Biomedical subjects

H Li

Publications and source records attributed to H Li.

At least 901 records · Page 50Linked to original sources

PubMed1999

Diagnosis of malignant catarrhal fever by PCR using formalin-fixed, paraffin-embedded tissues.

A previously described polymerase chain reaction (PCR) assay (amplification of a 238-bp fragment of ovine herpesvirus 2 [OHV-2] genomic DNA) for diagnosis of sheep-associated malignant catarrhal fever (MCF) was adapted for use on formalin-fixed, paraffin-embedded tissues. Variables affecting its use were examined. Archived tissues from cattle, white-tailed deer (Odocoileus virginianus), and bison (Bison bison) diagnosed with MCF by clinical signs or histologic lesions were obtained from 2 veterinary diagnostic laboratories. Tissues from healthy animals and from animals diagnosed with other common bovine viral diseases were examined as controls. A total of 86 blocks from 37 suspect MCF cases were examined. Forty-one blocks from healthy animals and animals with unrelated viral diseases were examined as controls. The assay was specific for sheep-associated MCF and did not yield false-positive signals from healthy animals or from cases of infectious bovine rhinotracheitis, bovine virus diarrhea, mucosal disease, or parainfluenza-3 virus infection. A wide variety of tissues were suitable substrates, including spleen, lymph node, intestine, brain, lung, and kidney. Extracted DNA provided a more suitable target than did unextracted tissue lysate. The highest levels of viral DNA were present in lymphoid organs and intestine, but the data indicate that in acute clinical cases, most organs contain sufficient viral DNA to serve as a suitable diagnostic specimen. Fixation of 0.5-cm3 blocks of tissue in 10% neutral buffered formalin was deleterious to the target DNA, and PCR signals progressively diminished after fixation for >45 days. Detection of genomic DNA of OHV-2 by PCR was successful for archived tissues that were 15 years old.

Animals↗

PubMed1999

Quantitation of sheep-associated malignant catarrhal fever viral DNA by competitive polymerase chain reaction.

A single-step, competitive polymerase chain reaction technique was developed to quantitate sheep-associated malignant catarrhal fever (SA-MCF) viral DNA. The assay employed coamplification of a fixed quantity of target DNA with graded amounts of a competitor, generated by truncation of the target sequence lying between the 2 primer binding sites. The assay yielded a linear response (r = 0.98) for DNA measurement within the range of 30-300,000 copies. Amplification efficiency analysis by coamplification of target and competitor in equal copy numbers for various numbers of cycles showed that the relative abundance of the coamplified products remained constant with increasing cycle numbers up to 40. Reproducibility was assessed by repetitively assaying a set of blind-coded samples from a variety of animals and tissues. Results indicated that the assay is reliable and reproducible for quantitation of SA-MCF viral DNA in samples from asymptomatically infected sheep and from animals with clinical SA-MCF.

Animals↗

PubMed1999

Metastasis stage, adjuvant treatment, and residual tumor are prognostic factors for medulloblastoma in children: conclusions from the Children's Cancer Group 921 randomized phase III study.

PURPOSE: From 1986 to 1992, "eight-drugs-in-one-day" (8-in-1) chemotherapy both before and after radiation therapy (XRT) (54 Gy tumor/36 Gy neuraxis) was compared with vincristine, lomustine (CCNU), and prednisone (VCP) after XRT in children with untreated, high-stage medulloblastoma (MB). PATIENTS AND METHODS: Two hundred three eligible patients with an institutional diagnosis of MB were stratified by local invasion and metastatic stage (Chang T/M) and randomized to therapy. Median time at risk from study entry was 7.0 years. RESULTS: Survival and progression-free survival (PFS) +/- SE at 7 years were 55%+/-5% and 54%+/-5%, respectively. VCP was superior to 8-in-1 chemotherapy, with 5-year PFS rates of 63%+/-5% versus 45%+/-5%, respectively (P = .006). Upon central neuropathology review, 188 patients were confirmed as having MB and were the subjects for analyses of prognostic factors. Children aged 1.5 to younger than 3 years had inferior 5-year estimates of PFS, compared with children 3 years old or older (P = .0014; 32%+/-10% v 58%+/-4%, respectively). For MB patients 3 years of age or older, the prognostic effect of tumor spread (MO v M1 v M2+) on PFS was powerful (P = .0006); 5-year PFS rates were 70%+/-5%, 57%+/-10%, and 40%+/-8%, respectively. PFS distributions at 5 years for patients with M0 tumors with less than 1.5 cm2 of residual tumor, versus > or = 1.5 cm2 of residual tumor by scan, were significantly different (P = .023; 78%+/-6% v 54%+/-11%, respectively). CONCLUSION: VCP plus XRT is a superior adjuvant combination compared with 8-in-1 chemotherapy plus XRT. For patients with M0 tumors, residual tumor bulk (not extent of resection) is a predictor for PFS. Patients with M0 tumors, > or = 3 years with < or = 1.5 cm2 residual tumor, had a 78%+/-6% 5-year PFS rate. Children younger than 3 years old who received a reduced XRT dosage had the lowest survival rate.

