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Biomedical subjects

F Li

Publications and source records attributed to F Li.

At least 253 records · Page 14Linked to original sources
PubMed1999

Serological evidence for swine hepatitis E virus infection in Australian pig herds.

Hepatitis E virus (HEV) is an enterically transmitted human pathogen, with some similarities to caliciviruses. A variant of HEV was recently identified in pigs in the USA, infecting almost 100% of animals in commercial herds. Phylogenetic analysis suggests that this is a true 'swine HEV' distinct from the human virus, but the swine virus may also infect man. Using an in-house ELISA based on a highly conserved, recombinant HEV protein, we have examined collections of sera from Australian pigs for evidence of HEV infection in local pig herds. Sera from one research herd (n = 32) were uniformly non-reactive, and this was used to establish an assay cut-off (= mean + 3 SD of reference pig serum reactivities). Screening of sera from other herds demonstrates that swine HEV is present in Australia, with reactivity observed in 30% (12/40) of random samples from two piggeries, 92-95% of pigs by the age of 16 weeks in two other piggeries (n = 45), and 17% (15/59) of wild-caught pigs. Further studies are required to examine whether HEV causes disease in pigs and to determine the risk of swine HEV transmission to man.

Age Factors↗
PubMed1999

Solution structure of the major alpha-amylase inhibitor of the crop plant amaranth.

alpha-Amylase inhibitor (AAI), a 32-residue miniprotein from the Mexican crop plant amaranth (Amaranthus hypochondriacus), is the smallest known alpha-amylase inhibitor and is specific for insect alpha-amylases (Chagolla-Lopez, A., Blanco-Labra, A., Patthy, A., Sanchez, R., and Pongor, S. (1994) J. Biol. Chem. 269, 23675-23680). Its disulfide topology was confirmed by Edman degradation, and its three-dimensional solution structure was determined by two-dimensional 1H NMR spectroscopy at 500 MHz. Structural constraints (consisting of 348 nuclear Overhauser effect interproton distances, 8 backbone dihedral constraints, and 9 disulfide distance constraints) were used as an input to the X-PLOR program for simulated annealing and energy minimization calculations. The final set of 10 structures had a mean pairwise root mean square deviation of 0.32 A for the backbone atoms and 1.04 A for all heavy atoms. The structure of AAI consists of a short triple-stranded beta-sheet stabilized by three disulfide bonds, forming a typical knottin or inhibitor cystine knot fold found in miniproteins, which binds various macromolecular ligands. When the first intercystine segment of AAI (sequence IPKWNR) was inserted into a homologous position of the spider toxin Huwentoxin I, the resulting chimera showed a significant inhibitory activity, suggesting that this segment takes part in enzyme binding.

Amino Acid Sequence↗
PubMed1999

The cancer antiapoptosis mouse survivin gene: characterization of locus and transcriptional requirements of basal and cell cycle-dependent expression.

Survivin is the first apoptosis inhibitor described to date to be expressed in G2-M in a cell cycle-dependent manner and to directly associate with mitotic spindle microtubules. To gain additional insights into this novel apoptotic checkpoint, we have now characterized the mouse survivin locus. Hybridization screening of mouse BAC libraries identified a survivin gene containing four exons and three introns, spanning >50 kb on the telomere of chromosome 11E2 and generating a 0.85-kb mRNA versus the 1.9-kb human transcript. A mouse survivin protein of 140 amino acids (Mr approximately 16,200) was 84% identical to its human orthologue and contained a structurally unique single baculovirus iap repeat (BIR) and a -COOH-terminus coiled domain instead of a RING finger. Analysis of the 5'-flanking region of the mouse survivin gene revealed a TATA-less promoter containing a canonical CpG island, numerous Sp1 sites, two cell cycle-dependent elements (CDEs), and one cell cycle gene homology region (CHR), typically found in G2-M-expressed genes. Primer extension and S1 nuclease mapping identified three transcription start sites at position -32, -36, and -40 from the initiating ATG. Transfection of survivin promoter-luciferase constructs identified a minimal promoter region within the most proximal 174 bp upstream of the first ATG. Mutagenesis of the CDE/CHR elements and Sp1 sites in this region, alone or in combination, reduced transcriptional activity by 40-60% in asynchronously growing cells and abolished cell cycle periodicity in G2-M-synchronized cells. These data demonstrate that cell cycle expression of survivin requires integration of typical CDE/CHR G1 repressor elements and basal transcriptional activity by Sp1. Disruption of these transcriptional requirements may provide an alternative strategy to block the overexpression of survivin in cancer.

