Biomedical subjects

Li Luo

Publications and source records attributed to Li Luo.

At least 19 recordsLinked to original sources

PubMed2026

TNFα-induced endothelial extracellular vesicles regulate astrocyte function: an integrated transcriptomic and proteomic study.

Endothelial cells and astrocytes are critical structural and functional components of the blood-brain barrier. In many neuroinflammatory diseases, endothelial cells are among the first to respond to inflammatory stimuli and release extracellular vesicles (EVs). However, whether inflammatory stimulation alters EV RNA cargo and subsequently regulates astrocyte function remains unclear. In this study, we performed integrated RNA sequencing and proteomic analyses to investigate the effects of TNFα-stimulated endothelial EVs on astrocytes. RNA profiling revealed significant alterations in EV cargo after TNFα stimulation, including 867 upregulated and 577 downregulated mRNAs, 317 upregulated and 15 downregulated lncRNAs, and 88 upregulated and 62 downregulated miRNAs. The results of functional enrichment analysis suggested that altered EV RNAs may primarily promote inflammatory responses, cell migration, and RNA splicing in astrocytes while reducing their regulatory effects on neuronal projection and calcium homeostasis. Further integrative analysis of EV RNAs and astrocytic proteomics revealed key overlapping targets, including upregulated expression of ICAM1, SOD2, TFPI2, and TNFAIP8, whereas NFKBIA expression was consistently decreased. Network analysis revealed NF-κB as the central regulatory node. Reduced levels of EV-derived NFKBIA mRNA were associated with decreased IκBα protein levels in astrocytes, which promoted NF-κB activation and inflammatory cytokine release. Finally, overexpression of IκBα in astrocytes significantly attenuated TNFα EV-induced IL-1β and IL-6 secretion. Collectively, these findings demonstrate that TNFα-stimulated endothelial EVs coordinately regulate astrocyte function through mRNA, lncRNA, and miRNA cargo and that the IκBα/NF-κB axis may be a key mechanism underlying endothelial EV-mediated inflammatory disruption of the blood-brain barrier.

Astrocytes↗

PubMed2026

Drug targets for lipid modification and risk of type 2 diabetes: a cis-Mendelian randomization study.

BACKGROUND AND AIMS: Reducing plasma levels of low-density lipoprotein cholesterol (LDL-C) is the cornerstone in the prevention of coronary artery disease (CAD) but may also increase risk of type 2 diabetes (T2D). A comprehensive examination of the genetic evidence of T2D related side-effects of all current lipid-modifying drugs, including those in development, has not yet been performed. METHODS: This cis-Mendelian randomization study used individual level data from the UK Biobank, Lifelines, and publicly available genome-wide association data. We identified loci that are either targeted directly with drugs, or alternatively, targeting their gene products (mRNA and/or protein). Included are, in alphabetical order, the loci ACLY, ANGPTL3, ANGPTL4, APOB, APOC3, CETP, HMGCR, LDLR, LIPG, LPA, MTTP, NPC1L1, and PCSK9. We used cis-genetic instruments weighted for LDL-C, HDL-C, triglycerides, and apolipoproteins as downstream proxies for the drug targets. Main outcomes were prevalent and incident T2D, with CAD as a contrast outcome. RESULTS: Lipid modification through HMGCR is predicted to reduce CAD risk and increase T2D risk. Modification through targeting APOC3, LDLR, LPA, MTTP, NPC1L1, and PCSK9 is predicted to reduce CAD risk without a change in T2D risk. Modification through ANGPTL4 and CETP is predicted to reduce risk of both CAD and T2D. For ACLY, ANGPTL3, APOB, and LIPG, we found evidence for neither CAD nor T2D. CONCLUSIONS: This study provides genetic evidence for variation in diabetes-related side-effects of different lipid-modifying drugs, with potential relevance for future clinical trials and individual treatment decisions.

Humans↗

PubMed2025

Extracellular vesicle proteomic expression is influenced by mining tenure in former uranium miners.

