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Q Chen

Publications and source records attributed to Q Chen.

At least 631 records · Page 35Linked to original sources
PubMed1994

Anti-CD11b monoclonal antibody reduces ischemic cell damage after transient focal cerebral ischemia in rat.

We investigated the effect of an anti-CD11b monoclonal antibody (1B6c) on ischemic cell damage after transient middle cerebral artery occlusion. We divided animals into three groups: MAb 1 group (n = 5)--rats were subjected to 2 hours of transient occlusion and 1B6c (1 mg/kg) was administered intravenously at 0 and 22 hours of reperfusion; MAb 2 group (n = 5)--same experimental protocol as MAb 1 group, except that the initial dose of 1B6c was increased to 2 mg/kg; and control group (n = 5)--same experimental protocol as MAb 2 group, except that an isotype-matched control antibody was administered. Animals were weighed and tested for neurological function before and after occlusion of the middle cerebral artery. Forty-six hours after reperfusion, brain sections were stained with hematoxylin and eosin for histology evaluation. We observed a significant reduction of weight loss and improvement in neurological function after ischemia in the MAb 2 animals compared to MAb 1 and vehicle-treated animals (p < 0.05). The lesion volume was significantly smaller in the MAb 2 group (19.5 +/- 1.9%) compared to MAb 1 (29.9 +/- 2.6%) and vehicle-treated (34.2 +/- 5.4%) groups (p < 0.01). Tissue polymorphonuclear cell numbers were reduced in both 1B6c-administered groups. Our data demonstrate that administration of anti-CD11b antibody results in a dose-dependent, significant functional improvement and reduction of ischemic cell damage after transient focal cerebral ischemia in the rat.

Animals↗
PubMed1994

Rapid induction of mRNAs for liver regeneration factor and insulin-like growth factor binding protein-1 in primary cultures of rat hepatocytes by hepatocyte growth factor and epidermal growth factor.

Liver regeneration factor belongs to the leucine-zipper family of transcription factors. It was originally cloned and characterized through differential screening of a regenerating rat liver cDNA library. The mRNA for liver regeneration factor-1 is barely detectable in normal rat liver but is dramatically induced after two-thirds hepatectomy, with a peak 1 to 3 hr after surgery. The nature of the signaling molecule(s) for this rapid induction is not known. It has been suggested that the liver regeneration factor-1 protein product, through complex interactions with other transcription factors such as c-Jun and Jun-B, controls expression of genes that are required during the G1 phase of hepatic growth. Hepatocyte growth factor has been shown to be the most potent mitogen for hepatocytes in vitro and in vivo. Plasma levels of hepatocyte growth factor rapidly (within 30 min) increase after loss of hepatic parenchyma induced by partial hepatectomy or carbon tetrachloride treatment. It has been postulated that hepatocyte growth factor plays a crucial role in stimulating the hepatocyte to enter the cell cycle. In this communication, we report that addition of pure hepatocyte growth factor to primary cultures of rat hepatocytes in the absence of serum and insulin results in rapid and transient induction of liver regeneration factor-1 mRNA (more than 20-fold) with a peak of expression 1 hr after treatment. The levels of jun-B and c-fos mRNAs, which are also known to be induced during the early hours of liver regeneration, were also increased after treatment of isolated hepatocytes with hepatocyte growth factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Activating Transcription Factor 3↗
PubMed1994

Early cellular events couple covalent binding of reactive metabolites to cell killing by nephrotoxic cysteine conjugates.