Amino Acid Sequence↗
PubMed1999

[Loss of heterozygosity and microsatellite instability in laryngeal carcinoma near p16 gene]

OBJECTIVE: To search for the minimal overlap region of tumor suppressor gene in laryngeal carcinoma and discuss the correlation of p16 gene with laryngeal carcinogenesis. METHODS: Five microsatellite polymorphism markers near p16 gene were selected to detect loss of heterozygosity (LOH) and microsatellite instability (MI) in 60 cases of laryngeal squamous cell carcinoma. RESULTS: The frequencies of LOH in 5 markers were less than 23.1%, while the frequencies of MI in 2 markers were higher, with the highest frequency (46.1%) in D9S1752. CONCLUSION: The results suggest that the deletion of p16 gene does not play an important role in the laryngeal carcinogenesis and there may exist a gene around D9S1752 participating in the development of laryngeal carcinoma, which correlates with the mutation of repair gene.

Journal Article↗
PubMed1999

Antioxidant properties of EPC-K1: a study on mechanisms.

Scavenging effects of L-ascorbic acid 2-[3,4-dihydro-2,5,7,8- tetramethyl-2-(4,8,12-trimethytridecyl)-2H-1-benzopyran- 6-yl-hydrogen phosphate] potassium salt (EPC-K1) on hydroxyl radicals, alkyl radicals and lipid radicals were studied with ESR spin trapping techniques. The inhibition effects of EPC-K1 on lipid peroxidation were assessed by TBA assay. The kinetics of EPC-K1 reacting with hydroxyl radicals and linoleic acid radicals were studied by pulse radiolysis. The active site of EPC-K1 and the structure-antioxidative activity relationships were discussed. The superoxide radicals scavenging capacity of the brain homogenate of EPC-K1-treated rats was measured. The results revealed that in comparison with Trolox and vitamin C, EPC-K1 showed better overall antioxidative capacity in vitro and in vivo. EPC-K1 was a moderate scavenger on hydroxyl radicals and alkyl radicals, a potent scavenger on lipid radicals, and an effective inhibitor on lipid peroxidation. EPC-K1 could react with hydroxyl radicals with a rate constant of 7.1 x 10(8) dm3 mol-1 s-1 and react with linoleic acid radicals with a rate constant of 2.8 x 10(6) dm3 mol-1 s-1. The active site of EPC-K1 was the enolic hydroxyl group. After administration of EPC-K1, the ability of rat brain to scavenge superoxide radicals was significantly increased. The potent scavenging effects of EPC-K1 on both hydrophilic and hydrophobic radicals were relevant with its molecular structure, which consisted of both hydrophilic and hydrophobic groups.

Animals↗
PubMed1999

Seroprevalence of antibodies to hepatitis E virus in the normal blood donor population and two aboriginal communities in Malaysia.

