Biomedical subjects

G Xu

Publications and source records attributed to G Xu.

At least 199 records · Page 11Linked to original sources

PubMed1999

[Inhibition of human breast cancer cell line BCap-37 by flavonoid extract of wheat germ in vitro].

Cell growth and proliferation were measured by microculture tetrazolium(MTT) assay, cell colony-forming assay and the synthesis of DNA by 3H-thymidine incorporation. Flavonoid extract of wheat germ resulted to a dose-dependent, time-dependent growth inhibition, reduction of colony and 3H-thymiding incorporation in DNA of human breast cancer cell BCap-37. These findings indicated that the flavonoid extract of wheat germ can inhibit tumor cell growth and proliferation by blocking DNA synthesis in vitro.

Antineoplastic Agents, Phytogenic↗

PubMed1999

Sol-gel thin-film immobilized soybean peroxidase biosensor for the amperometric determination of hydrogen peroxide in acid medium.

An acid-stable soybean-peroxidase biosensor was developed by immobilizing the enzyme in a sol-gel thin film. Methylene blue was used as a mediator because of its high electron-transfer efficiency. The sol-gel thin film and enzyme membrane were characterized by FT-IR, and the effects of pH, operating potential, and temperature were explored for optimum analytical performance by using the amperometric method. The H2O2 sensor exhibited a fast response (5 s), high sensitivity (27.5 microA/mM), as well as good thermostability and long-term stability. In addition, the performance of the biosensor was investigated using flow-injection analysis (FIA).

Enzymes, Immobilized↗

PubMed1999

Degradation mechanism of small molecule-based organic light-emitting devices

Studies on the long-term degradation of organic light-emitting devices (OLEDs) based on tris(8-hydroxyquinoline) aluminum (AlQ3), the most widely used electroluminescent molecule, reveal that injection of holes in AlQ3 is the main cause of device degradation. The transport of holes into AlQ3 caused a decrease in its fluorescence quantum efficiency, thus showing that cationic AlQ3 species are unstable and that their degradation products are fluorescence quenchers. These findings explain the success of different approaches to stabilizing OLEDs, such as doping of the hole transport layer, introducing a buffer layer at the hole-injecting contact, and using mixed emitting layers of hole and electron transporting molecules.

Journal Article↗

PubMed1999

Identification of a putative effector protein for rab11 that participates in transferrin recycling.

We have identified and cloned the cDNA for a 912-aa protein, rab11BP, that interacts with the GTP-containing active form of rab11, a GTP-binding protein that plays a critical role in receptor recycling. Although rab11BP is primarily cytosolic, a significant fraction colocalizes with rab11 in endosomal membranes of both the sorting and recycling subcompartments. In vitro binding of rab11 to native rab11BP requires partial denaturation of the latter to expose an internal binding site located between residues 334 and 504 that is apparently masked by the C-terminal portion of the protein, which includes six repeats known as WD40 domains. Within the cell, rab11BP must undergo a conformational change in which the rab11-binding site becomes exposed, because when coexpressed with rab11 in transfected cells the two proteins formed abundant complexes in association with membranes. Furthermore, although overexpression of rab11BP did not affect transferrin recycling, overexpression of a truncated form of the protein, rab11BP(1-504), that includes the rab11-binding site but lacks the WD40 domains inhibited recycling as strongly as does a dominant negative rab11 mutant protein that does not bind GTP. Strikingly, the inhibition caused by the truncated rab11BP was prevented completely when the cells also expressed a C-terminally deleted, nonprenylatable form of rab11 that, by itself, has no effect on recycling. We propose that rab11BP is an effector for rab11, whose association with this GTP-binding protein is dependent on the action of another membrane-associated factor that promotes the unmasking of the rab11-binding site in rab11BP.

3T3 Cells↗

PubMed1999

Function of a C-rich sequence in the polypyrimidine/polypurine tract of the promoter of the chicken malic enzyme gene depends on promoter context.