BACKGROUND: Chronic exposure to uranium (U) rich environments poses significant health risks, yet the molecular mechanisms underlying these effects remain poorly understood. Extracellular vesicles (EVs) are membrane-bound vesicles that transfer multiple biomolecules between cells and can regulate cellular function. OBJECTIVE: To determine whether U-mining tenure is associated with specific alterations in serum-derived EV proteomic and plasma cytokine profiles among former U-miners, and to assess the potential of EV-derived proteins as robust biomarkers of chronic U-exposure relative to canonical cytokines. METHODS: Serum and plasma samples were obtained from 39 former U-miners. Small and large EVs were isolated via differential ultracentrifugation and characterized by nanoparticle tracking and western blotting. EV proteomic profiles were analyzed using liquid chromatography-tandem mass spectrometry. Plasma cytokines were quantified using multiplex immunoassays. Age-adjusted linear regression was used to assess associations with mining tenure, and pathway enrichment analysis was performed on significant EV proteins. RESULTS: Eight small-EV and four large-EV proteins significantly correlated with mining tenure after age adjustment. Notably, Complement C1r subcomponent and Vitamin K-dependent protein S, and Fibrinogen alpha chain exhibited strong inverse correlations. Enrichment analyses highlighted immune-related and extracellular matrix pathways. Six cytokines were initially associated with mining tenure but lost significance after age adjustment. In contrast, EV protein associations appeared more robust for this confounding, underscoring their potential as exposure biomarkers. CONCLUSIONS: Serum EV-derived protein signatures were nominally associated with U-mining tenure independent of age, whereas cytokine profiles were confounded by age. These findings suggest that EV-derived proteins may provide sensitive biomarkers for monitoring long-term health effects of U-exposure, which warrants further investigation in larger cohorts.

Humans↗

PubMed2016

Variants in autophagy-related genes and clinical characteristics in melanoma: a population-based study.

Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy-related (ATG) genes have been investigated in relation to melanoma progression. We examined five single-nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population-based case-control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27-0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11-1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12-3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05-0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21-0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34-0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression.

Adult↗

PubMed2006

Sonic hedgehog protein promotes bone marrow-derived endothelial progenitor cell proliferation, migration and VEGF production via PI 3-kinase/Akt signaling pathways.

AIM: To investigate the effects of Sonic hedgehog (shh) protein on bone marrow- derived endothelial progenitor cells (BM-EPC) proliferation, migration and vascular endothelial growth factor (VEGF) production, and the potential signaling pathways involved in these effects. METHODS: Bone marrow-derived Flk-1(+) cells were enriched using the MACS system from adult Kunming mice and then BM-EPC was cultured in gelatin-coated culture dishes. The effects of shh N-terminal peptide on BM-EPC proliferation were evaluated using the MTT colorimetric assay. Cell migration was assayed using a modified Boyden chamber technique. The production of VEGF was determined by ELISA and immunofluorescence analysis. The potential involvement of PKC and PI3K signaling pathways was explored using selective inhibitor or Western blot. RESULTS: The proliferation, migration and VEGF production in BM-EPC could be promoted by endogenous shh N-terminal peptide at concentrations of 0.1 microg/mL to 10 microg/mL, and could be inhibited by anti-shh antibodies. Shh-mediated proliferation and migration in BM-EPC could be partly attenuated by anti-VEGF. Phospho-PI3-kinase expression in newly separated BM-EPC was low, and it increased significantly when exogenous shh N-terminal peptide was added, but could be attenuated by anti-human/mouse shh N-terminal peptide antibody. Moreover, the inhibitor of the PI3-kinase, but not the inhibitor of the PKC, significantly inhibited the shh-mediated proliferation, migration and VEGF production. CONCLUSION: Shh protein can stimulate bone marrow-derived BM-EPC proliferation, migration and VEGF production, which may promote neovascularization to ischemic tissues. This results also suggests that the PI3-kinase/Akt signaling pathways are involved in the angiogenic effects of shh.