The prevalence of antibodies to hepatitis E virus (HEV) has been examined in many countries, but such studies have generally been limited to majority populations such as those represented in healthy blood donors or cross sections of urban populations. Due to its major route of enteric transmission, large differences in HEV prevalence might be expected between populations in the same country but with different living conditions. Using an ELISA based on GST-ORF2.1 antigen, the prevalence of IgG-class antibodies to HEV was examined in three distinct populations in Malaysia: the normal (urban) blood donor population and two aboriginal communities located at Betau, Pahang and Parit Tanjung, Perak. IgG anti-HEV was detected in 45 (44%) of 102 samples from Betau and 15 (50%) of 30 samples from Parit Tanjung, compared to only 2 (2%) of 100 normal blood donors. The distribution of sample ELISA reactivities was also consistent with ongoing sporadic infection in the aboriginal communities, while there was no significant relationship between HEV exposure and age, sex, or malaria infection. The high prevalence of antibodies to HEV in the two aboriginal communities indicates that this group of people are at high risk of exposure to HEV compared to the general blood donors, and the results suggest that studies of HEV seroprevalence within countries must take into account the possibility of widely varying infection rates between populations with marked differences in living conditions.

Adolescent↗
PubMed1999

Direct injection of plasma to determine pseudoephedrine by high performance liquid chromatography with column switching.

An HPLC method has been developed for the determination of pseudoephedrine in plasma using column switching. Preparation of the sample was simple in that only 1000 microL of water was added to 200 microL of plasma before injection. A 900 microL aliquot was injected onto the precolumn. Double distilled water was used to elute and remove proteins and polar components in the sample. The components retained on the precolumn were flushed forward onto the analytical column by the mobile phase (acetonitrile-0.2 mol/L ammonium sulphate, 10:90 v/v) with automated column switching. The limit of determination of pseudoephedrine in plasma was 12 ng/mL. The relative standard deviations of intra- and inter-assay for the determination of pseudoephedrine in plasma were 1.2-9.8% over the concentration range 1020-21.8 ng/mL. The mean recovery by on-line solid phase extraction was 94.76% (RSD = 1.1%).

Calibration↗
PubMed1999

Determination of unbound drug concentration and protein-drug binding fraction in plasma.

The aim of this work was to provide a short overview of existing methods for the determination of free drug concentration and protein-drug binding fraction in plasma. Various methods have been described in terms of principles, evaluation of methods, and applications in recent years, with an emphasis on the chromatographic method, i.e. high-performance frontal analysis (HPFA).

Animals↗
PubMed1999

Neuroprotective effects of a novel broad-spectrum cation channel blocker, LOE 908 MS, on experimental focal ischemia: a multispectral study.

Thirty-four rats undergoing 90 minutes of temporary middle cerebral artery occlusion were randomly and blindly assigned to vehicle or (RS)-(3,4-dihydro-6, 7-dimethoxyisoquinoline-1-gamma1)-2-phenyl-N,N-di-2-(2, 3, 4-trimethoxyphenyl)ethyl acetamide (LOE 908 MS; 0.5 mg/kg) i.v. bolus at 30 minutes after arterial occlusion followed by a 5 mg/kg/hr i.v. infusion for 3.8 hours (n =17/group). Perfusion-, diffusion- and T(2)-weighted magnetic resonance imaging was performed before treatment and repeatedly after treatment. Multispectral analysis was used to define ischemic abnormalities. The size of the ischemic abnormalities, including the ischemic core and penumbra, was not different between the two groups before treatment. However, a significant difference in ischemic lesion size was detected beginning 1.5 hours after treatment. The size of the ischemic core was significantly smaller in the treatment group, while the size of the ischemic penumbra was similar in the two groups at 85 minutes after arterial occlusion. Postmortem infarct size at 24 hours was significantly smaller in the drug-treated group than in the placebo group. These results demonstrate that LOE 908 MS can reduce ischemic lesion size, which is probably attributable to inhibition of expansion of the ischemic core. J. Magn. Reson. Imaging 1999;10:138-145.

Acetamides↗
PubMed1999

Comparison of evoked cortical activity in conscious and propofol-anesthetized rats using functional MRI.