Adolescent↗

PubMed1999

Tissue-specific, hormonal, and developmental regulation of SCC-LacZ expression in transgenic mice leads to adrenocortical zone characterization.

We report here the study of the human CYP11A1 promoter in driving tissue-specific, developmentally and hormonally regulated reporter gene expression. A 4.4-kb fragment containing all known regulatory elements is more efficient than a short basal promoter fused to an upstream adrenal enhancer in driving reporter LacZ gene expression both in cell culture and in transgenic mice. The LacZ gene controlled by the 4.4- and 2.3-kb promoters was expressed in the adrenal cortex, testicular Leydig cells, ovarian corpora lutea, and granulosa cells. Transgene expression in the adrenals was stimulated by ACTH, indicating the presence of ACTH-responsive sequence. Beta-galactosidase activity was first detected in the adrenal primordia at 11.5 days postcoitum. Its expression continued throughout all stages of adrenal development in a pattern similar to that of the endogenous CYP11A1, which was expressed in all zones of the adrenal cortex, but was strongest in the X zone. The X zone grew before puberty but regressed afterward, as did the levels of CYP11A1 and LacZ gene expression in the X zone. Our study of the CYP11A1 promoter in transgenic mice led to characterization of the adrenocortical zones.

Adrenal Cortex↗

PubMed1999

Developmental expression of the peripheral-type benzodiazepine receptor and the advent of steroidogenesis in rat adrenal glands.

Although the precise mechanism whereby cholesterol is transported across the outer mitochondrial membrane is uncertain, a multimeric receptor complex termed the peripheral-type benzodiazepine receptor (PBR) appears essential for this process. We therefore predicted that adrenal cells at different developmental stages would express PBR coincidentally with the advent of steroidogenesis. Adrenals of neonatal rats demonstrate greatly reduced sensitivity to ACTH that gradually increases after the first 2 weeks of life. Thus, neonates have lower circulating corticosterone levels following exposure to stress. We examined mitochondrial PBR ligand binding activity, immunoreactive (ir) PBR content, and adrenal sensitivity to ACTH in vivo and in vitro. Ontogeny of both mitochondrial PBR ligand binding capacity and irPBR directly paralleled that of ACTH-inducible steroidogenesis in isolated rat adrenal cells and in rats injected with ACTH. In addition, neonatal PBR had approximately 2-fold higher affinity for PK11195, a synthetic ligand that binds with high affinity to PBR. No correlation was observed during neonatal life between ir-steroidogenic acute regulatory (StAR) protein content and steroidogenesis. These results are consistent with the hypothesis that PBR is an absolute prerequisite for adrenocortical steroidogenesis, and suggest that the stress hyporesponsive period of neonatal rats may result from decreased PBR expression. In addition, the higher affinity of neonatal PBR and the relatively high basal expression of StAR protein in neonatal adrenals may partly explain the high constitutive steroidogenesis characteristic of neonatal rat adrenal cells.

Adrenal Glands↗

PubMed1999

Diagnosis of hidden central hypothyroidism in survivors of childhood cancer.