Animals↗

PubMed2006

[Study on manpower allocation criteria of center of disease prevention and control in the context of province level, city level and county level].

OBJECTIVE: To set the manpower allocation criteria of center of disease prevention and control. METHODS: Expected allocation manpower criteria was obtained through adjusting the current manpower allocation of disease prevention and control centers. The principle was to fulfill public function and promote professional efficiency. RESULTS: Based on function requirement, in 3 - 5 years, the manpower allocation criteria of center of disease prevention and control at provincial-level is 336 persons, at city-level is 102 persons, and at county-level is 33 persons, that means in whole country 140016 persons should be needed. In 10 years, the manpower allocation criteria of center of disease prevention and control at provincial-level is 386 persons, at city-level is 112 persons, and at county-level is 38 persons, that means in whole country 159086 persons should be needed. CONCLUSION: The manpower allocation criteria advanced in the study indicated that current manpower quantity should be greatly reduced. It is an inevitable trend that disease prevention and control centers reduce the staff quantity and promote their quality.

China↗

PubMed2006

[A LuxR family regulator, ExpR regulates the expression of motC operon from Sinorhizobium meliloti].

In Sinorhizobium meliloti strain Rm1021, ExpR+ mutation results in the overproduction of EPS II, which is required for efficient invasion of root nodules on the host plant alfalfa. When rhizobia were grown in LB/MC medium for 36-hour then placed at room temperature, most of ExpR+ mutant (Rm8530) cells aggregated at the bottom of the tubes, but ExpR+ sinR double mutant Rm11528 and wild type Rm1021 did not. The ExpR+ mutant was also found to swim slower than Rm1021 on swarming plates, but the ExpR+ sinR- mutant showed almost the same as wild type. The average diameter of swarming plaques for Rm8530, Rm11528 and Rm1021 was 13, 16 and 16 mm respectively, when bacteria were incubated at 28 degrees C for two days. After four days, the plaques enlarged to 17, 22 and 20 mm, respectively. These results indicate that ExpR+ mutation causes a serious defection of motility in this condition. By flagella staining with silver nitrate method, it was noted that all three strains had flagella. It suggests that the swimming behavior of Rm8530 may not result from the change in components and structures of flagella. Based on DNA microarray data, Hoang speculated that the Sin system seemed to regulate a multitude of genes in S. meliloti, including genes that participate in succinoglycan production, motility, and chemotaxis, as well as other cellular processes (Hoang et al. 2004). And most of the regulation by the Sin system was dependent on the presence of the ExpR regulator. Accordingly, the expression of the flaA, cheY1 and motC operon was determined using promoter: lacZ fusion in different genetic backgrounds. The results showed two fold lower of motC expression activity in ExpR+ mutant strain Rm8530 than in wild-type strain Rm1021 at early exponential phase and this decrease was hold back by further mutation of sinR. However, the beta-galactosidase activity of motC-lacZ fusion was almost the same in three strains at later exponential phase. These results suggest that ExpR may repress the expression of motC operon in a low cell density, but this repression can be deprived in a higher cell density. It may be a good explanation to the motility of Rm8530 on swarming plates, since it is lower cell density of bacteria on the swarming plates. Therefore, it may be concluded that ExpR both involved in the regulation of EPS II production and motility in S. meliloti.

Bacterial Proteins↗

PubMed2006

[Effect of resveratrol on the cognitive ability of Alzheimeros mice].