Changes in cortical activity during foot shock were assessed under conscious and propofol-anesthetized conditions using functional magnetic resonance imaging (fMRI). Increases in signal intensity were observed in the contralateral somatosensory cortex in response to electrical shock of the hindpaw under both conditions. These increases in cortical signal ranged from 6% to 26% while awake and from 1% to 6% under propofol anesthesia. In each of the six animals studied, the largest increase in blood oxygenation level-dependent (BOLD)-based signal intensity was observed during consciousness. In three of six animals, propofol anesthesia depressed signal intensity by as much as 10-fold, showing that the level of cortical activity during foot shock is dampened by anesthesia. These results indicate it would be advantageous to use fully conscious animals to maximize BOLD-based MRI signal in certain behavioral studies using MR spectrometers with modest field strengths (1.0-2.0 T).

Anesthesia, General↗
PubMed1999

Reversal of acute apparent diffusion coefficient abnormalities and delayed neuronal death following transient focal cerebral ischemia in rats.

Twenty-two rats were subjected to 8, 15, 30, or 60 minutes of temporary middle cerebral artery occlusion (n = 5 per group) or sham occlusion (n = 2) in the magnetic resonance imaging unit. Diffusion-, perfusion-, and T2-weighted imaging were acquired before and during occlusion, and after reperfusion. A coregistration method was used to correlate the acute changes of the average apparent diffusion coefficient (ADCav) with the histology after 72 hours at the same topographic sites. The initially reduced ADCav values recovered completely in both the lateral caudoputamen and upper frontoparietal cortex in the 8-, 15-, and 30-minute groups, partially in the cortex, and not at all in the caudoputamen in the 60-minute group. The histology showed that the caudoputamen was either normal or had mild neuronal injury in the 8-minute group and invariably had some degree of neuronal death in the 15-, 30-, and 60-minute groups, whereas the cortex was either normal or had varying degrees of neuronal injury in all groups. No histological abnormalities were seen in the sham-operated rats. Our data suggest that acute ADCav reversal does not always predict tissue recovery from ischemic injury and that temporary focal ischemia for even 8-minute duration can cause delayed neuronal death that is more severe in the caudoputamen where the initial ADCav decline was greater than in the cortex.

Animals↗
PubMed1999

Basic FGF-induced down-regulation of IGF-I mRNA in cultured rat Müller cells.

Interactions among growth factors are important in a variety of physiological and pathological processes. The regulation of IGF-I mRNA expression by bFGF was investigated in cultured rat Müller cells and the mechanism of regulation studied. Müller cells from 1- to 3-day-old Sprague-Dawley rats were isolated and cultured with Eagle MEM+10% FCS. Cultured cells were identified by immunocytochemistry using antibodies against vimentin, carbonic anhydrase C, and glutamine synthetase. Cells of passage 1-4 were treated with bFGF, the PKC inhibitor H-7, calphostin C, the PKC activator PMA or the PKA inhibitor H-89, as well as the adenylate cyclase activator forskolin, or adenylate cyclase inhibitor SQ22536. IGF-I and bFGF expression levels were assessed by Northern blot analysis. The addition of bFGF to culture medium down-regulated IGF-I expression in a dose- and time-dependent manner. Decrease of IGF-I expression started at a bFGF concentration of 1 ng ml-1. IGF-I mRNA level declined to 44% of baseline level at 10 ng ml-1 of bFGF, and reached a trough of 40% at 50 ng ml-1. At 10 ng ml-1 of bFGF, down-regulation of IGF-I expression was observed as early as 4 hr (60%) after treatment, and reached a trough of 42% by 8 hr. The temporal and concentration dependence of IGF-I expression by addition of the PKC activator PMA, to culture medium was similar to that due to the addition of bFGF. The down-regulation of IGF-I expression by bFGF (10 ng ml-1) and PMA (0.1 microM) was blocked by the PKC inhibitors H-7 (30 microM) and calphostin C (1 microM). Forskolin (5 microM), an adenylate cyclase activator, had activator, had no effect on IGF-I expression. SQ22536 (100 microM), an adenylate cyclase inhibitor, and H-89, a PKA inhibitor, had no inhibitory effect on bFGF-induced down-regulation of IGF-I expression. These results indicate that bFGF down-regulates IGF-I expression in cultured rat M uller cells through PKC activation.

