Biomedical subjects

C Chen

Publications and source records attributed to C Chen.

At least 181 records · Page 10Linked to original sources

PubMed2001

DNA-mediated protection against classical swine fever virus.

Four eukaryotic expression plasmids containing the entire E2 gene sequence of classical swine fever virus (CSFV) were constructed: (a) pcDST, with 5' signal and 3' transmembrane sequences; (b) pcDSW, with 5' signal sequence only; (c) pcDWT, with transmembrane sequences only; and (d) pcDWW, containing the E2 gene alone. All four plasmids were readily transfected into BHK-21 cells, with pcDST and pcDSW resulting in secretion of E2 antigen. The latter two plasmids were also shown to induce a humoral immune response against CSFV in mice when administered intramuscularly, but no immune responses were detected with either pcDWT or pcDWW. The antibody level elicited by pcDSW was higher than that induced by pcDST. When pcDSW was used to immunize rabbits and pigs, both species were shown to be protected from challenge with virulent CSFV (hog cholera lapinized virus for rabbits and Shimen strain for pigs).

Animals↗

PubMed2001

Evidence that silencing of the HPRT promoter by DNA methylation is mediated by critical CpG sites.

The strong correlation between promoter hypermethylation and gene silencing suggests that promoter methylation represses transcription. To identify methylation sites that may be critical for maintaining repression of the human HPRT gene, we treated human/hamster hybrid cells containing an inactive human X chromosome with the DNA demethylating agent 5-azadeoxycytidine (5aCdr), and we then examined the high resolution methylation pattern of the HPRT promoter in single cell-derived lines. Reactivation of HPRT correlated with complete promoter demethylation. In contrast, the 61 5aCdr-treated clones that failed to reactivate HPRT exhibited sporadic promoter demethylation. However, three specific CpG sites remained methylated in all unreactivated clones, suggesting these sites may be critical for maintaining transcriptional silencing of the HPRT gene. Re-treatment of partially demethylated (and unreactivated) clones with a second round of 5aCdr did not increase the frequency of HPRT reactivation. This is consistent with mechanisms of methylation-mediated repression requiring methylation at specific critical sites and argues against models invoking overall levels or a threshold of promoter methylation. Treatment of cells with the histone deacetylase inhibitor, trichostatin A, failed to reactivate HPRT on the inactive X chromosome, even when the promoter was partially demethylated by 5aCdr treatment, suggesting that transcriptional repression by DNA methylation is unlikely to depend upon a trichostatin A-sensitive histone deacetylase.

Alleles↗

PubMed2001

The role of c-Myb in the up-regulation of methionine adenosyltransferase 2A expression in activated Jurkat cells.

Methionine adenosyltransferase (MAT) is a critical cellular enzyme which catalyses the formation of S-adenosylmethionine (SAM), the principal methyl donor. In mammals, two different genes, MAT1A and MAT2A, encode liver-specific and non-liver-specific MATs, respectively. SAM level increases during T-lymphocyte activation and is required for proliferation. A major mechanism for the increase in SAM level is increased MAT2A transcription. In the current work we examined the molecular mechanism of increased MAT2A expression in activated Jurkat cells. Treatment of Jurkat cells with interleukin-2 (IL-2), PMA or PMA plus phytohaemagglutinin (PHA) resulted in a 2-fold increase in MAT2A mRNA levels and a 2-fold increase in luciferase activity driven by the transfected human MAT2A promoter construct -571/+60 but not -270/+60. The region -571 to -270 of the human MAT2A contains a c-Myb consensus binding site. c-Myb is known to be induced during T-lymphocyte activation and its mRNA level was increased after treatment of Jurkat cells with IL-2, PMA or PMA plus PHA. Increased nuclear binding to the MAT2A c-Myb site was confirmed on electrophoretic mobility-shift and supershift analyses. Mutation of the MAT2A c-Myb site abolished the stimulatory effect of these agents on c-Myb nuclear binding and MAT2A promoter activities. Overexpression of c-Myb increased MAT2A promoter activity by 2-fold. Dexamethasone, a known inhibitor of lymphocyte activation, blocked the effect of these agents on MAT2A expression by preventing the increase in c-Myb expression.