Addition of the nephrotoxic cysteine conjugate, S-(1,2-dichlorovinyl)-L-cysteine (DCVC), to the LLC-PK1 line of renal epithelial cells leads to covalent binding of reactive intermediates followed by thiol depletion, lipid peroxidation, and cell death (Chen et al., 1990, J. Biol. Chem., 265:21603-21611). The present study was designed to determine if increased intracellular free calcium might play a role in this pathway of DCVC-induced toxicity by comparing the temporal relationships among increased intracellular free calcium, lipid peroxidation, and cytotoxicity. Intracellular free calcium increased 1 hr after DCVC treatment, long before LDH release occurred. The elevation of intracellular free calcium and cytotoxicity was prevented by inhibiting DCVC metabolism with AOA. The cell-permeable chelators, Quin-2AM and EGTA-AM, prevented the toxicity. Pretreatment of cells with a nontoxic concentration of ionomycin increased intracellular free calcium and potentiated DCVC-induced LDH release. However, the antioxidant, DPPD, which blocks lipid peroxidation and toxicity, did not affect the increase in intracellular free calcium, whereas buffering intracellular calcium with Quin-2AM or EGTA-AM blocked both lipid peroxidation and toxicity without preventing the depletion of nonprotein sulfhydryls by DCVC. Ruthenium red, an inhibitor of mitochondrial calcium uptake, also blocked cell death. We hypothesize that covalent binding of the reactive fragment from DCVC metabolism leads to deregulation of intracellular calcium homeostasis and elevation of intracellular free calcium. Increased intracellular free calcium may in turn be coupled to mitochondrial damage and the accumulation of endogenous oxidants which cause lipid peroxidation and cell death.

Aminooxyacetic Acid↗
PubMed1994

Signalling the molecular stress response to nephrotoxic and mutagenic cysteine conjugates: differential roles for protein synthesis and calcium in the induction of c-fos and c-myc mRNA in LLC-PK1 cells.

Nephrotoxic and mutagenic cysteine conjugates (NCC) are activated by the enzyme cysteine conjugate, beta-lyase, to reactive acylating species which bind covalently to cellular macromolecules. We now show that an early event after treatment of LLC-PK1 cells with NCC is the induction of mRNA for both c-fos and c-myc. Treatment with S-(1,2-dichlorovinyl)-L-cysteine (DCVC) induced c-fos (53-fold) and c-myc mRNA (20-fold) and increased transcription about 3-fold for both genes. Covalent binding was required for induction of both mRNAs. Dithiothreitol partially prevented induction of both c-fos and c-myc RNA. Buffering the DCVC-induced increase in cytosolic free calcium had no effect on c-fos mRNA, but partially blocked c-myc mRNA induction. Cycloheximide blocked the induction of c-myc mRNA in the absence of an effect on c-fos induction. The data suggest that the increase in c-fos mRNA is a primary response to DCVC toxicity and occurs without a requirement for protein synthesis or an increase in intracellular free calcium. In contrast, c-myc induction requires protein synthesis, suggesting that the presence of another primary response factor may regulate induction either transcriptionally or posttranscriptionally. The data suggest that different signalling pathways regulate induction of c-fos and c-myc mRNA in response to stress caused by reactive acylating species.

Animals↗
PubMed1994

Relative survival of striatal projection neurons and interneurons after intrastriatal injection of quinolinic acid in rats.

