epithelial cells, breast cancer cells have significantly elevated expression of E2F1, 4 and increased E2F DNA-binding activity. Moreover, chromatin immunoprecipitation experiments revealed that both E2F1 and 4 bind to the ARHI promoter in breast cancer cells in vivo. This binding was reduced when the cells were treated with the histone deacetylase (HDAC) inhibitor--trichostatin A (TSA). When SKBr3 cells were cotransfected with an ARHI/luciferase reporter and E2F-expression vectors, E2F1 and 4 reduced ARHI promoter activity 2-3-fold, and this reduction could be reversed by TSA treatment. The negative regulation by E2F-HDAC complexes could also be reduced by small interfering RNA of E2F1 and 4. While the retinoblastoma protein, pRB, alone had no effect on ARHI promoter activity, repression by E2F1, but not E2F4, was enhanced by the coexpression of pRB. Taken together, our results suggest that E2F1, 4 and their complexes with HDAC play an important role in downregulating the expression of the tumor suppressor gene ARHI in breast cancer cells.

Acetylation↗
PubMed2006

Identification and characterization of a novel zinc finger protein (HZF1) gene and its function in erythroid and megakaryocytic differentiation of K562 cells.

A novel zinc finger protein (HZF1) gene was identified and characterized by screening a human bone marrow cDNA library, using a new expression sequence tag probe that contains sequences encoding zinc finger motifs. There are at least three transcripts that may result from different splicing of the pre-mRNA, but the differences among them are only involved in 5' non-translation region of HZF1 mRNA. HZF1 gene contains four exons and three introns. The putative protein consists of 670 amino-acid residues including 15 typical C2H2 and 2 C2RH zinc finger motifs. This structure characterization of HZF1 and the nuclear location of the protein suggest that HZF1 may function as a transcription factor. HZF1 mRNA expression was detected in ubiquitous tissues and various hematopoietic cell lines. Increased HZF1 mRNA expression was observed following erythroid differentiation of K562 cells induced by hemin or megakaryocytic differentiation of K562 cells induced by phorbol myristate acetate (PMA). Both of the antisense method and RNA interference assay revealed that repression of the intrinsic expression of HZF1 blocked the hemin-induced erythroid differentiation and reduced the PMA-induced megakaryocytic differentiation of K562 cells, which suggested that HZF1 play important roles in erythroid and megakaryocytic differentiation.

Amino Acid Sequence↗
PubMed2006

Antimicrobial resistance in bacteria isolated from aquaculture sources in Australia.

AIMS: To carry out a preliminary assessment of the occurrence of resistance to antimicrobials in bacteria that has been isolated from a variety of aquaculture species and environments in Australia. METHOD AND RESULTS: A total of 100 Gram-negative (Vibrio spp. and Aeromonas spp. predominantly) and four Gram-positive bacteria isolated from farmed fish, crustaceans and water from crab larval rearing tanks were obtained from diagnostic laboratories from different parts of Australia. All the isolates were tested for sensitivity to 19 antibiotics and Minimal Inhibitory Concentrations were determined by the agar dilution method. Plasmid DNA was isolated by the alkali lysis method. Resistance to ampicillin, amoxycillin, cephalexin and erythromycin was widespread; resistance to oxytetracycline, tetracycline, nalidixic acid and sulfonamides was common but resistance to chloramphenicol, florfenicol, ceftiofur, cephalothin, cefoperazone, oxolinic acid, gentamicin, kanamycin and trimethoprim was less common. All strains were susceptible to ciprofloxacin. Multiple resistance was also observed and 74.4% of resistant isolates had between one and ten plasmids with sizes ranging 2-51 kbp. CONCLUSIONS: No antibiotics are registered for use in aquaculture in Australia but these results suggest that there has been significant off-label use. SIGNIFICANCE AND IMPACT OF STUDY: Transfer of antibiotic resistant bacteria to humans via the food chain is a significant health concern. In comparison with studies on terrestrial food producing animals, there are fewer studies on antibiotic resistance in bacteria from aquaculture enterprises and this study provides further support to the view that there is the risk of transfer of resistant bacteria to humans from consumption of aquaculture products. From the Australian perspective, although there are no products registered for use in aquaculture, antimicrobial resistance is present in isolates from aquaculture and aquaculture environments.