Animals↗
PubMed1999

A Trypanosoma brucei bloodstream form mutant deficient in ornithine decarboxylase can protect against wild-type infection in mice.

A Trypanosoma brucei bloodstream mutant in which both copies of the ornithine decarboxylase (ODC) gene were knocked out (ODC mutant) was used to determine the biological functions of ODC in T. brucei. Growth of the mutant cells ceased within 12-24 h in regular culture medium deficient in polyamines, but could be rescued by supplementation with 1 mM putrescine. A mouse model of T. brucei infection was used to determine whether the mutant was still infective and was found to develop either extremely low or undetectable levels of parasitemia, suggesting that in T. brucei, ODC activity is essential for establishing an infection. Furthermore, when these mice were subsequently challenged with wild-type T. brucei cells expressing the same variant surface glycoprotein (VSG), they did not develop any parasitemia, indicating that inoculating the mice with the attenuated ODC mutant had conferred protection against challenge by wild-type cells. These results were reproduced in C57BL/6J mice deficient in alpha-beta and gamma-delta T-cell receptors. However, no protection was observed in rag-2 knockout mice deficient in both B and T lymphocytes or in C57BL/10J mice deficient only in B lymphocytes. The results thus suggest that the ODC mutant could induce a T-lymphocyte-independent but B-lymphocyte-dependent immunity against wild-type cells of the same VSG. Such a mechanism of immunity has been elicited only by live T. brucei cells, but not by isolated VSGs or radiation-killed trypanosomes. This ODC mutant may thus represent a genuinely attenuated T. brucei bloodstream form capable of immunizing mammals against infections by African trypanosomes of the same VSG subtype without causing detectable infection by itself. The observation also raises the interesting likelihood that the in vivo treatment of T. brucei bloodstream forms with alpha-DL-difluoromethylornithine is a de facto attenuation of the parasitic organisms, which may very well result in B-lymphocyte-dependent host immune responses to subsequent infections by parasites of the same VSG subtypes.

Africa South of the Sahara↗
PubMed1999

Chronic pressure overload cardiac hypertrophy and failure in guinea pigs: I. Regional hemodynamics and myocyte remodeling.

A chronic pressure overload animal model was created in young guinea pigs by surgical constriction of the descending thoracic aorta. Hemodynamics, echocardiography and myocyte size characterization demonstrated compensated pressure overloaded left ventricular (LV) hypertrophy at 4 weeks (4 wk), and congestive left heart failure 6 months (6 mo) after aortic constriction. Compared to age-matched sham-surgery control groups, the cell length and length/width ratio of isolated LV myocytes were significantly increased at 6 mo but not at 4 wk. LV myocyte lengthening was statistically correlated to an increase in LV chamber dimension and diastolic wall stress at 6 mo. These data demonstrate that myocyte lengthening occurs in mechanical overload-induced congestive heart failure, contributes to LV chamber dilatation, and is associated with increased end-diastolic wall stress. Myocytes of the other three chambers remained morphometrically normal at 4 wk. Hypertrophy of left atrial (LA) and right ventricular and atrial myocytes was evident at 6 mo. Increases in both cell length and cross-sectional area contributed significantly to the hypertrophy in the three chambers. More than 85% of LV myocytes were binucleate and the binucleation remained unchanged in the sham-surgery group from the tested 4 wk to 6 mo time point. LV hypertrophy and failure showed no significant effects on the binucleation of LV myocytes. By contrast, over 96% of LA myocytes were mononucleate. The mononucleate percent of LA myocytes was not appreciably altered during either normal growth or hypertrophy induced by secondary hemodynamic overload due to LV failure.

Animals↗
PubMed1999

Chronic pressure overload cardiac hypertrophy and failure in guinea pigs: II. Cytoskeletal remodeling.