Cell Extracts↗

PubMed2001

A computationally simple test of homogeneity of odds ratios for twin data.

It is of interest to compare measures of association of binary traits among samples of bivariate data. One example is the comparison of association within a sample of monozygotic (MZ) twins to that within a sample of dizygotic (DZ) twins. A larger association in the MZ twins suggests that the trait of interest may have a genetic component. The Bivariate data in this example are binary traits for the twins in each pair. Another example is the comparison of a measure of Hardy-Weinberg disequilibrium across several populations. The bivariate data in this example are the two alleles comprising the genotype of interest. We propose using derived logistic regression equations from the full exponential model for the bivariate outcomes to test for homogeneity. We adjust for correlation among outcomes via generalized estimating equations. This modeling approach allows for adjustment for individual-level and pair-level covariates and thereby allows for testing for gene x environment interactions. Further, we extend the model to allow for simultaneous analysis of two diseases, which allows for testing for a genetic component to the coaggregation of two diseases. In contrast to approaches proposed by previous authors, no special software is required; our approach can be easily implemented in standard software packages. We compare our results to those of other methods proposed in the literature for data from the Vietnam Era Twins Study. We apply our methods also to the Anqing Twin Study and to data on major depression and generalized anxiety disorder from the Virginia Twin Register.

Disease↗

PubMed2001

Defining a common region of deletion at 13q21 in human cancers.

Previous molecular genetic analyses identified a region of deletion at 13q21 in a variety of human cancers, suggesting the existence of a tumor suppressor gene(s) at this locus. In our earlier study on prostate cancer, the region of deletion was confined to a 3.1 cM interval between D13S152 and D13S162. At present, however, no known gene located in this interval has been firmly implicated in cancer, and the region remains too large for gene identification. To fine-map the area of interest, we established a contig of bacterial artificial chromosome (BAC) clones, narrowed the region of deletion by loss of heterozygosity (LOH) and homozygosity-mapping-of-deletion (HOMOD) analyses in different types of cancers, and tested a candidate gene from the region for mutation and alteration of expression in prostate cancers. The contig consisted of 75 overlapping BAC clones. In addition to the generation of 47 new sequence-tagged-site (STS) markers from the ends of BAC inserts, 76 known STS and expressed sequence tag markers were mapped to the contig (25 kb per marker on average). The minimal region of deletion was further defined to be about 700 kb between markers D13S791 and D13S166 by LOH analysis of 42 cases of prostate cancer, and by HOMOD analysis of eight prostate cancer cell lines/xenografts and 49 cell lines from cancers of the breast, ovary, endometrium, and cervix, using 18 microsatellite markers encompassing the deletion region. A gene that is homologous to the WT1 tumor suppressor gene, AP-2rep (KLF12), was mapped in this region and was analyzed for its expression and genetic mutation. In addition to low levels of expression in both normal and neoplastic cells of the prostate, this gene did not have any mutations in a group of aggressive prostate cancers and cell lines/xenografts, as assessed by the methods of polymerase chain reaction-single strand conformational polymorphism analysis and direct sequencing. These studies suggest that a 700 kb interval at 13q21 harbors a tumor suppressor gene(s) that seems to be involved in multiple types of cancer, and that the AP-2rep gene is unlikely to be an important tumor suppressor gene in prostate cancer. The BAC contig and high-resolution physical map of the defined region of deletion should facilitate the cloning of a tumor suppressor gene(s) at 13q21.

Chromosome Deletion↗

PubMed2001

Correlation of the apparent diffusion coefficient and the creatine level in early ischemic stroke: a comparison of different patterns by magnetic resonance.