Animals↗
PubMed2005

[Ex-vivo gene therapy with BMP-4 for critically sized defects and enhancement of fracture healing in an osteoporotic animal model].

Fractures in osteoporotic bones or segment defects are problematic bone lesions with a reduced biological capability of regeneration. We tested the hypothesis that cell-mediated ex vivo gene therapy to deliver BMP4 can heal critically sized defects and improve bone healing in osteoporotic rats. Primary muscle-derived cells were isolated from the hindlimb muscle of rats and retrovirally transduced to express bone morphogenic protein 4 (BMP4). The bone formation was evaluated following local application of these cells in critically sized defects and in fractures of osteoporotic bones. Radiographic analysis revealed bridging callus formation in a critically sized defect in all specimens using muscle-derived cells expressing BMP4 at 12 weeks. These findings were confirmed by histological evaluation, which revealed callus bone formation with good integration to the distal and proximal bone. Following treatment with muscle-derived cells expressing BMP4, the bone healing process in the osteoporotic bone was improved to the level similar to that of normal bone. The ex vivo gene therapy could be a promising tool for the treatment of osteoporotic fractures and critically sized defects. The reduced number of complications (nonunions, loss of reduction, and fragment dislocation), shortening of hospitalization period, and improvement of bone strength are decisive advocates for this treatment option.

Animals↗
PubMed2005

Non-specific tolerance induced by staphylococcal enterotoxin B in treating high risk corneal transplantation in rats.

AIMS: To explore the role of staphylococcal enterotoxin B (SEB) in treating high risk corneal keratoplasty in rats. METHODS: Rat corneal high risk transplantation rejection models were set up using Fisher 344 and Lewis rats. The experimental rats were injected intraperitoneally with 0.2 ml SEB at different concentrations before keratoplasty. The rejection indexes of the allograft were recorded and the lymphocyte infiltration in the allograft and the percentage of the lymphocyte subpopulation in the lymphatic organs were also examined. Lymphocyte proliferation ability and the concentration of IL-2 and IL-10 in the serum were also evaluated. RESULTS: Compared with the control group, SEB prolonged the survival time of the allograft significantly from 7 to 12 days. It could also reduce CD4(+) and CD8(+) lymphocyte infiltration in the allograft and minimise the percentage of CD4(+) and CD8(+) lymphocytes in the lymphatic organs. The lymphocyte proliferation ability was also weakened. However, the percentage of CD4(+) NK T lymphocytes in the lymphatic organs was raised. The serum concentration of IL-10 was higher but IL-2 was lower in the SEB treated groups. CONCLUSIONS: SEB prolonged the survival time of the allograft in high risk rat corneal allo-transplantation, which may be caused by T cell deletion and acquisition of non-specific tolerance.

Animals↗
PubMed2005

The role of TNF related apoptosis-inducing ligand in neurodegenerative diseases.

A hallmark of all forms of neurodegenerative diseases is impairment of neuronal functions, and in many cases neuronal cell death. Although the etiology of neurodegenerative diseases may be distinct, different diseases display a similar pathogenesis, for example abnormal immunity within the central nervous system (CNS), activation of macrophage/microglia and the involvement of proinflammatory cytokines. Recent studies show that neurons in a neurodegenerative state undergo a highly regulated programmed cell death, also called apoptosis. TNF-related apoptosis-inducing ligand (TRAIL), a member of the TNF family, has been shown to be involved in apoptosis during many diseases. As one member of a death ligand family, TRAIL was originally thought to target only tumor cells and was not present in CNS. However, recent data showed that TRAIL was unregulated in HIV-1-infected and immune-activated macrophages, a major disease inducing cell during HIV-1-associated dementia (HAD). TRAIL is also induced on neuron by beta-amyloid protein, an important pathogen for Alzheimer's disease. In this review, we summarize the possible common aspects that TRAIL involved those neurodegenerative diseases, TRAIL induced apoptosis signaling in the CNS cells, and specific role of TRAIL in individual diseases.

