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Biomedical subjects

X Ma

Publications and source records attributed to X Ma.

At least 253 records · Page 14Linked to original sources
PubMed1998

Comparative genotoxicity of quinolone and quinolonyl-lactam antibacterials in the in vitro micronucleus assay in Chinese hamster ovary cells.

The in vitro micronucleus assay is gaining increased attention as a potential alternative to the standard in vitro metaphase analysis assay. In particular, the in vitro micronucleus assay has been proposed as a useful method for chemicals that induce both structural and numerical chromosome alterations, such as DNA gyrase/topoisomerase inhibitors. In this study, we compared the micronucleus-inducing activity of quinolonyl-lactam antibacterials that inhibit DNA-gyrase and bind to penicillin-binding proteins relative to the activity of structurally related quinolone antibacterials that also inhibit DNA-gyrase. All of the quinolones that were structurally related to the quinolonyl-lactams were cytotoxic and induced large increases in the frequency of micronucleated binucleated cells (MNBC) at concentrations between 0.02 and 0.16 mM. These changes were larger than those seen with the commercial quinolones, ciprofloxacin (cytotoxic at > or = 0.57 mM and MNBC at > or = 0.3 mM) and nalidixic acid (cytotoxic at 1.8 mM and no MNBC up to this dose). In contrast, the quinolonyl-lactams were not cytotoxic up to 1.0 mM concentrations and induced either no MNBC or a low frequency of MNBC at higher concentrations compared to the quinolones. Quinolonyl-lactams appear to be less cytotoxic and genotoxic than structurally related quinolones. These results add to the growing database on the in vitro micronucleus assay in general, and more specifically to the relatively small database for the in vitro micronucleus assay in Chinese hamster ovary cells.

Animals↗
PubMed1998

Positive and negative regulation of interleukin-12 gene expression.

Interleukin-12 (IL-12) is a pivotal cytokine representing the link between the cellular and humoral branches of an effective host immune defense apparatus. IL-12 is a heterodimer produced by phagocytic, B, dendritic, and possibly other accessory cells in both innate and adaptive immune responses. It is a key factor in the induction of T cell-dependent and independent activation of macrophages, generation of T helper type 1 (Th1) and cytotoxic T cells, suppression of IgG1 and IgE production, induction of organ-specific autoimmunity, and resistance to bacterial and parasitic infections [1]. IL-12 has a powerful anti-tumor and anti-metastatic activity against many murine tumors [2-5] as well as human tumors [6-17]. The genes encoding the two heterologous chains of IL-12, p40 and p35 are located on different human chromosomes. Together, p40 and p35 form the biologically active IL-12. Their expressions are highly coordinated during an effective immune response. However, under some pathological conditions, IL-12 is under- or overexpressed, resulting either in a lack of resistance to microbial infection and to uncontrolled tumor growth, or in destructive inflammation, respectively. A transient or irreversible dysregulation of IL-12 production may reflect a pathogen/tumor cell-induced disruption in the highly coordinated expression of p40 and p35. The understanding of the molecular mechanisms governing the expression of IL-12 p40 and p35 genes in the context of interactions between pathogens and the immune system is essential in efforts aimed at designing therapeutic strategies to treat infectious and malignant diseases.

Animals↗
PubMed1998

Preliminary clinical experience with the pullback atherectomy catheter and the study of proliferation in coronary plaques.

BACKGROUND: Clues to the biology of coronary artery disease can be obtained through the study of proliferation in human coronary artery plaques. Previously, immunocytochemistry has been used to detect the proliferating cell nuclear antigen to demonstrate low levels of proliferation in directional coronary atherectomy tissue fragments resected from human coronary arteries. OBJECTIVES: To describe the proliferative profile of coronary artery tissue by using a more sensitive marker for cell replication. PATIENTS AND METHODS: Ten patients with unstable or stable angina pectoris underwent coronary atherectomy with a newer coronary atherectomy device, the Arrow-Fischell pullback atherectomy catheter. The histological features of the specimens were studied by using light microscopy, and cell proliferation was assessed with the use of in situ hybridization for the S phase-specific mRNA species, histone H3. RESULTS: Pullback coronary atherectomy immediately followed by percutaneous transluminal coronary angioplasty resulted in angiographic improvement in the lumen diameter in all but one patient, who required insertion of a stent. The atherectomy specimens consisted of a combination of atheromatous plaque and media. Four specimens had a small amount of adventitia. Five of the 10 specimens had no proliferating cells. Three specimens had between one and five proliferating cells per slide, while two specimens had relatively high proliferation indexes (2.5% and 4.2% of all cells per atherectomy cross-section). Both smooth muscle cells and macrophages were identified in areas with proliferating cells. The histology and proliferation profiles of the tissue resected from patients with stable and unstable angina were similar. CONCLUSIONS: Pullback atherectomy can be used effectively to debulk coronary artery lesions. By using a sensitive marker for cell replication, it was determined that the majority of the tissue specimens have low proliferation indexes.