The cytoskeleton is a major regulator of cell shape. To explore potential mechanisms for maladaptation of cardiac myocyte shape in pressure overload-induced congestive heart failure, the abundance and organization of major intra- and extra-myofibrillar cytoskeleton of cardiac myocytes were examined with western blotting and confocal microscopy in guinea pigs with chronic aortic stenosis. It was found that: (1) the amount and distribution of alpha-actinin and myomesin remained unchanged at both the compensated hypertrophy and the congestive heart failure stages; (2) loss of titin was associated with myocyte lengthening in heart failure; (3) desmin protein and filaments in LV myocytes increased progressively with mechanical overload cardiac hypertrophy and subsequent heart failure; (4) a newly developed and validated quantitative confocal microscopic approach disclosed that the microtubule density in isolated LV myocytes increased by 21% at 4 weeks and by 48% 6 months after aortic constriction; (5) at the heart failure stage, microtubule density in LV myocytes showed a statistically significant inverse correlation to the LV maximum +dP/dt and a direct correlation to LV myocyte lengthening; (6) the increased microtubule density in LV myocytes in this model was not due to an increase in total tubulin; and (7) microtubule density in left atrial and right ventricular myocytes also increased when they underwent hypertrophy secondary to left heart failure. These results suggest that the down-regulation of titin and up-regulation of microtubule and desmin filaments may contribute to myocyte lengthening and malfunction in pressure overload congestive heart failure.

Actinin↗
PubMed1999

Small peripheral carcinomas of the lung: thin-section CT and pathologic correlation.

The aim of this study was to clarify the thin-section CT features of small peripheral carcinomas of the lung on the basis of pathologic findings of tumor growth patterns. Thin-section CT and pathologic correlation was evaluated in 19 patients with surgically verified small peripheral carcinomas of the lung ( < 20 mm in size) that had been detected in a screening trial for lung cancer using spiral CT. Four thin-section CT types of nodules were observed: (a) type L1 (4 of 19, 21 %), a fairly well-defined nodule with ground-glass attenuation, corresponding to tumor lepidic growth without alveolar collapse; (b) type L2 (4 of 19, 21 %), a partly lobulated nodule with a low but inhomogeneous attenuation, corresponding to tumor lepidic growth with scattered foci of alveolar collapse; (c) type L3 (4 of 19, 21 %), an ill-defined nodule with an irregularly shaped higher-density central zone in a ground-glass attenuation peripheral zone, accompanied by convergence of the bronchovascular structures from the surrounding lung parenchyma, which corresponded to desmoplastic response in the central zone and to tumor lepidic growth in the peripheral zone; and (d) type H (7 of 19, 37 %), a well-defined nodule with a solid homogeneous attenuation, corresponding to tumor hilic growth. Thin-section CT features of small peripheral carcinomas of the lung can be classified into four types, based on the density distribution of the tumor, which reflect the histologic findings.

Adenocarcinoma↗
PubMed1999

Serum iron and ferritin levels in patients with colorectal cancer in relation to the size, site, and disease stage of cancer.

We investigated blood loss from colorectal cancer in 92 men seen between January 1990 and June 1997, in relation to the size and site of the tumor, Dukes stage, pathologic type of cancer, and serum carcinoembryonic antigen (CEA) positivity. We used indirect methods, measuring serum hemoglobin, iron, and ferritin concentrations. The means of these three concentrations were significantly lower in patients with a tumor >3cm than in those with a tumor < or =3cm in largest diameter. The means of the three values were lower in patients with proximal colon cancer than in those with distal colon cancer, but only the difference in serum hemoglobin concentration was significant. Cancers of the ulcerative type were found more often in the proximal colon. The proportion of patients with Dukes stage C or D was not different between those with proximal colon cancer and those with distal colon cancer. There was a positive correlation between tumor size and Dukes stage. There were no differences in serum hemoglobin, iron, and ferritin concentrations with respect to the pathologic type of cancer and CEA positivity. These findings show that blood loss from colorectal cancer is closely related to the size and site of the tumor.

Adenocarcinoma↗