AIDS Dementia Complex↗
PubMed2004

SEB combined with IL-1ra could prolong the survival of the rat allografts in high-risk corneal transplantation.

PURPOSE: To determine whether the superantigen Staphylococcal enterotoxin B (SEB) combined with interleukin-1 receptor antagonist (IL-1ra) prolong allograft survival better than individual agents in high-risk corneal transplantation in a rat model. METHODS: Fisher 344 donor corneas were transplanted into Lewis recipients. High-risk transplantation meant that the transplants were sutured into the recipient beds with corneal neovascularization induced by placing three interrupted sutures in the host cornea. All of the recipients were divided in blinded fashion into four groups. Group I was injected with saline buffer. Group II was injected intraperitoneally with 0.2 mL SEB (75 microg/kg) at 4-day intervals on three occasions before transplantation. Group III was injected with 0.1 mL IL-1ra (1 mg/mL) subconjunctivally from the first day after transplantation for 2 weeks. Group IV received both SEB and IL-1ra. All transplants were evaluated for signs of rejection for 4 weeks after surgery. Ten days after transplantation, two recipients in each group were sacrificed for histopathological and immunological evaluation. RESULTS: The mean survival time of the allografts in the control group was 5.89 +/- 0.79 days; in SEB group, 10.70 +/- 2.52 days; in IL-1ra group, 8.25 +/- 0.71 days; in the SEB and IL-1ra group, 17.36 +/- 2.39 days. CD4+ and CD8+ lymphocyte infiltration into the allografts and the percentage of the lymphocytes in the spleen and mandibular lymphatic nodes was significantly decreased among the treated groups with dampened lymphocyte reactivity. The SEB plus IL-1ra combination group showed the strongest inhibition. CONCLUSION: SEB and IL-1ra are most effective in combination to treat high-risk corneal transplants.

Animals↗
PubMed2004

Efficient inhibition of multidrug-resistant human tumors with a recombinant bispecific anti-P-glycoprotein x anti-CD3 diabody.

Overexpressing of P-glycoprotein (Pgp) has been shown to be responsible for cancer resistance to multiple chemotherapeutic agents. Immunotherapy with biological agents, such as bispecific antibodies (BsAbs), may represent a promising approach to overcome the emergence of drug resistance. Here we constructed a recombinant BsAb, a diabody, with specificities to both CD3 on human T-lymphocyte and Pgp on cancer cells. The diabody was produced in Escherichia coli in a soluble functional form and purified by an affinity chromatography with a yield of >4 mg/l culture medium in shaker flask. The diabody binds to both CD3 on T-lymphocytes and Pgp on multidrug-resistant (MDR) tumor cells with affinities that are comparable to its respective parental single chain Fv molecules. In the presence of activated human peripheral blood lymphocytes (PBLs), the diabody mediates effectively the lysis of the Pgp-overexpressing human leukemia K562/A02 and epidermoid carcinoma KBv(200) cells, but is much less potent in mediating the lysis of the parent K562 and KB cells. Further, the diabody localized selectively within the K562/A02 xenografts in mice. When combined with activated PBL, the diabody significantly inhibited the growth of K562/A02 and KBv(200), but had no effect on K562 and KB xenografts. In contrast, treatment with doxorubicin, a standard chemotherapeutic agent, only inhibited the growth of K562 and KB, but had no effect on K562/A02 and KBv(200) xenografts. Taken together, our results suggest that the anti-Pgp x anti-CD3 diabody may have a great potential in the treatment of various MDR cancers.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2004

Cloning and identification of Rab cDNAs from Limulus polyphemus.