Angioplasty, Balloon, Coronary↗
PubMed1997

Inhibition of IL-12 production by thalidomide.

The immunomodulatory properties of thalidomide are currently being exploited therapeutically in conditions as diverse as erythema nodosum leprosum, chronic graft-vs-host disease, rheumatoid arthritis, and sarcoidosis. The relevant mechanism of action of thalidomide in these diseases remains unclear. The important role recently ascribed to IL-12, a cytokine critical to the development of cellular immune responses, in the pathogenesis of several of these conditions led us to examine whether thalidomide affects the production of IL-12. Thalidomide potently suppressed the production of IL-12 from human PBMC and primary human monocytes in a concentration-dependent manner. Thalidomide-induced inhibition of IL-12 production was additive to that induced by suboptimal inhibiting doses of dexamethasone, and occurred by a mechanism independent of known endogenous inhibitors of IL-12 production. These results suggest that thalidomide may have therapeutic utility in a wide range of immunologic disorders that are characterized by inappropriate cellular immune responses.

Antibodies, Monoclonal↗
PubMed1997

A novel link between REC2, a DNA recombinase, the retinoblastoma protein, and apoptosis.

The REC2 recombinase is essential for recombinational repair following DNA damage as well as for successful meiosis and gene targeting in the corn smut Ustilago maydis. Here we report that overexpression of REC2 induced apoptotic cell death in human HuH-7, Hep G2, and Hep 3B hepatoma cells. Apoptosis was related to recombinase activity and was significantly increased by inhibition of retinoblastoma (Rb) expression with transforming growth factor-beta1. REC2-induced apoptosis was associated with a significantly reduced percentage of cells in the G1 phase of the cell cycle and a significant reduction in G2/M only in the Rb(-/-) Hep 3B cells. Overexpression of REC2 resulted in increased abundance of the hyperphosphorylated form of Rb. However, by immunoprecipitation REC2 was associated primarily with hypophosphorylated Rb, suggesting that REC2 may be involved in modulating the phosphorylation state of Rb. The A and B pocket domains with the spacer amino acid sequence and the carboxyl-terminal region of Rb were required for maximal binding to REC2. Overexpression of Rb significantly inhibited REC2-induced apoptosis even in the presence of transforming growth factor-beta1. Taken together, these data suggest a novel interaction of Rb with the recombinase REC2 and a role for this complex in bridging DNA recombination and apoptosis.

Apoptosis↗
PubMed1997

Identification and characterization of a novel Ets-2-related nuclear complex implicated in the activation of the human interleukin-12 p40 gene promoter.

Interleukin-12 (IL-12) is a proinflammatory cytokine produced by antigen-presenting cells in response to many microbial infections. IL-12 plays an important role in the generation of T helper type-1 cells, which favor cell-mediated immune response. IL-12 is composed of two different subunits, p40 and p35, whose expression can be regulated concomitantly or differentially. Monocytic cells, the major producers of IL-12, can be primed by interferon-gamma (IFN-gamma) to produce optimal amounts of IL-12 in response to LPS stimulation as a consequence of bacterial infection. The priming effect is exerted primarily at the transcriptional level on the p40 promoter in conjunction with the effects of LPS, possibly by inducing specific transcription factors, which individually have no direct effect but which cooperatively can activate the promoter. We examined in detail one of these DNA-protein interactions observed around an Ets-2 element situated at -211/-207 of the p40 promoter, which is known to be a functionally critical site. This region interacts with a nuclear complex termed F1 that appears to be highly inducible by either IFN-gamma treatment for 16 h or lipopolysaccharide stimulation for 8 h. F1 binding to the Ets-2 site requires a considerable amount of spacing around the Ets-2 site, as revealed by gel mobility shift and in vitro methylation assays. Supershift experiments and DNA affinity purification indicated that both Ets-2 and a novel, antigenically related protein with an approximate molecular mass of 109 kDa are part of the F1 complex, together with additional components including IRF-1 and c-Rel. This novel protein is designated GLp109 for its inducibility by IFN-gamma or lipopolysaccharide. Its possible role in the activation of the IL-12 p40 promoter is discussed.