It has been reported that reduction of the apparent diffusion coefficient (ADC) after stroke can persist for several days, after which the ADC increases gradually to an abnormally high level. We evaluated ADC values of stroke lesions and compared the results to the cellular density of the lesion by means of the creatine (Cre) level. This two-parameter estimation is of particular relevance in ascertaining the underlying cellular status. Lesion-to-contralateral ADC ratios (ADCn) were obtained based on diffusion-weighted echo-planar and fast spin-echo imaging. Single-voxel localized spectroscopy was used for quantification of cerebral metabolites in infarcted regions. Their levels were also compared to that in homotopic contralateral regions. Fifteen patients with ischemic stroke were examined at times ranging from 18-88 hours following the onset of symptoms. In the stroke lesion, there was a significant correlation between the ADC and the Cre level showing that the higher the cell density the lower the ADC value. For ADCn vs. the lesion Cre concentration and the lesion-to-contralateral Cre ratio (Cre(n)), the strengths of relationship were R2 = 0.70 and 0.58, respectively. It is concluded that ADC is a good reflection of cell density. Greatly lowered ADC values occur within the context of a stable cellularity. ADC and the Cre level have complementary roles in the characterization of stroke lesion with regard to the sequential stage.

Adult↗

PubMed2001

An 800-kb region of deletion at 13q14 in human prostate and other carcinomas.

Deletions of regions at 13q14 have been detected by various genetic approaches in human cancers including prostate cancer. Several studies have defined one region of loss of heterozygosity (LOH) at 13q14 that seems to reside in a DNA segment of 7.1 cM between genetic markers D13S263 and D13S153. To define the smallest region of overlap (SRO) for deletion at 13q14, we first applied tissue microdissection and multiplex PCR to detect homozygous deletion and/or hemizygous deletion at 13q14 in 134 prostate cancer specimens from 114 patients. We detected deletions at markers D13S1227, D13S1272, and A005O48 in 13 (10%) of these tumor specimens. Of the 13 tumors with deletions, 12 were either poorly differentiated primary tumors or metastases of prostate cancer. To fine-map the deletion region, we then constructed a high-resolution YAC/BAC/STS/EST physical map based on experimental and database analyses. Several markers encompassing the deletion region were analyzed for homozygous deletion and/or hemizygous deletion in 61 cell lines/xenografts derived from human cancers of the prostate, breast, ovary, endometrium, cervix, and bladder, and a region of deletion was defined by duplex PCR assay between markers A005X38 and WI-7773. We also analyzed LOH at 13q14 in the 61 cell lines/xenografts using the homozygosity mapping of deletion approach and 26 microsatellite markers. We found 24 (39%) of the cell lines/xenografts to show LOH at 13q14 and defined a region of LOH by markers M1 and M5. Combination of homozygous or hemizygous deletion and LOH results defined the SRO for deletion to be an 800-kb DNA interval between A005X38 and M5. There are six known genes located in or close to the SRO for deletion. This region of deletion is at least 2 Mb centromeric to the RB1 tumor-suppressor gene and the leukemia-associated genes 1 and 2, each of which is located at 13q14. These data suggest that the 800-kb DNA segment with deletion contains a gene whose deletion may be important for the development of prostate and other cancers. This study also provides a framework for the fine-mapping, cloning, and identification of a novel tumor-suppressor gene at 13q14.

Adult↗

PubMed2001

Complete suppression of insulitis and diabetes in NOD mice lacking interferon regulatory factor-1.