Small GTPases of the Rab family are essential for the control of membrane transport between intracellular compartments. Trafficking of the sodium-dependent facilitative insulin responsive glucose transporter (GLUT 4) has been shown to be associated with the intracellular redistribution of Rabs 4, 5 and 11 in adipose and muscle tissues. As a prelude to studies of the endosomal trafficking of the choline cotransporter (ChCoT), we describe herein our initial efforts to identify Rab proteins in Limulus polyphemus central nervous system (CNS) tissue. The studies were initiated after results from Microarray analysis of Limulus RNA hybridized to mouse gene chips suggested the presence of RNA transcripts for Rab 7 protein. Subsequently, more than 30 sequences for different Rab proteins were aligned and several consensus segments were selected for degenerate primer design to produce Rabs 2, 4, 7, 9 and 11. The expected PCR fragment sizes were obtained using RT-PCR and subcloned into pCR II TOPO vector and transferred into E. coli Top 10. The nucleotide sequences indicated that the recombinants encoded partial amino acid sequences for Rabs 1a, 1b, 1c, 2, 2a, 2b, 3a, 4, 5a, 7a, 7b, 11a, 11b, 14, 33b1 and 33b2. Northern blot analyses showed that the molecular sizes of Limulus Rabs 3a, 4, 7, 11a and 11b ranged from approximately 1.94.6 Kb. These Rab proteins, particularly Rabs 4, 7 and 11, will be studied further to determine their possible roles in the trafficking of the Limulus ChCoT

Amino Acid Sequence↗
PubMed2003

The chemorepellent semaphorin is expressed in the horseshoe crab, Limulus polyphemus.

Semaphorins are a family of soluble and membrane-bound proteins that play a critical role in axonal guidance and other processes of neuronal development. Currently, more than twenty semaphorins have been identified, all of which share a conserved 500 amino acid domain near the amino terminus. Semaphorins are divided into eight classes according to species of origin and structural similarities. Classes 1 and 2 are found in invertebrates, classes 3 through 7 are present in vertebrates and viruses encode class V semaphorin. Microarray analysis of Limulus CNS RNA revealed the presence of a semaphorin-like gene in Limulus polyphemus. Based on these data, we aligned 31 different sequences and designed degenerate primers for the consensus domains (WTT/SFLKA) and (DPY/VCA/GW). RT-PCR products were generated using 6 forward primers and 4 reverse primers. The expected size PCR products (750 bp) was obtained and then ligated with pCR II TOPO vector and transferred into E. coli Top 10. Five partial semaphorin cDNAs were found in Limulus: semaphorins 1a, 1b, 2a, 2b and F (now known as 5) were partially cloned. Subsequent Northern blot analyses using these Limulus specific-probes revealed hybridization with total RNAs purified from six different tissues.

Animals↗
PubMed2002

Ex vivo gene therapy with stromal cells transduced with a retroviral vector containing the BMP4 gene completely heals critical size calvarial defect in rats.

In order to develop a successful gene therapy system for the healing of bone defects, we developed a murine leukemia virus (MLV)-based retroviral system expressing the human bone morphogenetic protein (BMP) 4 transgene with high transduction efficiency. The bone formation potential of BMP4 transduced cells was tested by embedding 2.5 x 10(6) transduced stromal cells in a gelatin matrix that was then placed in a critical size defect in calvariae of syngenic rats. Gelatin matrix without cells or with untransduced stromal cells were the two control groups. The defect area was completely filled with new bone in experimental rats after 4 weeks, while limited bone formation occurred in either control group. Bone mineral density (BMD) of the defect in the gene therapy group was 67.8 +/- 5.7 mg/cm(2) (mean +/- s.d., n = 4), which was 119 +/- 10% of the control BMD of bone surrounding the defect (57.2 +/- 1.5 mg/cm(2)). In contrast, BMD of rats implanted with untransduced stromal cells was five-fold lower (13.8 +/- 7.4 mg/cm(2), P < 0.001). Time course studies revealed that there was a linear increase in BMD between 2-4 weeks after inoculation of the critical size defect with 2.5 x 10(6) implanted BMP4 cells. In conclusion, the retroviral-based BMP4 gene therapy system that we have developed has the potential for regeneration of large skeletal defects.