Animals↗
PubMed1997

Targeting determinants and proposed evolutionary basis for the Sec and the Delta pH protein transport systems in chloroplast thylakoid membranes.

Transport of proteins to the thylakoid lumen is accomplished by two precursor-specific pathways, the Sec and the unique Delta pH transport systems. Pathway selection is specified by transient lumen-targeting domains (LTDs) on precursor proteins. Here, chimeric and mutant LTDs were used to identify elements responsible for targeting specificity. The results showed that: (a) minimal signal peptide motifs consisting of charged N, hydrophobic H, and cleavage C domains were both necessary and sufficient for pathway-specific targeting; (b) exclusive targeting to the Delta pH pathway requires a twin arginine in the N domain and an H domain that is incompatible with the Sec pathway; (c) exclusive targeting to the Sec pathway is achieved by an N domain that lacks the twin arginine, although the twin arginine was completely compatible with the Sec system. A dual-targeting signal peptide, constructed by combining Delta pH and Sec domains, was used to simultaneously compare the transport capability of both pathways when confronted with different passenger proteins. Whereas Sec passengers were efficiently transported by both pathways, Delta pH passengers were arrested in translocation on the Sec pathway. This finding suggests that the Delta pH mechanism evolved to accommodate transport of proteins incompatible with the thylakoid Sec machinery.

Amino Acid Sequence↗
PubMed1997

Reduced evoked release of acetylcholine in the rodent neocortex following traumatic brain injury.

Neocortical acetylcholine (ACh) release was examined in awake, freely-moving rats at 14 days following lateral controlled cortical impact. Extracellular ACh was measured prior to and after an intraperitoneal administration of scopolamine, which evokes ACh release by blocking autoreceptors. At 14 days post-injury there was a significant reduction in scopolamine-evoked ACh release. The data suggest that neocortical cholinergic neurotransmission is chronically compromised, and may contribute to post-traumatic memory deficits.

Acetylcholine↗
PubMed1997

Interleukin-12: an immunoregulatory cytokine produced by B cells and antigen-presenting cells.

Interleukin 12 (IL-12) is a heterodimeric protein produced by B cells, phagocytic cells, and other antigen-presenting cells. IL-12 was originally purified from the supernatant fluids of human EBV-transformed cell lines and later observed to be produced by the large majority of such cell lines, especially and at high levels from those derived from AIDS-associated lymphomas. However, phagocytic cells rather than B cells appear to be the most important physiological producers of IL-12. There are two pathways of IL-12 induction in phagocytic cells: a T-cell-independent one, induced primarily by bacteria, bacterial products, or intracellular parasites and important in the early inflammatory response of innate resistance; and a T-cell-dependent one, induced by the interaction of CD40L on activated T cells with CD40 receptor on IL-12-producing cells (phagocytic cells and antigen-presenting cells) and important in the regulation of adaptive immunity. IL-12 induces production of cytokines, especially interferon-gamma, from both T and NK cells, enhances the cytotoxic activity of NK cells and the generation of cytotoxic T cells, and has a proliferative activity on T and NK cells. Both in vivo and in vitro, IL-12 is a powerful inducer of T helper type 1 (Th1) response, whereas it inhibits Th2-type responses.

Antigen-Presenting Cells↗
PubMed1997

Basal nitric oxide expresses endogenous cardioprotection during reperfusion by inhibition of neutrophil-mediated damage after surgical revascularization.