Interferon regulatory factor-1 (IRF-1), a transcriptional factor, regulates type I interferon and interferon-induced genes. It was reported that IRF-1 regulates important molecules required for inflammation and immune reactions. To investigate the role of IRF-1 in the development of autoimmune diabetes, we established IRF-1 deficient (IRF-1(-/-)) non-obese diabetic (NOD) mice. IRF-1-deficient C57BL/6J mice were out-crossed to NOD mice, and F1 were backcrossed to NOD mice. At the N8 generation, the heterozygote for IRF-1 mutation was intercrossed and N8F1 was obtained. Out of three NOD genotypes, IRF-1(+/+) and IRF-1(+/-) developed spontaneous diabetes with an incidence of 47% (9/19) and 50% (10/20) by 30 weeks of age, respectively; whereas IRF-1(-/-) did not develop diabetes (0/18, P< 0.01 vs. (+/+) and (+/-)). Histologically, IRF-1(+/+) and IRF-1(+/-) had various degrees of insulitis, but IRF-1(-/-) had no insulitis. In comparison with IRF-1(+/+), the percentage of CD4(+) and Mac-1(+) splenic cells significantly increased, whereas CD3(+), CD8(+) and B220(+) cells decreased in IRF-1(-/-). Furthermore, spleen cell proliferation in response to Con A or murine GAD65 peptide, a major autoantigen of the pancreatic beta-cell, significantly increased, and the IFN-gamma/IL-10 ratio in the culture supernatant significantly decreased in IRF-1(-/-), suggesting Th2 deviation in cytokine balance. These results indicate that IRF-1 plays a key role in developing insulitis and diabetes in NOD mice.

Animals↗

PubMed2001

Opposing effects of delta and xi PKC in ethanol-induced cardioprotection.

Low amounts of ethanol reduce cardiac damage induced by ischemia. The protection from ischemic damage by acute exposure to low amounts of ethanol in isolated myocytes and intact heart have been attributed to activation of protein kinase C (PKC). We previously found that two PKC isozymes, delta and xi, are activated by ethanol in several cell models. Here, we perfused isozyme-selective agonist and antagonist peptides that we have generated into intact heart to determine the role of these two isozymes in ethanol-induced protection from transient ischemia. Whereas xi PKC activation was required for ethanol-induced protection, delta PKC activation led to further damage. These data explain the conflicting reports on the role of acute exposure to ethanol in protection from cardiac ischemia. The clinical implications of these findings are also discussed.

Animals↗

PubMed2001

Effects of nicotine and cotinine on porcine arterial endothelial cell function.

UNLABELLED: BACKGROUND. There has been a significant amount of research on the effects of nicotine on vascular biology; however, little is known about the effects of cotinine, the metabolic product of nicotine. This study used a novel vascular perfusion system to study the effects of nicotine and cotinine on the vascular endothelial cell function. METHODS: Porcine common carotid arteries were cultured in a novel vascular perfusion system with nicotine or cotinine or as controls. After 24 h, vessels were precontracted with norepinephrine and subsequently relaxed with acetylcholine. Vessel diameters were recorded and analyzed. After culture, samples were taken for en face, immunohistochemistry, and RT-PCR for eNOS. Porcine coronary arteries were incubated as controls or with nicotine or cotinine and tested on a myograph system to measure contraction and relaxation. RESULTS: Porcine carotid arteries treated with nicotine and cotinine showed a 27.2% and a 41.2% reduction in endothelial-dependent relaxation, respectively, as compared to control vessels (P<0.05). Rings of coronary arteries treated with nicotine relaxed similarly to control rings while cotinine-treated rings failed to relax to endothelial-dependent stimulation. RT-PCR for eNOS mRNA showed a 23. 2 and a 24.1% reduction in eNOS expression for nicotine- and cotinine-treated vessels, respectively (P<0.01). Additionally, immunohistochemical staining for eNOS showed less dense staining on nicotine- and cotinine-treated vessels as compared to controls. En face preparations showed normal endothelial cell morphology in all groups, but cell density decreased slightly in vessels treated with nicotine and cotinine. CONCLUSION: These results indicate that cotinine may have even more effect on the impairment of endothelial-dependent vasorelaxation than nicotine for the regulation of vessel tone in porcine carotid and coronary arteries.

Animals↗

PubMed2001

Apoptosis and Fas-ligand expression correlate to the histopathological grade of gastric smooth muscle tumors.