An excitotoxic process mediated by the NMDA type glutamate receptor may be involved in striatal neuron death in Huntington's disease (HD). To explore this possibility, we have injected an NMDA-receptor-specific excitotoxin, quinolinic acid (QA), into the striatum in adult rats and 2-4 months postlesion explored the relative patterns of survival for the various different types of striatal projection neurons and interneurons and for the striatal efferent fibers in the different striatal projection areas. The perikarya of specific types of striatal neurons were identified by neurotransmitter immunohistochemical labeling or by retrograde labeling from striatal target areas, while the striatal efferent fiber plexuses were identified by neurotransmitter immunohistochemical labeling. The pattern of survival for the perikarya of each neuron type as a function of distance from the center of the injection site was determined, and the relative survival of each type was compared. For the fibers in target areas, computer-assisted image analysis was used to determine the degree of fiber loss for each projection target. In the study of perikaryal vulnerability, we found that the somatostatin-neuropeptide Y (SS/NPY) interneurons were the most vulnerable to QA and the cholinergic neurons were invulnerable to QA. The perikarya of all projection neuron types (striatopallidal, striatonigral, and striato-entopeduncular) were less vulnerable than the SS/NPY interneurons and more vulnerable than the cholinergic interneurons. Among projection neuron perikarya, there was evidence of differential vulnerability, with striatonigral neurons appearing to be the most vulnerable. Examination of immunolabeled striatal fibers in the striatal target areas indicated that striato-entopeduncular fibers better survived intrastriatal QA than did striatopallidal or striatonigral fibers. The apparent order of vulnerability observed in this study among projection neurons and/or their efferent fiber plexuses and the invulnerability observed in this study of cholinergic interneurons is similar to that observed in HD. The vulnerability of the SS/NPY interneurons to QA is, however, in stark contrast to their invulnerability in HD. The results thus suggest that although the excitotoxin hypothesis of striatal neuron death in HD has merit, QA injections into adult rat striatum do not strictly mimic the outcome in HD. This suggests that either adult rats are not a completely suitable subject for mimicking HD or the HD excitotoxic process does not involve a freely circulating excitotoxin such as QA.

Animals↗
PubMed1994

Is the swelling in brain edema isotropic or anisotropic?

A study was conducted to examine whether swelling of the brain due to vasogenic-type and cytotoxic-type edema is isotropic or anisotropic. Vasogenic edema was induced by cryogenic injury in cats, and coronal sections of the brain were examined at 4-5 h after injury. The swelling of the edematous white matter longitudinal to and transverse to the subcortical neuronal fibers was 2.3% and 91.1%, respectively. Ischemic edema was examined using cortical tissue specimens of cat brain subjected to either middle cerebral artery occlusion for 3 h or immersion in saline after decapitation for 3 h. The swelling parallel to the left-right axis, caudo-rostral axis and antero-posterior axis was 9.6%, 10.1% and 8.5%, respectively. Neuroglial cell swelling was prominent in the ischemic cortex. Thus swelling of the white matter in vasogenic-type edema was anisotropic, whereas that of gray matter in cytotoxic-type (ischemic) edema was isotropic. This observed difference in the biomechanical properties of brain tissue should be taken into account when the etiology of edema-mediated tissue injury, such as herniation, secondary bleeding or ischemia is investigated.

Animals↗
PubMed1994

Biomechanical characteristics of brain edema: the difference between vasogenic-type and cytotoxic-type edema.

Some of the basic biomechanical properties of edematous brain tissue have yet to be clarified. Therefore we measured regional tissue compliance and swelling isotropy/anisotropy in cat brain during development of vasogenic-type and cytotoxic-type edema. In vasogenic-type edema induced by cryogenic injury, the edematous white matter showed an increase of regional tissue compliance (indentation method), which paralleled the increase in the regional tissue water content (gravimetry). Swelling of the white matter due to edema was anisotropic, in which expansion transverse to the neuronal fibers caused by their dissociation was 91.1%, whereas longitudinal expansion was 2.3%. In cytotoxic-type edema induced by cerebral ischemia for 3 h, regional tissue compliance was decreased in the area suffering energy failure, which was visualized as an area of reduced succinic dehydrogenase activity. The ischemic gray matter showed isotropic swelling, and morphologically, prominent swelling of neuroglial cells. These marked differences in basic biomechanical properties between vasogenic-type and cytotoxic-type edema should be taken into account when analyzing the mechanism of edema-mediated tissue injury.

Animals↗
PubMed1994

Evaluation of single-photon emission tomography imaging of supratentorial brain gliomas with technetium-99m sestamibi.