Ischemia-reperfusion damages endothelium and impairs basal production of nitric oxide. Basally released nitric oxide is cardioprotective by its inhibition of neutrophil activities. Loss of endogenous nitric oxide with endothelial injury may occur during two phases: cardioplegic ischemia and reperfusion (aortic declamping). This study tested the hypothesis that inhibition of endogenously released nitric oxide in hearts subjected to regional ischemia, cardioplegic arrest, and reperfusion (1) restricts endogenous cardioprotection and permits neutrophil-mediated damage and (2) expresses damage during the reperfusion phase. L-Nitro-arginine was used to block basal nitric oxide production. In 22 anesthetized dogs, the left anterior descending artery was ligated for 90 minutes followed by 1 hour of arrest with cold multidose (every 20 minutes) blood cardioplegia. Dogs were divided into three groups: the first group received standard unsupplemented blood cardioplegia (group 1, n = 8), in the second group L-nitro-arginine was administered as an additive to blood cardioplegic solution (1 mmol) and as an infusion during reperfusion (34 mg/kg) (group 2, n = 7), and in the third group L-nitro-arginine was administered only at reperfusion (group 3, n = 7). The ligature was released during the second infusion of cardioplegic solution. Infarct size (triphenyltetrazolium chloride) was increased in group 3 (L-nitro-arginine only at reperfusion) compared with that in group 1 (standard blood cardioplegia) (49% +/- 6% vs 34% +/- 2%, respectively), but was not further extended in group 2 (L-nitro-arginine as an additive to blood cardioplegic solution and at reperfusion) (56% +/- 3%, p > 0.05 vs group 3), which suggests primarily a reperfusion process. Polymorphonuclear neutrophil-specific myeloperoxidase activity in the area at risk was elevated comparably in groups 2 and 3 (group 2: 2.9 +/- 0.5 units/gm tissue, p = 0.06 vs group 1; group 3: 3.9 +/- 1.0 units/gm tissue, p < 0.05 vs group 1) compared with that in the standard blood cardioplegia group (1.7 +/- 0.3 units/gm tissue), suggesting polymorphonuclear neutrophil accumulation occurs primarily during reperfusion. Polymorphonuclear neutrophil adherence in ischemic-reperfused left anterior descending artery segments was comparably greater in group 2 (L-nitro-arginine as an additive to blood cardioplegic solution and at reperfusion: 195 +/- 21 polymorphonuclear neutrophils/mm2 of artery, p < 0.05 vs group 1) and group 3 (L-nitro-arginine only at reperfusion: 224 +/- 20 polymorphonuclear neutrophils/mm2 of artery, p < 0.05 vs group 1) relative to that in group 1 (108 +/- 19 polymorphonuclear neutrophils/mm2 of artery). There was no significant adherence to nonischemic circumflex arteries. We conclude that blockade of endogenous nitric oxide augments postischemic injury mediated by polymorphonuclear neutrophils, and this damage is expressed primarily during the reperfusion phase.

Animals↗
PubMed1997

The cytoskeleton and the extracellular matrix in sensitized canine tracheal smooth muscle.

To investigate the mechanisms responsible for the increased shortening capacity (delta Lmax) of airway smooth muscle in ragweed pollen sensitized dogs, the alterations of biophysical and biochemical properties of cytoskeleton and extracellular collagen in tracheal smooth muscle (TSM) were studied. Smooth muscle passive elastic properties were not significantly altered by removal of cytoskeleton with guanidine HCI plus 2-mercaptoethnol; collagenase digestion reduced smooth muscle force development, but did not affect its delta Lmax and passive elastic properties in both sensitized and control dogs. There were no significant differences in the amount of cytoskeletal intermediate filament proteins, desmin and vimentin between sensitized and control TSM. The content of total collagen, collagen type I, and collagen cross-linking in sensitized TSM were significantly greater than in control. Collagen fibres in sensitized TSM was more resistant to collagenase attack. We conclude that increased delta Lmax in sensitized canine TSM is not the result of alterations in passive cytoskeletal and extracellular collagen structures.

Allergens↗
PubMed1997

Polyenylphosphatidylcholine prevents carbon tetrachloride-induced lipid peroxidation while it attenuates liver fibrosis.

BACKGROUND/AIMS: Polyenylphosphatidylcholine protects against alcoholic cirrhosis in the baboon and carbon tetrachloride-induced cirrhosis in rats. This study addresses the possible mechanism of the protective effect of polyenylphosphatidylcholine. METHODS: For 8 weeks, rats were injected with either carbon tetrachloride in peanut oil or peanut oil alone (control), and pair-fed nutritionally adequate liquid diets with equivalent amounts of linoleic acid either as polyenylphosphatidylcholine or as safflower oil. Other rats were injected for 9 weeks with heterologous albumin and fed the same liquid diets. Lipid peroxidation was measured by F2-isoprostanes and 4-hydroxynonenal. RESULTS: Carbon tetrachloride-induced lipid peroxidation was strikingly attenuated with polyenylphosphatidylcholine supplementation. Levels of hepatic F2-isoprostanes and 4-hydroxynonenal paralleled liver fibrotic scores and collagen accumulation. Polyenylphosphatidylcholine also attenuated the fibrosis induced in rats with human albumin, but in this case, levels of hepatic 4-hydroxynonenal did not change, nor were they significantly affected by polyenylphos-phatidylcholine. Neither carbon tetrachloride injection nor polyenylphosphatidylcholine treatment changed the arachidonic acid content (a major precursor of F2-isoprostanes and 4-hydroxynonenal) in liver phospholipids, and hepatic vitamin E was not significantly altered. CONCLUSIONS: The hepatic protection of polyenylphosphatidylcholine against carbon tetrachloride appears to be due, at least in part, to an antioxidant effect, whereas the protection against heterologous albumin-induced fibrosis suggests that an additional mechanism, such as stimulation of collagenase activity, may also be responsible.