BACKGROUND: Apoptosis is associated with the tumor grade in various types of carcinomas or lymphomas, but less is understood about the association of apoptosis in mesenchymal tumors. In the prior studies, expression of apoptotic regulatory proteins, Bcl-2, Fas and its ligand, Fas-ligand, has been related to apoptotic index (AI) and histopathological grade of tumors. Our study investigated the incidence of apoptosis in gastric smooth muscle tumor and the correlation of the apoptotic index (AI) with the histopathological grade of the tumors. We evaluated the relationship of apoptotic regulatory proteins to the AI and tumor grade. METHODS AND MATERIALS: Using immunohistochemistry and the terminal deoxynucleotidyl transferase (TdT)-mediated digoxigenin-dUTP nick end-labeling (TUNEL) assay, we analyzed the expression of Bcl-2, Fas, Fas-ligand, and AI in 26 cases of gastric smooth muscle tumors. RESULTS: The incidence of greater than 10 apoptotic cells per 10 high-power fields (HPFs) was 73% (19/26 cases). The AI was significantly associated with malignant tumors (P = 0.006) and mitotic counts (P = 0.006) but not with tumor size. Bcl-2, Fas, and Fas-ligand were detected in 13 (50%), 14 (53.8%), and 19 (73%) cases, respectively. Interestingly, Fas-ligand was significantly correlated to malignancy (P = 0.006), mitotic counts (P = 0.006), and AI (P = 0.035) but not to tumor size. Fas expression was significantly associated with high levels of AI (P = 0.014). In contrast, Bcl-2 expression was inversely associated with AI (P = 0.004). Expression of Bcl-2 and Fas did not show a statistically significant correlation with tumor grade, mitotic counts, or tumor size. CONCLUSION: Apoptosis and Fas-ligand expression are statistically correlated to the histopathological grade of gastric smooth muscle tumors. This suggests that detection of apoptotic cells and Fas-ligand expression using the TUNEL assay or immunohistochemistry are useful for the evaluation of the malignant potential of gastric smooth muscle tumors.

Adult↗

PubMed2001

Cyclosporine directly causes oxidative stress and promotes Epstein-Barr virus transformation of human B cells.

BACKGROUND: We have previously shown that oxidative stress alone can promote transformation of human B cells infected with Epstein-Barr virus (EBV) in vitro, an accepted model mimicking posttransplant lymphoproliferative disorders (PTLDs). Our laboratory has investigated the direct effects of cyclosporine A (CyA) as an oxidant promoting B-cell transformation and we have proposed that CyA directly promotes B-cell transformation and that this effect can be blocked by antioxidants. METHODS: Human splenocytes were prepared by centrifugation and plating technique to provide a greater than 80% pure preparation of B cells that was used for the direct oxidative stress experiments. These cells were cocultured with CyA (500 ng/ml) and hydrogen peroxide (H(2)O(2), 0.15 mM) with or without antioxidant vitamin E (40 microM). Oxidative stress was evaluated by using a commercial lipid hydroperoxide (LPO) assay kit. In another set of three separate experiments, human B lymphocytes infected with EBV were cultured with CyA (500 ng/ml), H(2)O(2) (0.15 mM), and vitamin E (40 microM). B-Cell transformation by EBV was evaluated by counting colony number and [(3)H]-thymidine incorporation. RESULTS: At therapeutic concentrations, CyA (500 ng/mL) had an oxidative effect on human splenocytes in vitro, similar to the effect of H(2)O(2) (90 and 97% increases, respectively in LPO production over control P < 0.005), which was abrogated by the addition of vitamin E. Similarly, both CyA and H(2)O(2) promoted transformation of B cells infected with EBV(75 and 108% increases respectively in colony counts over control, P < 0.005). This effect was also blocked by vitamin E. CONCLUSIONS: Both CyA and H(2)O(2) have a direct oxidative effect on human B cells and cause promotion of EBV-induced transformation of B cells. These effects are blocked by the antioxidant vitamin E. These findings may have future therapeutic implications for PTLDs.

Antioxidants↗

PubMed2001

In vivo proton MR spectroscopy of chorea-ballismus in diabetes mellitus.