OBJECTIVE: To explore the effect of resveratrol on the cognition of Alzheimer's mice (AD) and its mechanism, and to assess its action on the reproduction system. METHODS: According to the results of step-down test, 84 Kunming female mice were randomly divided into 6 groups: Group A [sham operated+1% CMC-Na (0.01 mL/g)], Group B [ovariectomy+D-galactose+1% CMC-Na (0.01 mL/g)], Group C [ovariectomy+D-galactose+0.05 mg/(kg.d) Diethylstilbestrol], Group D [ovariectomy+D-galactose+15 mg/(kg.d) Res], and Group E [ovariectomy+D-galactose injected+45 mg/(kg.d) Res], and Group F [ovariectomy+D-galactose +135 mg/(kg.d) Res]. Experimental cycle was 60 days. RESULTS: Resveratrol of every dosage could improve the performance records of behavior tests in AD mice,could inhibit the SOD vitality and the MDA level both in the serum and in the brain, and could suppress the acetylcholinesterase vitality and the bax expression. Resveratrol has no endometrial hyperplasia effect. CONCLUSION: Resveratrol can improve the cognitive ability of AD mice, which may contribute to the resveratrol's antioxidation and antiapoptosis, and can modulate acetylcholinesterase. Resveratrol has no side-effect of endometrial hyperplasia on AD mice.

Alzheimer Disease↗

PubMed2005

Expansive effects of aorta-gonad-mesonephros-derived stromal cells on hematopoietic stem cells from embryonic stem cells.

BACKGROUND: Hematopoietic stem cells (HSCs) give rise to all blood and immune cells and are used in clinical transplantation protocols to treat a wide variety of refractory diseases, but the amplification of HSCs has been difficult to achieve in vitro. In the present study, the expansive effects of aorta-gonad-mesonephros (AGM) region derived stromal cells on HSCs were explored, attempting to improve the efficiency of HSC transplantation in clinical practice. METHODS: The murine stromal cells were isolated from the AGM region of 12 days postcoitum (dpc) murine embryos and bone marrow (BM) of 6 weeks old mice, respectively. After identification with flow cytometry and immunocytochemistry, the stromal cells were co-cultured with ESCs-derived, cytokines-induced HSCs. The maintenance and expansion of ESCs-derived HSCs were evaluated by detecting the population of CD34+ and CD34+Sca-1+ cells with flow cytometry and the blast colony-forming cells (BL-CFCs), high proliferative potential colony-forming cells (HPP-CFCs) by using semi-solid medium colonial culture. Finally, the homing and hematopoietic reconstruction abilities of HSCs were evaluated using a murine model of HSC transplantation in vivo. RESULTS: AGM and BM-derived stromal cells were morphologically and phenotypically similar, and had the features of stromal cells. When co-cultured with AGM or BM stromal cells, more primitive progenitor cells (HPP-CFCs) could be detected in ESCs derived hematopoietic precursor cells, but BL-CFC's expansion could be detected only when co-cultured with AGM-derived stromal cells. The population of CD34+ hematopoietic stem/progenitor cells were expanded 3 times, but no significant expansion in the population of CD34+Sca-1+ cells was noted when co-cultured with BM stromal cells. While both CD34+ hematopoietic stem/progenitor cells and CD34+Sca-1+ cells were expanded 4 to 5 times respectively when co-cultured with AGM stromal cells. AGM region-derived stromal cells, like BM-derived stromal cells, could promote hematopoietic reconstruction and HSCs' homing to BM in vivo. CONCLUSIONS: AGM-derived stromal cells in comparison with the BM-derived stromal cells could not only support the expansion of HSCs but also maintain the self-renewal and multi-lineage differentiation more effectively. They are promising in HSC transplantation.

Animals↗

PubMed2005

The effect of glow discharge plasma surface modification of polymers on the osteogenic differentiation of committed human mesenchymal stem cells.

Little is known of the effect of material surfaces on stem cell differentiation. The present study has addressed the hypothesis that the interaction of mesenchymal stem cells (MSCs) with material surfaces modified by glow discharge plasma is a major regulator of osteogenic differentiation. We found that biaxially oriented polypropylene (BOPP) plasma treated in ammonia significantly reduced up-regulation of expression of osteogenic marker genes, such as alkaline phosphatase (ALP), bone sialoprotein (BSP) and osteocalcin (OC). In contrast, ALP expression was up-regulated when cultured on treated Nylon-6 polyamide (Ny-t) but was substantially reduced when cultured on its pristine counterpart (Ny-p) on day 3. On day 7, ALP expression was down-regulated with MSCs cultured on Ny-t although its expression level was up again on day 14. BSP was expressed weakly on day 3, but was up-regulated when cultured on Ny-t and Ny-p. Its expression reached its maximum on day 14 when cultured on a polystyrene control, while it was cyclically up-regulated on Ny-t. Similarly, there was a slight increase in OC expression when MSCs were cultured on Ny-t and Ny-p on day 3, when compared to control. Thus, the nature of the surface can directly influence MSCs differentiation, ultimately affecting the quality of new tissue formation with BOPP-t suppressing osteogenic differentiation.