Analysis of Variance↗
PubMed1997

Inhibition of human interleukin-12 production by pentoxifylline.

Pharmacological control of interleukin-12 (IL-12) production may be a key therapeutic strategy for modulating immunological diseases dominated by type-1 cytokine responses. In this study, we investigated the effects of pentoxifylline on the production of IL-12 by human blood mononuclear cells and primary human monocytes stimulated with heat-killed Staphylococcus aureus Cowan strain I (SAC) or lipopolysaccharide (LPS). Pentoxifylline potently suppressed production of IL-12 in a concentration-dependent manner. In these same experiments, tumour necrosis factor-alpha (TNF-alpha) production was inhibited and IL-10 and prostaglandin E2 (PGE2) production was enhanced by treatment with pentoxifylline. Suppression of IL-12 production by pentoxifylline was found to be independent of several known endogenous inhibitors of IL-12, such as IL-10, transforming growth factor-beta (TGF-beta), IL-4 and PGE2. RNase protection assays revealed that pentoxifylline inhibited accumulation of both IL-12 p40 and p35 mRNA, suggesting a predominant mRNA locus for pentoxifylline-induced IL-12 inhibition. Low levels of pentoxifylline added to the suppression of IL-12 production by suboptimal inhibiting doses of dexamethasone, suggesting that this drug combination may have therapeutic utility. These results provide a firm rationale for the use of pentoxifylline in clinical trials of immunological disorders characterized by inappropriate type-1 immune responses.

Cell Culture Techniques↗
PubMed1997

Effects of CDP-choline treatment on neurobehavioral deficits after TBI and on hippocampal and neocortical acetylcholine release.

The exogenous administration of cytidine-5'-diphosphate (CDP)-choline has been used extensively as a brain activator in different neurological disorders that are associated with memory deficits. A total of 50 rats were utilized to (a) determine whether exogenously administered CDP-choline could attenuate posttraumatic motor and spatial memory performance deficits and (b) determine whether intraperitoneal (i.p.) administration of CDP-choline increases acetylcholine (ACh) release in the dorsal hippocampus and neocortex. In the behavioral study, traumatic brain injury (TBI) was produced by lateral controlled cortical impact (2-mm deformation/6 m/sec) and administered CDP-choline (100 mg/kg) or saline daily for 18 days beginning 1 day postinjury. At 1 day postinjury, rats treated with CDP-choline 15 min prior to assessment performed significantly better than saline-treated rats. Between 14-18 days postinjury, CDP-choline-treated rats had significantly less cognitive (Morris water maze performance) deficits that injured saline-treated rats. CDP-choline treatment also attenuated the TBI-induced increased sensitivity to the memory-disrupting effects of scopolamine, a muscarinic antagonist. The microdialysis studies demonstrated for the first time that a single i.p. administration of CDP-choline can significantly increase extracellular levels of ACh in dorsal hippocampus and neocortex in normal, awake, freely moving rats. This article provides additional evidence that spatial memory performance deficits are, at least partially, associated with deficits in central cholinergic neurotransmission and that treatments that enhance ACh release in the chronic phase after TBI may attenuate cholinergic-dependent neurobehavioral deficits.

Acetylcholine↗
PubMed1997

Discordant hepatic expression of the cell division control enzyme p34cdc2 kinase, proliferating cell nuclear antigen, p53 tumor suppressor protein, and p21Waf1 cyclin-dependent kinase inhibitory protein after WY14,643 ([4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid) dosing to rats.