The most common cause of chorea-ballismus (CB) is a vascular lesion; it is also associated with nonketotic hyperglycaemia in diabetes mellitus (DM) and may be the first manifestation of this disorder. We describe the CT, MRI and proton MR spectroscopy (1H-MRS) of CB in eight patients. Six had hemichorea-hemiballismus (HC-HB) and two bilateral CB. Single-voxel (SV) 1H-MRS was performed using point-resolved spectroscopy (PRESS). Voxels were positioned in the basal ganglia of the patients and control subjects. PRESS was also used to obtain spectroscopic imaging (1H-MRSI) of the slice of interest in two patients. CT showed a slightly dense striatum in all the patients with CB, and T1-weighted images revealed high signal. The CB correlated well with the neuroimaging findings. SV 1H-MRS showed the mean (+/- SD) N-acetylaspartate (NAA)/ creatine (Cr) ratio to be 1.45 +/- 0.19 in HC-HB and 1.82 +/- 0.06 on the opposite normal side (P = 0.01). The choline (Cho)/ Cr ratio was 1.3 +/- 0.12 in HC-HB and 1.11 +/- 0.13 on the opposite normal side (P = 0.005). A lactate peak was seen in seven patients. The NAA/Cr ratio was 1.44 +/- 0.15 in bilateral CB and 1.74 +/- 0.16 in the controls (P = 0.017); the Cho/Cr ratios were 1.36 +/- 0.1 and 1.19 +/- 0.07 (P = 0.015). The low NAA/Cr suggests neuronal loss or damage and the high Cho/Cr probably indicates gliosis. The presence of lactate may suggest mild ischaemia due to acute vascular events during hyperglycaemia and underlying chronic focal cerebrovascular diseases in DM.

Aged↗

PubMed2001

Over-expression of beta-1,4-galactosyltransferase I, II, and V in human astrocytoma.

PURPOSE: beta-1,4-Galactosyltransferase (beta-1,4-GalT) I, II, and V are the enzymes responsible for the biosynthesis of N-acetyllactosamine on N-glycans by transferring UDP-galactose to the terminal N-acetylglucosamine (N-GlcNAc) residues with the formation of a beta-1,4-linkage. Neoplasms undergo various changes in the carbohydrate of their glycoconjugates, indicating the possible changes in glycosyltransferases themselves. METHOD: Therefore, we compared the expression of beta-1,4-GalTs between astrocytoma and normal brain tissues. RESULTS: Our reverse-transcription polymerase chain reaction (RT-PCR) results showed that beta-1,4-GalT I transcript was absent in normal adult brain but detectable in grade II, III, and IV astrocytomas; the level of beta-1,4-GalT II transcript was increased in grade II, III, and IV astrocytomas while only a trace amount was found in normal brain; beta-1,4-GalT V transcript existed in normal brain and increased in the process of astrocytoma progress, with the highest level in grade IV astrocytoma. By Ricinus communis agglutinin-1 (RCA-1) lectin blot assay, we also found the more extensive galactosylated bands in astrocytomas compared with normal brain. A major 61kD protein was galactosylated in astrocytoma but not in normal brain tissues. CONCLUSION: These results indicate that the increase of galactosylation in astrocytomas may be caused by the alterations of gene expression of beta-1,4-GalT I, II, and V and that the malignant degree of astrocytoma is correlated with the expression of beta-1,4-GalT V.

Astrocytoma↗

PubMed2001

Fine genetic mapping and BAC contig development for the citrus tristeza virus resistance gene locus in Poncirus trifoliata (Raf.).

A map-based cloning strategy has been employed to isolate Ctv, a single dominant gene from Poncirus trifoliata that confers resistance to citrus tristeza virus (CTV), the most important viral pathogen of citrus. Cloning of this gene will allow development of commercially acceptable, virus-resistant cultivars. A high-resolution genetic linkage map of the Ctv locus region was developed using a backcross population of 678 individuals. Three DNA markers that were closely linked or co-segregated with Ctv were identified and used to screen BAC libraries derived from an intergeneric hybrid of Poncirus and Citrus. Through chromosome walking and landing, two BAC contigs were developed: one encompassing the Ctv region, and the other spanning the allelic susceptibility gene region. The resistance gene contig consists of 20 BAC clones and is approximately 550 kb in length; the susceptibility gene contig consists of 16 BAC clones and extends about 450 kb. The Ctv locus was localized within a genomic region of approximately 180 kb by genetic mapping of BAC insert ends. The BAC contigs were integrated with the genetic map; variation in the ratio of genetic to physical distance was observed in the vicinity of Ctv. Southern hybridization data indicated that a few copies of NBS-LRR class sequences are distributed at or around the Ctv locus. Efforts are being made to assign the Ctv locus to a smaller genomic fragment whose function can be confirmed through genetic complementation of a CTV susceptible phenotype. These results indicate that map-based gene cloning is feasible in a woody perennial.