To determine how often central hypothyroidism remains undetected by routine out-patient tests of thyroid hormone, we studied 208 pediatric cancer survivors referred for evaluation because of signs of subtle hypothyroidism or hypopituitarism. Of the 208 (68 females and 140 males), 110 had brain tumors, 14 had other head/neck tumors, 11 had solid tumors remote from head and neck, and 73 had leukemia. Patients were evaluated 1-16 yr (mean, 6.1+/-4.1 yr) after tumor diagnosis. The nocturnal TSH surge and response to TRH were measured. Of 160 patients with free T4 in lowest third of normal, 34% had central hypothyroidism (blunted TSH surge or low/delayed TSH peak or delayed TSH decline after TRH); 9% had central hypothyroidism with mild TSH elevation (mixed hypothyroidism). Another 16% had mild primary hypothyroidism (TSH, 5-15 mU/L). Of 48 with free T4 in the upper two thirds of normal, 14% had central hypothyroidism; 17% had mild primary hypothyroidism. Incidence of central, mixed, and mild primary hypothyroidism 10 yr after tumor diagnosis was significantly related to total cranial radiation dose (P < 0.0001). Of 62 patients with central hypothyroidism, 34% had not developed GH deficiency. TSH surge identified 71%, and response to TRH identified 60% of those with central hypothyroidism. More than half of the slowly growing patients who have received cranial or craniospinal radiation for childhood cancer develop subtle hypothyroidism. In our study group, 92% of patients with central hypothyroidism and 27% with mixed hypothyroidism would have remained undiagnosed using baseline thyroid function tests alone. Both TSH surge and response to TRH must be evaluated to identify all of these patients.

Adolescent↗

PubMed1999

The effect of kampo formulae on bone resorption in vitro and in vivo. II. Detailed study of berberine.

We previously isolated berberine from aqueous extracts of tsu-kan-gan, a Kampo formula used for the treatment of osteoporosis. Berberine caused an inhibitory effect on parathyroid hormone (PTH)-stimulated bone resorption in neonatal mouse bone. In this report we describe the inhibitory effect of berberine on the formation of osteoclast-like multinucleated cells (OCLs) in the co-culture of mouse osteoblastic cells and bone marrow cells in the presence of 1alpha,25-dihydroxyvitamin D3 [1alpha,25(OH)2D3], PTH and interleukin-1alpha (IL-1alpha). Berberine dose-dependently inhibited the formation of tartrate-resistant acid phosphatase (TRAP)-positive OCLs induced by 1alpha25(OH)2D3, PTH and IL-1alpha. We prepared OCLs in the co-culture of osteoblastic cells and bone marrow cells. The effect of berberine on pit formation by OCLs was examined using dentin slices. As OCLs are terminally differentiated multinucleated cells, the survival of OCLs affects the bone-resorbing activity of OCLs. This prompted us to count the number of TRAP-positive OCLs on the slices. Berberine dose-dependently inhibited pit formation and caused a decrease in the number of TRAP-positive OCLs. Calcitonin (CT) inhibited pit formation without affecting the number of OCLs. Berberine accelerated the cell death in OCLs cultivated on a culture plate, but CT did not affect the cell death of OCLs. This suggests that the decrease in the number of OCLs on dentin slices may be due to apoptotic cell death in OCLs. In fact, Hoechst 33258 staining revealed that the treatment of OCLs with berberine resulted in condensed nuclei and a decrease in cell size. Oral administration of the berberine (30 and 50 mg/kg/d) to ovariectomized rats prevented a decrease in bone mineral density (BMD) of the lumbar vertebra without affecting the weight of the uterus and plasma concentration of estradiol. These results suggested that berberine prevented a decrease in BMD in vivo by inhibiting osteoclastic bone resorption.

Animals↗

PubMed1999

Effects of removal of stratum corneum, delipidization and addition of enhancers, ethanol and l-menthol, on skin permeation of benzoic acid and its 4-n-alkyl substituents in excised guinea pig dorsal skin.