The hepatocarcinogen and peroxisome proliferator WY14,643 ([4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid) was examined for its ability to induce changes in the intracellular protein expression of hepatic p34cdc2 kinase (CDK1), proliferating cell nuclear antigen (PCNA), p53 tumor suppressor protein, and p21Waf1 CDK inhibiting protein. Young adult male rats were administered 45 mg-kg/day WY14,643 intraperitoneally for 1, 2, 3, 4, or 5 days or fed diets containing 0% or 0.08% WY14,643 for 1, 2, 3, or 4 weeks. WY14,643 dosing increased concentrations of hepatic proteins of 34- and 37-kDa molecular mass, which were identified through immunoprecipitation as CDK1 and PCNA, respectively. Gel filtration of the hepatic S9 fractions determined by enzyme-linked immunosorbent assay confirmed the increased expression of CDK1 and PCNA immunoreactivity in livers from WY14,643-treated rats. Also, gel filtration revealed that the native CDK1 and PCNA in hepatic S9 from WY14,643-treated rats chromatographed as a major peak with an apparent molecular mass of 70 and 76 kDa, respectively. Immunoblotting of the 70-kDa fraction with anti-CDK1 revealed a single band of molecular mass of 34 kDa. Thus, the CDK1 in the major immunoreactive peak of WY14,643-treated rat liver S9 seems to exist as a heterodimer or homodimer. Immunohistochemistry of formalin-fixed liver demonstrated a cytosolic localization of immunoreactive CDK1 and nuclear localization of immunoreactive PCNA in proliferating cells of WY14,643-treated rat livers. WY14,643 increased hepatic CDK1 content by 1.9-6.3-fold through postdosing days 1-5. Hepatic PCNA content was increased 1.9-5-fold over the same period. In the 4-week feeding study, CDK1 and PCNA expression were increased at all weekly time points by an average of 15-50-fold, respectively. Furthermore, the dietary administration of 0.08% WY14,643 resulted in sustained, overexpression of hepatic p53 tumor suppressor protein from week 1 through week 4 and of p21Waf1 CDK inhibitory protein from week 3 to week 4.

Animals↗
PubMed1997

Interactions between heterologous FtsA and FtsZ proteins at the FtsZ ring.

FtsZ and FtsA are essential for cell division in Escherichia coli and colocalize to the septal ring. One approach to determine what regions of FtsA and FtsZ are important for their interaction is to identify in vivo interactions between FtsA and FtsZ from different species. As a first step, the ftsA genes of Rhizobium meliloti and Agrobacterium tumefaciens were isolated and characterized. In addition, an FtsZ homolog that shared the unusual C-terminal extension of R. meliloti FtsZ1 was found in A. tumefaciens. In order to visualize their localization in cells, we tagged these proteins with green fluorescent protein (GFP). When R. meliloti FtsZ1-GFP or A. tumefaciens FtsZ-GFP was expressed at low levels in E. coli, they specifically localized only to the E. coli FtsZ ring, possibly by coassembly. When A. tumefaciens FtsA-GFP or R. meliloti FtsA-GFP was expressed in E. coli, they failed to localize detectably to the E. coli FtsZ ring. However, when R. meliloti FtsZ1 was coexpressed with them, fluorescence localized to a band at the midcell division site, strongly suggesting that FtsA from either A. tumefaciens or R. meliloti can bind directly to its cognate FtsZ. As expected, GFP-tagged FtsZ1 and FtsA from either R. meliloti or A. tumefaciens localized to the division site in A. tumefaciens cells. Therefore, the 61 amino acid changes between A. tumefaciens FtsA and R. meliloti FtsA do not prevent their direct interaction with FtsZ1 from either species, suggesting that those residues are not essential for protein-protein contacts. Moreover, the failure of the two non-E. coli FtsA derivatives to interact strongly with E. coli FtsZ in this in vivo system unless their cognate FtsZ was also present suggests that FtsA-FtsZ interactions have coevolved and that the residues which differ between the E. coli proteins and those of the two other species may be important for specific interactions.

Agrobacterium tumefaciens↗
PubMed1997

[The free radicals and nickel carcinogenesis].

The relationship between free radicals and the carcinogenesis of nickel and its compounds was summarized. Ni(II) could enhance the production of free radicals mainly in three pathways: Fenton reaction, enhancing lipid peroxidation and decreasing cellular antioxidantive defense system. Thus free radacals lead cell carcinogenesis. It suggested that the carcinogenesis of Ni(II) was mainly related to the effect of free radicals.

Animals↗