Single-photon emission tomography (SPET) with technetium-99m sestamibi (MIBI) was carried out in 61 adult patients with supratentorial expanding brain lesions. Thirty-one patients had pathologically proven malignant glioma. Ten patients had pathologically proven low-grade glioma, while another 12 patients had a clinical diagnosis of low-grade glioma. The other eight patients had a variety of lesions including radiation necrosis (3), abscess (2), ischaemic stroke (2) and primary brain lymphoma (1). SPET was performed 15 min after administration of 740-930 MBq MIBI and transverse, sagittal and coronal views were reconstructed. Using computed tomography or magnetic resonance imaging guidance, a MIBI uptake index was computed as the ratio of counts in the lesion to counts in the contralateral homologous region. In high-grade gliomas, the MIBI index ranged from 1.9 to 6.6 (mean 3.6 +/- 1.4) whereas it ranged from 0.8 to 1.7 (1.1 +/- 0.2) in the pathologically proven low-grade group (P < 0.01). No significant difference was found between the two low-grade groups (1.1 +/- 0.2 vs 1.1 +/- 0.2). No overlap was found between high-grade and low-grade glioma index values. Patients with suspected radiation necrosis, cerebral abscess or ischaemic stroke did not demonstrate high MIBI uptake (0.9-2.2), whereas one patient with brain lymphoma did (3.9). This study suggests that MIBI SPET imaging is of value in distinguishing low-from high-grade supratentorial gliomas in adults.

Adult↗
PubMed1994

Radioimmunolocalization of human pancreatic carcinoma xenograft by 99mTc-labeled YPC3 monoclonal antibody.

Monoclonal antibodies specific to tumor cells may be a useful tool for the diagnosis and treatment of carcinomas. In this study, YPC3 mAb, a specific monoclonal antibody against the human pancreatic carcinoma cell line Capan-2, was labeled directly with 99mTc after being pretreated with 2-mercaptoethanol. The radiolabeling efficiency was found to be high (88%-95%) and the immunoreactivity retained, as assessed by immunohistochemistry and enzyme-linked immunosorbent assay. The biodistribution of 99mTc-YPC3 mAb in nude mice bearing Capan-2 pancreatic carcinoma xenografts was studied and compared with that of labeled mouse immunoglobulin G(99mTc-nmIgG). The xenograft uptake values per gram of tissue 6 h and 24 h after injection of 99mTc-YPC3 mAb were found to be, respectively, 4.72%ID/g and 8.42%ID/g, and the tumor/blood ratios 1.16 and 2.24. At 6 h and 24 h after injection of 99mTc-nmIgG, the uptakes were 2.89%ID/g and 1.80%ID/g, and the tumor/blood ratios 0.84 and 1.02 respectively. External imaging by single-proton emission computed tomography, 24 h after injection of 99mTc-YPC3 mAb, revealed clear scintigraphic visualization of Capan-2 xenografts, whereas injection of 99mTc-nmIgG did not. This study suggests that 99mTc labeling of monoclonal antibody YPC3 might be of practical value in localization diagnosis of human pancreatic carcinoma.

Animals↗
PubMed1994

T cell recognition of melanoma antigens in association with HLA-A1 on allogeneic melanoma cells.

Previous studies have shown that recognition of melanoma by cytotoxic T lymphocytes may be restricted by HLA-A1, A2 and other HLA antigens. The present study examined the cytotoxic specificity and major histocompatibility complex restriction of cloned cytotoxic T lymphocytes (CTL) isolated from a patient with the HLA phenotype A3,31 who had been immunized with a vaccine prepared from HLA-A1,3 melanoma cells. Cytotoxic assays against HLA-typed allogeneic melanoma cells indicated that cloned CTL from the patient were able to kill allogeneic melanoma cells expressing HLA-A1 but not other HLA-A1-positive cells. Studies on a representative clone indicated that proliferation and cytokine (tumour necrosis factor alpha) production in response to melanoma cells was also associated with HLA-A1 on melanoma cells. Response to the melanoma cells was associated with interleukin-4 (IL-4) rather than IL-2 production. The antigen recognized in the context of HLA-A1 on allogeneic melanoma cells was detected in cytotoxic assays on cells from 9 of 12 HLA-A1+ melanoma cell lines and did not appear to be the product of the MAGE-1 or -3 genes. These findings suggest that T cells can recognize melanoma antigens in the context of alloantigens and that allogeneic vaccines containing "immunodominant" alloantigens may generate CTL that are ineffective against autologous melanoma. The study does not, however, exclude the possibility that CTL with specificity to the latter may be activated by allogeneic vaccines, and further studies are needed to answer this question.