Aged↗

PubMed2005

Selective inhibition of type X collagen expression in human mesenchymal stem cell differentiation on polymer substrates surface-modified by glow discharge plasma.

Recent evidence indicates that a major drawback of current cartilage- and disc-tissue engineering is that human mesenchymal stem cells (MSCs) rapidly express type X collagen-a marker of chondrocyte hypertrophy associated with endochondral ossification. Some studies have attempted to use growth factors to inhibit type X collagen expression, but none to date has addressed the possible effect of the substratum on chondrocyte hypertrophy. Here, we sought to examine the growth and differentiation potential of human MSCs cultured on two polymer types, polypropylene and nylon-6, both of which have been surface-modified by glow discharge plasma treatment in ammonia gas. Cultures were performed for up to 14 days in Dulbecco's modified Eagle medium + 10% fetal bovine serum. Commercial polystyrene culture dishes were used as control. Reverse transcriptase-polymerase chain reaction was used to assess the expression of types I, II, and X collagens and aggrecan using gene-specific primers. Glyceraldehyde-3-phosphate dehydrogenase was used as a housekeeping gene. Types I and X collagens, as well as aggrecan, were found to be constitutively expressed by human MSCs on polystyrene culture dishes. Whereas both untreated and treated nylon-6 partially inhibited type X collagen expression, treated polypropylene almost completely inhibited its expression. These results indicate that plasma-treated polypropylene or nylon-6 may be a suitable surface for inducing MSCs to a disc-like phenotype for tissue engineering of intervertebral discs in which hypertrophy is suppressed.

Aged↗

PubMed2005

Effect of cobalt and chromium ions on MMP-1, TIMP-1, and TNF-alpha gene expression in human U937 macrophages: a role for tyrosine kinases.

Previous reports have suggested that the imbalance of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) activity may contribute to prosthetic loosening. However, the mechanisms controlling these enzymes in the periprosthetic environment is unknown. We examined the effect of Co2+ and Cr3+ ions on the expression of genes encoding MMP-1, one of the principal proteinases capable of degrading native fibrillar collagens in the extracellular matrix (ECM), its inhibitor TIMP-1, and TNF-alpha, a cytokine that plays a central role in the induction of implant osteolysis. Human U937 macrophages were incubated in suspension or on phosphorylcholine (PC)-polymer coated surfaces for 24h with Co2+ and Cr3+ ions. The level of mRNAs was determined by reverse transcription-polymerase chain reaction (RT-PCR). Results show that both Co2+ and Cr3+ ions induce the expression of MMP-1, TIMP-1, and TNF-alpha mRNA in a dose-dependent manner in cell suspensions. Tyrosine kinase inhibitors have different effects on these stimulatory effects. Indeed, genistein has only partial inhibitory effect on MMP-1 and TIMP-1, with even less effect on TNF-alpha expression. In contrast, herbimycin A completely blocks MMP-1 and TNF-alpha while partially inhibiting TIMP-1. However, Co2+ and Cr3+ ions had no effect on the expression of MMP-1 and TIMP-1 in macrophages cultured on the PC-polymer, suggesting that the attachment of U937 macrophages to the PC-polymer surfaces may modify their gene expression. In fact, MMP-1 and TIMP-1 seems to be constitutively up-regulated in this condition. However, the effect of Co2+ and Cr3+ ions on macrophages cultured on PC-polymer coated surfaces is similar to what was observed in suspension. Together, these findings indicate that activation of MMP-1, TIMP-1, and TNF-alpha by Co2+ and Cr3+ ions is regulated by tyrosine kinases.