Skin penetration of benzoic acid and its 4-alkyl substituents (methyl, ethyl, n-propyl and n-butyl) through excised guinea pig dorsal skin was examined, and effects of removal of stratum corneum, delipidization and addition of the penetration enhancers, ethanol and l-menthol plus ethanol, were observed. Permeability coefficients, which increased with the increase in their alkyl chain lengths, depended on the ratio of undissociated form of the derivatives. Removal of stratum corneum by tape stripping and delipidization by a chloroform-methanol mixture, whose effects on the permeation were similar, increased the permeability coefficients of the derivatives, especially those of relatively hydrophilic derivatives. Addition of 1% l-menthol plus 15% ethanol increased the permeability coefficient of benzoic acid, but decreased those of ethyl-, n-propyl- and n-butyl-substituents, and differences in the permeability coefficients among these acids almost disappeared. A similar though weaker tendency was observed for the effects of 15% ethanol itself. Analysis of transfer free energy of the methylene group from vehicle to skin revealed that tape stripping and delipidization induced the reduction of lipophilic barrier property, although it still remained after these treatments. The analysis also showed that the addition of the enhancers made the skin relatively more hydrophilic compared to the vehicle, which induced an increase in permeability coefficient of benzoic acid and decreases in those of its lipophilic substituents.

Animals↗

PubMed1999

Sensitization components of post-traumatic stress disorder: implications for therapeutics.

Behavioral sensitization to psychomotor stimulants and stressors involves increasing reactivity to repetition of the same dose (or intensity) of the stimulus over time. In cocaine-induced behavioral sensitization, conditioned components are prominent and the underlying pharmacological and neuroanatomical substrates differ as a function of stage of its evolution. Since there is cross-sensitization between cocaine-induced behavioral sensitization and stress-induced behavioral sensitization and, as well, a high comorbidity of stimulant abuse with post-traumatic stress disorder, many of the mechanisms and principles of cocaine-induced behavioral sensitization may be pertinent to post-traumatic stress disorder. The extent and duration of cocaine-induced behavioral sensitization/stress-induced behavioral sensitization are a function of age, genetic strain, and gender of the organism, as well as magnitude, frequency, duration, quality, and environmental contingencies of the inducing stimuli. These effect a spatiotemporal evolution of cascades of alterations in gene expression involving a host of immediate early and late effector genes, including neurotrophic and apoptotic factors. They may change the physiology, biochemistry, and neuroanatomy of the developing brain and, in adults, substrates critical for learning and memory. Suggestions are made for differential strategies of therapeutic intervention as primary prevention, in the immediate post-traumatic period, and in the late phases of post-traumatic stress disorder evolution.

Animals↗

PubMed1999

GnRH agonist treatment decreases progesterone synthesis, luteal peripheral benzodiazepine receptor mRNA, ligand binding and steroidogenic acute regulatory protein expression during pregnancy.

We have demonstrated that continuous administration of a gonadotropin-releasing hormone agonist (GnRH-Ag) suppresses luteal steroidogenesis in the pregnant rat. We further demonstrated that the peripheral-type benzodiazepine receptor (PBR) and the steroidogenic acute regulatory protein (StAR) play key roles in cholesterol transport leading to steroidogenesis. The purpose of this study was to understand the cellular and molecular mechanisms involved in the suppression of luteal steroidogenesis leading to a fall in serum progesterone levels in GnRH-Ag-treated rats during early pregnancy. Pregnant rats were treated individually starting on day 8 of pregnancy with 5 microgram/day GnRH-Ag using an osmotic minipump. Sham-operated control rats received no treatment. At 0, 4, 8 and 24 h after initiation of the treatment, rats were killed and corpora lutea (CL) were removed for PBR mRNA, protein and radioligand binding analyses, immunoblot 1-D gel analysis of StAR, P450 scc and 3beta-hydroxysteroid dehydrogenase as well as 2-D gel analysis of StAR. The treatment decreased the luteal PBR mRNA expression at all time periods starting at 4 h compared with that in corresponding sham controls. GnRH-Ag also reduced, in the CL, the PBR protein/ligand binding, the StAR protein and P450 scc protein and its activity as early as 8 h after the treatment and they remained low compared with those in corresponding sham controls. The data from 2-D gel studies suggest that the majority of the decrease in StAR protein appears to be in the phosphorylated forms of StAR. Thus, we have demonstrated, for the first time, the presence of PBR and StAR in the pregnant rat CL and that the coordinated suppression of these proteins involved in the mitochondrial cholesterol transport along with P450 scc by GnRH-Ag leads to reduced ovarian steroidogenesis.

3-Hydroxysteroid Dehydrogenases↗

PubMed1999

Clinical and genetic characteristics of type 2 diabetes with and without GAD antibodies.