Blotting, Southern↗

PubMed2001

Can we do better with postoperative pain management?

BACKGROUND: In the last decade, there has been heightened awareness that pain management needs to be a priority for all health care settings and clinicians. The article will overview practice guidelines and new technology, and assess their impact on pain relief in inpatient and outpatient surgeries from a patient's perspective. METHODS: Literature was retrieved by searches from 1996 to 2000 Medline and CINAHL (nursing database), using keywords "postoperative pain," "postsurgical pain," "patient outcomes," "pain outcomes," "survey," "questionnaire," and "practice guidelines." RESULTS: Overall, current practice standards have had minimal impact on decreasing patients' reports of pain. The incidence of moderate to severe pain with cardiac, abdominal, and orthopedic inpatient procedures has been reported as high as 25% to 50%, and incidence of moderate pain after ambulatory procedures is 25% or higher. CONCLUSIONS: Despite the advances, the incidence of pain remains high. Yet the future is promising, with new standards from the Joint Commission on Accreditation of Health care Organizations paving the way for reduction of institutional barriers and improved implementation of guidelines.

Ambulatory Surgical Procedures↗

PubMed2001

The length dependence of translational diffusion, free solution electrophoretic mobility, and electrophoretic tether force of rigid rod-like model duplex DNA.

In this work, boundary element modeling is used to study the transport of highly charged rod-like model polyions of various length under a variety of different aqueous salt conditions. Transport properties considered include free solution electrophoretic mobility, translational diffusion, and the components of the "tether force" tensor. The model parameters are chosen to coincide with transport measurements of duplex DNA carried out under six different salt/temperature conditions. The focus of the analysis is on the length dependence of the free solution electrophoretic mobility. In a solution containing 0.04 M Tris-acetate buffer at 25 degrees C, calculated mobilities using straight rod models show a stronger dependence on fragment length than that observed experimentally. By carrying out model studies on curved rod models, it is concluded that the "leveling off" of mobility with fragment length is due, in part at least, to the finite curvature of DNA. Experimental mobilities of long duplex DNA in monovalent alkali salts are reasonably well explained once account is taken of long-range bending and the simplifying assumptions of the model studies.

DNA↗

PubMed2001

Feeding behavior during sialodacryoadenitis viral infection in rats.

Sialodacryoadenitis (SDA) is a highly contagious common viral infection in rats, akin to mumps in humans. Anorexia occurs during such viral infection. But the pattern of the decrease in food intake (a decrease in either meal size and meal number or both) during spontaneous viral infection has not been previously characterized. We observed the onset of anorexia and an abnormal feeding pattern during an opportunistic SDA viral infection in our rat colony. We thus studied seven male rats. Before the viral infection there was a positive association between food intake and meal number (P<.05). After infection food intake decreased by 68%. This occurred via a significant decrease in meal size (by 69%) (P<.05); and a nonsignificant decrease in meal number (P=.71). This pattern of decreased food intake is similar to that occurring during indomethacin-induced ulcerative ileitis, where we previously measured an increase in plasma tumor-necrosis factor (TNF)-alpha. Anorexia in response to bacterial lipopolysaccharide administration, which is also linked to plasma TNF-alpha, is however, caused only via a decrease in meal number. The differences in the decrease in the feeding pattern between the SDA viral and a bacterial infection suggest that factors other than TNF-alpha alone play a significant role in the mechanism of anorexia during a viral infection.

Animals↗