Antibodies, Monoclonal↗
PubMed1994

Assays of oxidative DNA damage biomarkers 8-oxo-2'-deoxyguanosine and 8-oxoguanine in nuclear DNA and biological fluids by high-performance liquid chromatography with electrochemical detection.

High-performance liquid chromatography with electrochemical detection is a highly sensitive and selective method for detecting oxo8dG and oxo8Gua, biomarkers of oxidative DNA damage. When employed together with the DNA isolation and monoclonal antibody-based immunoaffinity purification methods described, oxo8dG and oxo8Gua in DNA and urine can be readily detected and quantitated, offering a powerful approach for assessing oxidative DNA damage in vivo. Application of the technique to the detection of oxo8dG from DNA permits quantitation of the steady-state levels of this oxidatively modified deoxynucleoside and overcomes the detection problems associated with the extremely low levels present in DNA. In addition, the selectivity gained by this detection method eliminates the problem of separating the signal for oxo8dG from those of normal deoxynucleosides. The quantitation of oxo8dG and oxo8Gua in biological fluids is noninvasive and complements the measurement of oxo8dG in DNA by estimating the rate of oxidative DNA damage occurring within the body or in a population of cells. This analytical approach may allow one to estimate oxidative DNA damage in an animal or individual exposed to prooxidant conditions associated with lifestyle, genetic predisposition, degenerative diseases, or environmental toxins. Furthermore, these assays may allow one to assess the potentially beneficial effects of intervention strategies that protect DNA from such damage.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

Altered monamine metabolism in caudate-putamen of iron-deficient rats.

The effect of iron deficiency on brain monoamine metabolism using in vivo microdialysis techniques has not been previously reported. We, therefore, examined the monoamines, dopamine and norepinephrine, and their metabolites at steady state by in vivo microdialysis in rat brain caudate-putamen in 11-week-old iron-deficient anemic (hemoglobin < 7 g/dl) and control rats (Hb > 14 g/dl). Caudate-putamen dopamine (DA), dihydroxyphenyl acetic acid (DOPAC), and homovanillic acid (HVA) concentrations were increased by 53%, 57%, and 30% (p < 0.001), respectively, in iron-deficient rats in samples collected over a 4-h period. While diminished numbers of D2 receptors have been previously reported, the present findings suggest an additional defect in monoamine uptake and catabolism.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Cytogenetic analysis of soft tissue sarcomas. Recurrent chromosome abnormalities in malignant peripheral nerve sheath tumors (MPNST).

Malignant peripheral nerve sheath tumors (MPNST) are known to develop in patients with neurofibromatosis 1 (NF1), thus providing an excellent model for the study of multistep carcinogenesis in genetically predisposed individuals. To determine the sites of gene(s) involved in such a process, we have performed cytogenetic analysis on 10 tumors. The patients were five males and five females ranging in age from 15 to 77 years. Nine patients had NF1. Karyotypic analysis of these tumors exhibited complex clonal abnormalities of several chromosomes. Recurrent abnormalities (numerical as well as structural) of chromosomes 1, 11, 12, 14, 17, and 22 occurred in a substantial proportion of tumors studied. Although abnormalities of these chromosomes have been seen in a variety of other tumors, the aberrations of chromosomes 17 and 22 are of particular interest; chromosomes 17 and 22 carry the genes for NF1 and NF2, respectively. In addition to other clonal aberrations, six tumors had abnormalities of both chromosomes 17 and 22, while three tumors only had an abnormality of chromosome 17. In eight tumors a structural abnormality of chromosome 17 included deletion or a relative deficiency of 17p; in four of the tumors there was also either deletion or rearrangement of the NF1 locus at the cytogenetic level. One tumor had monosomy of chromosome 17. The abnormality of chromosome 22 was deletion of 22q11.2-->qter. This study suggests that the germline mutation in one of the copies accompanied by loss or inactivation of the second copy of the NF1 gene and tumor suppressor gene(s) on 17p and 22q may be associated with the neoplastic transformation; abnormalities of other chromosomes may be related to progression of MPNST. Although the role of the p53 gene in carcinogenesis is well documented in several tumor types, the role of the NF2 gene or other unidentified tumor suppressor gene(s) on chromosomes 22q, 1p, 11, 12, 14 remains to be seen.