The aim of the study was 1) to establish the prevalence of GAD antibodies (GADab) in a population-based study of type 2 diabetes in western Finland, 2) to genetically and phenotypically characterize this subgroup, and 3) to provide a definition for latent autoimmune diabetes in adults (LADA). The prevalence of GADab was 9.3% among 1,122 type 2 diabetic patients, 3.6% among 558 impaired glucose tolerance (IGT) subjects, and 4.4% among 383 nondiabetic control subjects. Islet antigen 2 antibodies (IA2ab) or islet cell antibodies were detected in only 0.5% of the GADab- patients. The GADab+ patients had lower fasting C-peptide concentrations (median [interquartile range]: 0.46 [0.45] vs. 0.62 [0.44] nmol/l, P = 0.0002) and lower insulin response to oral glucose compared with GADab- patients. With respect to features of the metabolic syndrome, the GADab+ patients had lower systolic (140 [29.1] vs. 148 [26.0] mmHg, P = 0.009) and diastolic (79.2 [17.6] vs. 81.0 [13.1] mmHg, P = 0.030) blood pressure values, as well as lower triglyceride concentrations (1.40 [1.18] vs. 1.75 [1.25] mmol/l, P = 0.003). GADab+ men had a lower waist-to-hip ratio compared with GADab- patients. Compared with GADab- patients and control subjects, the GADab+ patients had an increased frequency HLA-DQB1*0201/0302 (13 vs. 4%; P = 0.002) and other genotypes containing the *0302 allele (22 vs. 12%; P = 0.010). However, the frequency of these high-risk genotypes was significantly lower in GADab+ type 2 patients than in type 1 diabetes of young or adult onset (0201/0302 or 0302/X: 36 vs. 66 vs. 64%, P < 0.001). The GADab+ type 2 group did not differ from control subjects with respect to genotypes containing the protective DQB1-alleles *0602 or *0603, nor with respect to the type 1 high-risk genotype in the IDDM1 (Hph1 +/+). We conclude that GADab+ patients differ from both GADab- type 2 diabetic patients and type 1 diabetic patients with respect to beta-cell function, features of the metabolic syndrome, and type 1 diabetes susceptibility genes. Further, we propose that LADA be defined as GADab positivity (>5 relative units) in patients older than 35 years at onset of type 2 diabetes.

Alleles↗

PubMed1999

Effects of graft-versus-host reaction on intrahepatic islet transplants.

The use of donor-specific bone marrow transplantation might represent a valuable approach for the induction of hyporesponsiveness to concurrent allogeneic organ and tissue grafts. In this setting, the occurrence of subclinical forms of graft-versus-host reaction (GVHR) can seldom be formally ruled out. When systemic administration of donor-specific bone marrow is performed together with intraportal transplantation of islets of Langerhans, GVHR might damage the implanted islets through an innocent bystander mechanism. The liver is, in fact, a prominent target of GVHR, and islets are sensitive to the noxious effects of proinflammatory mediators, including selected cytokines produced during GVHR. A parent (Lewis) to F1 (Lewis x Brown Norway) splenocyte transfer model was used to induce GVHR in rats. Islets were also obtained from Lewis donors and implanted into F1 recipients to examine the effects of GVHR on islet function in the absence of rejection. Selected doses of splenocytes were infused in F1 recipients to induce GVHR. When 150 x 10(6) cells were administered, all recipients developed clinical lethal GVHR. When 100 x 10(6) or 80 x 10(6) cells were given, lethal GVHR was observed in 40 and 20% of the F1 animals, respectively. A transient clinical syndrome occurred in the remaining animals and spontaneously subsided; histological findings consistent with persistent low-grade GVHR were observed in these animals at the time of death several months after splenocyte inoculation. When simultaneous splenocyte infusions and islet grafts were performed in chemically diabetic animals, no adverse effect of either clinical or subclinical GVHR was observed on islet function. Blood glucose profiles were normal, as were intravenous glucose tolerance test profiles. In conclusion, GVHR does not seem to adversely influence function of islets of Langerhans implanted intrahepatically in this parent to F1 experimental model.

Animals↗

PubMed1999

Determinants of plasma fibrin D-dimer sensitivity for acute pulmonary embolism as defined by pulmonary angiography.