Cell Line↗

PubMed2005

Adhesion of human U937 macrophages to phosphorylcholine-coated surfaces.

A new type of amphiphilic phosphorylcholine (PC) polymer was used in this work to develop a cell culture surface that allows the attachment of U937 macrophages. The PC polymer was a random copolymer of N-isopropylacrylamide (45%), N-(phosphorylcholine)-N'-(ethylenedioxy-bis(ethyl)) acrylamide (41%), and the hydrophobic monomer N-(n-octadecyl) acrylamide (14%). Polypropylene (PP) films (1 cm2) were coated with the polymer solution by immersion. U937 macrophage suspensions were applied on PC polymer-coated surfaces and incubated for up to 72 h at 37 degrees C. While U937 cells did not adhere to PP, ammonia, nitrogen, or oxygen plasma-treated surfaces, they attached rapidly on PC-coated surfaces (< 1 h), proliferated, and stayed attached to the modified surface for at least 72 h, suggesting that unique features of the PC polymer, and the U937 macrophages, are responsible for the attachment of these cells. We compared the effect of Co2+ and Cr3+ ions on the expression of bone-resorbing cytokines (TNF-alpha, IL-6, IL-1beta) in U937 macrophages cultured on PC-coated surfaces to the response of U937 macrophages in suspension. Cytokine gene expression was analyzed by reverse transcription polymerase chain reaction (RT-PCR). Addition of Co2+ and Cr3+ ions led to a significant increased expression of TNF-alpha in both cultured and suspension cells. On the other hand, Co2+ and Cr3+ ions had a weak stimulatory effect or no effect on IL-1beta and IL-6, respectively, in both cultured and suspension cells. In conclusion, the use of PC polymer-modified surfaces might offer promising new opportunities for the culture of human U937 cells and may also point to the mechanism by which macrophages interact with lipid bilayers of biological membranes.

Animals↗

PubMed2005

Role of oxyR from Sinorhizobium meliloti in regulating the expression of catalases.

The process of symbiotic nitrogen fixation results in the generation of reactive oxygen species such as the superoxide anion (O2-) and hydrogen peroxide (H2O2). The response of rhizobia to these toxic oxygen species is an important factor in nodulation and nitrogen fixation. In Sinorhizobium meliloti, one oxyR homologue and three catalase genes, katA, katB, and katC were detected by sequence analysis. This oxyR gene is located next to and divergently from katA on the chromosome. To investigate the possible roles of oxyR in regulating the expression of catalases at the transcriptional level in S. meliloti, an insertion mutant of this gene was constructed. The mutant was more sensitive and less adaptive to H2O2 than the wild type strain, and total catalase/peroxidase activity was reduced approximately fourfold with the OxyR mutation relative to controls. The activities of KatA and KatB and the expression of katA::lacZ and katB::lacZ promoter fusions were increased in the mutant strain compared with the parental strain grown in the absence of H2O2, indicating that katA and katB are repressed by OxyR. However, when exposed to H2O2, katA expression was also increased in both S. meliloti and Escherichia coli. When exposed to H2O2, OxyR is converted from a reduced to an oxidized form in E. coli. We concluded that the reduced form of OxyR functions as a repressor of katA and katB expression. Thus, in the presence of H2O2, reduced OxyR is converted to the oxidized form of OxyR that then results in increased katA expression. We further showed that oxyR expression is autoregulated via negative feedback.

Catalase↗

PubMed2005

Two new Sinorhizobium meliloti LysR-type transcriptional regulators required for nodulation.