Animals↗
PubMed2002

Fractalkine (CX3CL1) and brain inflammation: Implications for HIV-1-associated dementia.

Leukocyte migration and activation play an important role in immune surveillance and the pathogenesis of a variety of neurodegenerative disorders, including human immunodeficiency virus (HIV)-1-associated dementia (HAD). A novel chemokine named fractalkine (FKN, CX3CL1), which exists in both membrane-anchored and soluble isoforms, has been proposed to participate in the generation and progression of inflammatory brain disorders. Upon binding to the CX3C receptor one (CX3CR1), FKN induces adhesion, chemoattraction, and activation of leukocytes, including brain macrophages and microglia (MP). Constitutively expressed in the central nervous system (CNS), mainly by neurons, FKN is up-regulated and released in response to proinflammatory stimuli. Importantly, FKN is up-regulated in the brain tissue and cerebrospinal fluid (CSF) of HAD patients. Together, these observations suggest that FKN and its receptor have a unique role in regulating the neuroinflammatory events underlying disease. This review will examine how FKN contributes to the recruitment and activation of CX3CR1-expressing MP, which are critical events in the neuropathogenesis of HAD.

AIDS Dementia Complex↗
PubMed2002

Chromosome location and characterization of the human nicotinic acetylcholine receptor subunit alpha (alpha) 9 (CHRNA9) gene.

The human nicotinic acetylcholine receptor (nAChR) subunit alpha9 gene (CHRNA9) codes for a component of the AChR in hair cells of the inner ear. While no direct evidence presently links this gene to known hearing disorders, it may underlie individual susceptibility to acoustic inner ear injury, and is associated with the autoimmune skin disorder Pemphigus vulgaris. Future studies will depend upon a thorough characterization of the nAChR alpha9 gene. CHRNA9 was localized to chromosome 4p15.1-->p14 by FISH analysis. Radiation hybrid mapping further localized the gene between markers D4S405 and D4S496 (Stanford G3 panel), and between markers WI-3875 and D4S1231 (Genebridge 4 panel), representing a distance of approximately 3.1 cR. The D4S405 marker has been linked to a non-syndromic form of hereditary hearing loss, DFNB-25. The gene contains five exons, separated by four introns. Exons 1-5 are 78, 145, 154, 532 and 877 bases, respectively. Introns 1-4 are 294, 1239, 11517, and 4571 bases, respectively. The intron-exon splice junction sites correlate identically with those of the rat alpha9 gene and are nearly identical to those of the human alpha10 gene. Sequence promoter analysis reveals a number of potential regulatory elements, including several in common with the nAChR alpha10 gene, whose expressed protein is assumed to combine with alpha9 in the inner ear.

Amino Acid Sequence↗
PubMed2001

DOC-2/hDab-2 inhibits ILK activity and induces anoikis in breast cancer cells through an Akt-independent pathway.

DOC-2/hDab-2 was identified due to the loss of its expression in primary ovarian cancer cells. It is believed that loss of DOC-2/hDab-2 expression is one of the early events of ovarian malignancy. These results suggest a function of DOC-2/hDab-2 as a tumor suppressor. However, it is not clear how DOC-2/hDab-2 negatively regulates cancer cell growth. In this report, we demonstrate that DOC-2/hDab-2 expression in breast cancer cells resulted in sensitivity to suspension-induced cell death (anoikis). This event was associated with the down-regulation of the integrin-linked kinase (ILK) activity. Since ILK is a key factor in regulating the cellular signaling in responding to the extracellular signals through adhesion molecules like integrins, our results indicate that DOC-2/hDab-2 may prevent tumor growth and invasion by modulating the anti-apoptotic ILK pathway.

Adaptor Proteins, Signal Transducing↗