BACKGROUND: The reported operating characteristics of the plasma fibrin D-dimer level for the diagnosis of acute pulmonary embolism vary widely. OBJECTIVE: To determine the sensitivity, specificity, predictive value, and clinical utility of the D-dimer for the diagnosis of pulmonary embolism, and to describe the effect of D-dimer assay method (enzyme-linked immunosorbent assay [ELISA], latex agglutination, membrane ELISA) and discriminate level, patient location at onset, comorbid disease, duration and intensity of concurrent heparin administration, and duration of symptoms on these operating characteristics. DESIGN: Prospective laboratory investigation. SETTING: Community and tertiary care teaching hospital. PATIENTS: Consecutive patients with suspected acute pulmonary embolism referred for pulmonary angiography from April 1993 through March 1996. MEASUREMENTS: Baseline characteristics, the duration and intensity of heparin anticoagulation, the time interval between symptom onset and plasma D-dimer testing, pulmonary angiography, and the D-dimer level on the day of pulmonary angiography. RESULTS: Of 105 consenting patients, 33 (31%) had a positive pulmonary angiogram. The D-dimer sensitivity/ negative predictive value for the ELISA, latex agglutination (American Bioproducts Co/Diagnostica Stago and Biopool International), and membrane ELISA were 100%/100%, 94%/94%, 100%/100%, and 97%/96%, respectively, at a discriminate level of 250 microg/L or less. The clinical utility, defined as the prevalence of a negative test, ranged from 17% to 33%. D-dimer sensitivity was unaffected by patient location at onset, comorbid disease, or heparin therapy but was inversely related to the duration of symptoms. CONCLUSIONS: The sensitivity of the plasma fibrin D-dimer for the diagnosis of pulmonary embolism depends on the assay method, the assay-specific discriminate level, and the duration of symptoms. At the appropriate discriminate level, the plasma D-dimer is a sensitive but nonspecific test for the diagnosis of pulmonary embolism.

Aged↗

PubMed1999

Intracerebral adenovirus-mediated p53 tumor suppressor gene therapy for experimental human glioma.

Malignant gliomas of astrocytic origin are good candidates for gene therapy because they have proven incurable with conventional treatments. Although mutation or inactivation of the p53 tumor suppressor gene occurs at early stages in gliomas and is associated with tumor progression, many tumors including high-grade glioblastoma multiforme carry a functionally intact p53 gene. To evaluate the effectiveness of p53-based therapy in glioma cells that contain endogenous wild-type p53, a clinically relevant model of malignant human glioma was established in athymic nu/nu mice. Intracerebral, rapidly growing tumors were produced by stereotactic injection of the human U87 MG glioma cell line that had been genetically modified for tracking purposes to express the Escherichia coli lacZ gene encoding beta-galactosidase. Overexpression of the p53 gene by adenovirus-mediated delivery into the tumor mass resulted in rapid cell death with the eradication of beta-galactosidase-expressing glioma cells through apoptosis. In long-term experiments, the survival of mice treated with the p53 adenoviral recombinant was significantly longer than that of mice that had received control adenoviral recombinant. During the observation period of 1 year, a complete cure was achieved in 27% of animals after a single injection of p53 adenoviral recombinant, and 38% of the animals were tumor free in the group receiving multiple injections of p53 adenoviral recombinant into a larger tumor mass. These experiments demonstrate that overexpression of p53 in gliomas, even in the presence of endogenous functional wildtype p53, leads to efficient elimination of tumor cells. These results point to the potential therapeutic usefulness of this approach for all astrocytic brain tumors.

Adenoviridae↗

PubMed1999

A model of port-site metastases of gallbladder cancer: the influence of peritoneal injury and its repair on abdominal wall metastases.