The establishment of an effective nitrogen-fixing symbiosis between Sinorhizobium meliloti and its legume host alfalfa (Medicago sativa) depends on the timely expression of nodulation genes that are controlled by LysR-type regulators. Ninety putative genes coding for LysR-type transcriptional regulators were identified in the recently sequenced S. meliloti genome. All 90 putative lysR genes were mutagenized using plasmid insertions as a first step toward determining their roles in symbiosis. Two new LysR-type symbiosis regulator genes, lsrA and lsrB, were identified in the screening. Both the lsrA and lsrB genes are expressed in free-living S. meliloti cells, but they are not required for cell growth. An lsrA1 mutant was defective in symbiosis and elicited only white nodules that exhibited no nitrogenase activity. Cells of the lsrA1 mutant were recovered from the white nodules, suggesting that the lsrA1 mutant was blocked early in nodulation. An lsrB1 mutant was deficient in symbiosis and elicited a mixture of pink and white nodules on alfalfa plants. These plants exhibited lower overall nitrogenase activity than plants inoculated with the wild-type strain, which is consistent with the fact that most of the alfalfa plants inoculated with the lsrB1 mutant were short and yellow. Cells of the lsrB1 mutant were recovered from both pink and white nodules, suggesting that lsrB1 mutants could be blocked at multiple points during nodulation. The identification of two new LysR-type symbiosis transcriptional regulators provides two new avenues for understanding the complex S. meliloti-alfalfa interactions which occur during symbiosis.

Agrobacterium tumefaciens↗

PubMed2005

[Reform steps of reestablishing disease prevention and control system of China].

OBJECTIVE: To develop and demonstrate the reform steps of reestablishing disease prevention and control system of China. METHODS: A model named "strategies of fulfilling public functions of disease prevention and control system of China" has been employed to develop reform steps. 154 centers for disease prevention and control (CDC) have been sampled to consult the opinions about the reform steps developed by research team. RESULTS: To reestablish the disease prevention and control system of China, the following reform steps should be kept to: (1) increase government's attention to disease prevention and control, (2) insure feasible government investment to disease prevention and control, (3) increase the stability and efficiency of government financing, (4) reform management system to enhance the operation efficiency of the CDC, (5) revise labor regulation to attract and stabilize specialists, (6) be carefully to dispose the non-public-service now delivered by the CDC. The consent percent of all sampling CDC was 98.7%.

China↗

PubMed2005

[A study on the cause of public health service delivery insufficiency of disease prevention and control system of China].

OBJECTIVE: To demonstrate the cause of public health service delivery insufficiency of disease prevention and control system of China. METHODS: 205 literatures in 8 national academic journals concerning health service management have been reviewed. The method of boundary analysis has been employed to conclude the various causes of public health service delivery insufficiency of disease prevention and control system of China. RESULTS: Literatures review demonstrated that the financing from government to disease prevention and control system of China was insufficiency and show lower efficiency, which has been agreed by 99.3% of CDC. Literatures review demonstrated that the financing administration idea of permitting charging service caused the fee-for-service played a key role in the economic reimbursement of various levels of CDC, which has been agreed by 96.0% of CDC. CONCLUSION: The causes of public health service delivery insufficiency of disease prevention and control system of China were the government financing insufficiency and the defective administration strategies.

China↗

PubMed2005

[Fundamental strategies to address the problem of public health service delivery insufficiency of disease prevention and control system of China].

OBJECTIVE: To develop and demonstrate the strategies to solve the problem of public health service delivery insufficiency of disease prevention and control system of China. METHODS: 205 literatures in 8 national academic journals concerning health service management have been reviewed. The method of boundary analysis has been employed to conclude the various reform strategies. Based on the causes and mechanism of public health service delivery insufficiency of disease prevention and control system, the logic analysis has been employed to develop fundamental strategies, which has been demonstrated by 154 CDC using intention questionnaires. RESULTS: There are fundamental strategies to which the agreeing rate for sampling CDC was over 95%: to make sure government should afford the financing function of disease prevention and control and secure the feasible investment for centers of disease prevention and control. Meanwhile, the working efficiency of CDC should be improved through strengthening management and reforming government investing manner.

China↗