Adolescent↗
PubMed1994

Chronic mild acidosis specifically reduces functional expression of N-methyl-D-aspartate receptors and increases long-term survival in primary cultures of cerebellar granule cells.

Previous studies suggest that chronic depolarization by addition of 25 mM KCl or N-methyl-D-aspartate to primary cultures of cerebellar granule cells promotes expression of the N-methyl-D-aspartate subtype of glutamate receptor, as determined by electrophysiological responsiveness and susceptibility to excitotoxicity. Recent studies have demonstrated that acute mild acidosis reduces N-methyl-D-aspartate receptor channel activity by a non-competitive action of H+ on an extracellular site of the receptor channel complex. Since the level of N-methyl-D-aspartate receptor expression in granule cell cultures is activity-dependent, we examined whether chronic mildly acidotic culture conditions would selectively diminish the level of N-methyl-D-aspartate responsiveness in granule cells, in effect producing a functional level of expression more comparable to that observed in vivo. To test this, cerebellar granule cells from eight-day neonatal rats were grown in an HCO3-buffered medium containing elevated K+ (25 mM KCl) either under standard conditions (95% air/5% CO2, pH 7.4), or under chronic mildly acidotic conditions (90% air/10% CO2, estimated pH of 7.1). Glutamate receptor subtype expression was subsequently assessed using standard neurotoxicity assays, a quantitative immunoblotting assay for N-methyl-D-aspartate receptors and whole cell patch clamp recordings. Cells grown in the 10% CO2 environment exhibited a significant reduction in susceptibility to L-glutamate neurotoxicity (at least 10-fold), but not kainate-induced neurotoxicity, relative to cells grown in 5% CO2. In both culture conditions, L-glutamate- and kainate-induced toxicity were mediated by activation of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors, respectively, as determined by the sensitivity of agonist-induced toxicity to specific receptor antagonists. Using polyclonal antibodies generated against a peptide sequence recognizing five of eight splice variants in the common "R1" subunit of N-methyl-D-aspartate receptors, a 31% reduction in the amount of immunoreactive protein was observed in membrane preparations from cells grown in 10% CO2, relative to the amount detected in cells grown in 5% CO2. Moreover, perfusion of cells with glutamate (50 microM) in a nominally Mg(2+)-free solution containing glycine (2 microM) elicited N-methyl-D-aspartate antagonist-sensitive inward currents in proportionately fewer cells cultured in 10% CO2, relative to cells cultured in 5% CO2. Long-term survival was also significantly enhanced in cells exposed chronically to mild acidotic culture conditions, relative to cells grown under standard pH conditions (22 days, 10% CO2 vs 16 days, 5% CO2).(ABSTRACT TRUNCATED AT 400 WORDS)

Acidosis↗
PubMed1994

Inhibition of wheat embryo calcium-dependent protein kinase by acridines and azaacridines.