BACKGROUND: Recent surgical literature contains several reports of wound metastases of unexpected gallbladder cancer after laparoscopic cholecystectomy. We hypothesized that peritoneal injury caused by trocar insertion potentiates wound metastases. This study was designed to determine the effect of peritoneal injury on tumor implantation. METHODS: Cultured human gallbladder cancer cells were injected into the peritoneal cavity of mice immediately after surgical procedures. In a peritoneal injury group muscle and the peritoneum were perforated; in a peritoneal injury and repair group each muscle and peritoneal wound was sutured carefully; in a laparoscopic model group animals underwent peritoneal insufflation with carbon dioxide gas and tumor cell injection and then the abdominal wall was perforated. Some mice (controls) were not subjected to any surgical procedure. All mice (n = 178) were killed 2 weeks after tumor cell injection and were examined for tumor implantation. RESULTS: Although no control mice showed intraperitoneal tumor, all mice in the peritoneal injury group showed tumors at the injured sites. In the laparoscopic model group, 90% of injured sites had tumors. The traumatized site-specific implantation rate in the peritoneal injury and repair group was only 40%, whereas it was 100% in the peritoneal injury group (P < .001). CONCLUSIONS: Peritoneal injury enhances peritoneal implantation of carcinoma cells. Repair of injured peritoneum at trocar sites may reduce the frequency of wound metastases in laparoscopic surgery for unexpected gallbladder carcinoma.

Abdominal Muscles↗

PubMed1999

Defibrillation and the upper limit of vulnerability to fibrillation in a transthoracic guinea pig model.

Recent studies have shown sustained tachyarrhythmias in guinea pigs. We hypothesized that guinea pigs could be used as a model of ventricular fibrillation, focusing on defibrillation waveform efficacy and the upper limit of vulnerability to fibrillation. In 10 male guinea pigs, an esophageal/apical pacing electrode configuration was used. The electrocardiogram (ECG) and arterial blood pressure were continuously monitored. T-wave and defibrillation shocks were applied transthoracically. A modified up-down protocol was used. After up-down testing was completed, a tachyarrhythmia was induced without electrical termination. All animals died of a sustained tachyarrhythmia. The monophasic DFT50 (the 50% successful defibrillation voltage, 496 +/-176 V) was larger than the biphasic DFT50 (364+/-94 V, P < .005). The upper limit of vulnerability to fibrillation (ULV50) (the 50% successful induction voltage) was correlated with the DFT50 for both monophasic (r = .82, P < .005) and biphasic shocks (r = .88, P < .005). Its low cost and ease of handling may make the guinea pig a preferred model for some fibrillation and defibrillation studies.

Animals↗

PubMed1999

[Inhibitory effect of replication and expression of HDV by antisense oligodeoxynucleotides in H1 delta 9 cell].

OBJECTIVE: To study inhibitory effect of an antisense oligodeoxynucleotide (ASODN) and its phosphorothioate (S-ASODN) on replication and expression of HDV in H1 delta 9 cell. METHODS: In previous studies, it was proved that the ASODNs which are complementary to genomic HDV ribozyme self-cleavage site and stem I regions can inhibit availably genomic HDV ribozyme activity. In the present study, a 15-mer ASODN and S-ASODS which are complementary to this region (nucleotide 684-698) were added to medium of cultured H1 delta 9 cell. HDAg and HDV cDNA were detected by ELISA and Dot blot hybridization. RESULTS: Twenty-fourth hour after 6 mumol/L ASODN and S-ASODN were added, both the secreting amount of HDAg in the supernatant and HDV RNA were inhibited. The inhibiting rates were 76.14% and 84.50% respectively. When the concentration of S-ASODN was 2, 4, 6 mumol/L, the inhibiting rate showed the feature of dosage dependence. Inhibitory effect of ASODN and S-ASODN were similar in the same dosage. CONCLUSION: The results suggest that ASODN and S-ASODN can availably inhibit replication and expression of HDV in H1 delta 9 cell.

Hepatitis Delta Virus↗

PubMed1999

Effect of verbascoside on decreasing concentration of oxygen free radicals and lipid peroxidation in skeletal muscle.

AIM: To detect the effects of verbascoside on decreasing the concentration of oxygen free radicals (OFR) and lipid peroxidation in skeletal muscle resulting from exhaustive exercise. METHODS: Electron spin resonance (ESR) technique and thiobarbituric acid reaction (TBAR) method were used to detect the concentration of OFR in intact gastrocnemius muscle and the contents of milondialdehyde (MDA) in muscle homogenate. RESULTS: Verbascoside decreased the concentration of OFR (P < 0.05) and the level of lipid peroxidation (P < 0.05) in muscle caused by exercise. CONCLUSION: Verbascoside has the effects of reducing oxidative stress in muscle caused by exhaustive exercise by decreasing the concentration of free radicals and the level of lipid peroxidation.

Animals↗