The inhibition of wheat Ca(2+)-dependent protein kinase (CDPK) by substituted acridines and substituted 5-, 6-, 7- and 8-azaacridines (5-AA, 6-AA, 7-AA and 8-AA) was examined. Of a total of 71 substituted acridines and azaacridines examined, only 20 have IC50 values for wheat CDPK of less than 200 microM. Of these, effective compounds all have neutral or basic 4-substituents, except for 2,7-dibromo-4-carboxy-5-AAO (IC50 73 microM), the carboxymethyl ester of which is a much better inhibitor (IC50 20 microM). There is a large aza position effect so that various 4-substituted azaacridines can be either very active or very poor inhibitors depending upon the azaacridine nucleus substituted. One of the most potent inhibitors found is the 8-AA 4-N-(2-dimethylaminoethyl)carboxamide (4-P) derivative (IC50 1.5 microM), but the corresponding 4-substituted acridine analogue is a very poor inhibitor. Other potent inhibitors found include 1-nitro-4-P-8-AA (IC50 4 microM) and 7-bromo-4-methyl-5-AA (IC50 0.7 microM). These potent and relatively specific CDPK inhibitors may be useful in obtaining evidence for CDPK involvement in plant cell responses to specific signals.

Acridines↗
PubMed1994

Selective distribution of medial thickening in the renal vessels in experimental hypertension.

Direct effects, especially the distribution of medial thickening due to chronic hypertension on the renal arterial tree, were examined pathologically and morphometrically in cats with one-kidney DOCA-salt hypertension. Twenty-one adult male cats were divided into three groups: (i) an experimental group of one-kidney DOCA-salt hypertension (12 cats): (ii) a uninephrectomized group without administration of DOCA and salt (four cats); and (iii) a group without uninephrectomy and administration of DOCA and salt (five cats). The duration of hypertension varied from 3 weeks to 4 months and the aortic blood pressure was monitored every 5 min. The increase of mean blood pressure (MBP) of the experimental group was 15-44 mmHg. A significant medial thickening of the right renal arterial tree was evaluated by a comparison of the right and left regression lines of each case between the midwall radius (R) and medial thickness (D) of arteries in a distended state. The evaluation was made separately for arteries with R values above or below 40 microns, because a regression line between R and D showed a maximum bend at a level of R from 30 to 40 microns. The arteries of the right kidney with a diameter less than 40 microns, corresponding to the interlobular arteries and afferent arterioles, showed significant medial thickening in six cases. Medial thickening was absent in other cats of the experimental group and cats of a control group given uninephrectomy alone. Increase of MBP during the hypertensive phase of these six cases was above 34.6 mmHG and all values of other cats without medial thickening were below this level.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Chromosome-mediated 2,3-dihydroxybenzoic acid is a precursor in the biosynthesis of the plasmid-mediated siderophore anguibactin in Vibrio anguillarum.

We have isolated a recombinant clone harboring the chromosomal aroC gene, encoding chorismate synthase, from Vibrio anguillarum 775 by complementation of the Escherichia coli aroC mutant AB2849 which was transfected with a cosmid gene bank of the plasmidless V. anguillarum H775-3. The nucleotide sequence was determined, and an open reading frame that corresponds to a protein of 372 amino acids was found. The calculated mass of 40,417 Da was correlated with the size of the V. anguillarum aroC product detected in vitro. The homology of the V. anguillarum aroC gene to the aroC genes of E. coli and Salmonella typhi is 68% at the nucleotide level and 78% at the protein level. The expression of the aroC transcript is not regulated by iron, as determined by Northern (RNA) blot hybridization analysis. After insertion of an antibiotic resistance gene cassette within the cloned aroC gene, an aroC mutant of V. anguillarum was generated by allelic exchange. This mutant is deficient in the production of 2,3-dihydroxybenzoic acid (2,3-DHBA). Our bioassay and complementation experiments with this mutant demonstrate that the chromosome-mediated 2,3-DHBA is a precursor of the pJM1 plasmid-mediated siderophore anguibactin.

Amino Acid Sequence↗