The promoters of many genes contain C-rich polypyrimidine/polypurine (PPY/PPU) sequences that are important for gene expression. The promoter of the chicken malic enzyme gene contains a long PPY/PPU tract that can act as an alternative promoter. This tract can be separated functionally into a C-rich and (CT)7 sequences. The (CT)7 region together with some 3' nucleotides is essential for function of the alternative transcription start site and the C-rich sequence as a regulatory element. In constructs that contained the PPY/PPU tract or the -147/+31-bp promoter of the malic enzyme gene connected to a reporter gene, deletion of the C-rich region increased gene expression. In constructs containing 5.8-kb 5'-flanking DNA of the gene, deletion of the same C-rich region decreased expression of the reporter gene. Positive function of the C-rich sequence required two upstream DNA regions, -237 to -147 bp and -3474 to -2715 bp. To understand the mechanism(s) by which the same sequence exerts different effects, we examined the transcription start sites in the construct where the C-rich region was deleted. We directly visualized transcription start sites by performing 5'-rapid amplification of cDNA ends and a subsequent primer extension on a single-stranded template. Deletion of the C-rich region from constructs containing 5.8 kb of 5'-flanking DNA almost completely abolished transcription initiation from the PPY/PPU promoter and reduced transcription from the major endogenous start site. DEAE fractionation of hepatic nuclear extract revealed more than 10 proteins that bound specifically to C-rich DNA. These results suggest that interactions between upstream DNA elements and the C-rich sequence and the selective use of DNA-binding activities may bestow different functions on the same nucleotide sequence.

Animals↗

PubMed1999

Depentylation of [3H-pentyl]methyl-n-amylnitrosamine by rat esophageal and liver microsomes and by rat and human cytochrome P450 isoforms.

Methyl-n-amylnitrosamine (MNAN) induces esophageal cancer in rats, probably involving activation by cytochromes P450. We studied the metabolic depentylation of MNAN. [3H-4,5-pentyl]MNAN and [3H-2,3-pentyl]-MNAN were synthesized, purified, and incubated with rat esophageal microsomes (REM) or rat liver microsomes (RLM) to give [3H]pentaldehyde (depentylation), an indicator of MNAN activation. [3H]Pentaldehyde was determined by high-performance liquid chromatography of its 2,4-dinitrophenylhydrazone. Adding 5 mM semicarbazide to incubations increased the observed depentylation (except that due to CYP2E1) by >60%. MNAN depentylation by REM and uninduced and induced RLM showed Km values of 64, 610, and 170-330 microM, respectively (Vmax: 20, 220, and 160-1270 pmol/mg protein/min, respectively). The depentylation of 100 microM MNAN by REM was inhibited 98% by CO and 65% by coumarin preincubated for 15 min with REM (Ki, 120 microM) but was unaffected by antibodies inhibitory to various P450s. MNAN inhibited coumarin 7-hydroxylation by RLM and CYP2A6 (Ki, 3000 and 320 microM, respectively). REM showed slight coumarin 7-hydroxylase activity. MNAN depentylation by RLM was 41% inhibited by an antibody to CYP2C11. Km for rat CYP2E1, human CYP2E1, and human CYP2A6 was 210, 115, and 17 microM, respectively (Vmax: 900, 570, and 120 pmol/nmol P450/min, respectively). We conclude that MNAN activation by REM is probably due to a P450 related to CYP2A3, a rodent nasal P450.

Animals↗

PubMed1999

Model peptide studies of sequence repeats derived from the intracrystalline biomineralization protein, SM50. I. GVGGR and GMGGQ repeats.

We report solution-state pulsed field gradient nmr studies of a native sequence-derived 23-residue peptidomimetic, N alpha-acetyl-QPGVGGRQPGMGGQPGVGGRQPG-C alpha-amid, that incorporates the prevalent GVGGR and GMGGQ repeats found in the sea urchin embryo intracrystalline spicule matrix protein, SM50 (Strongylocentrotus purpuratus). These repeats are sequence homologues of elastin protein repeats (VPGVG, VGGVG, and APGVGV) and spider dragline silk protein repeats (GPGG, GQGG, and QPGYG). Using rotating frame nuclear Overhauser effect (ROE) connectivities, CH alpha proton conformational shifts, 3JNH-CH alpha coupling constants, amide temperature shift coefficients, and pulsed field gradient ROE spectroscopy solvent exchange measurements, we find that the 23-mer peptidomimetic possesses a multiple beta-turn structure in aqueous solution, in equilibria with an extended or coil structure (60% beta-turn: 40% random coil). The GVGGR sequence adopts a double beta-turn conformation that is stabilized by two hydrogen bonds (R7-->V4, R20-->V17; G6-->G3, G19-->G16). The GMGGQ region adopts a single beta-turn conformation that is stabilized by a hydrogen bond involving residues Q14 and M11. Repeating beta-turn structures, or beta-spirals, may play an important role with regard to matrix assembly, protein stability, molecular elasticity, and/or protein-crystal recognition within the spicule mineralized matrix.

Amino Acid Sequence↗

PubMed1999

Squamous cell carcinoma of temporal bone: reported on 33 patients.

BACKGROUND: This study assessed the treatment results of a series of 33 patients with squamous cell carcinoma (SCC) of the temporal bone and evaluated the efficacy of mastoidectomy combined with perioperative radiation therapy protocol. METHODS: Thirty-three patients with biopsy-proven SCC invaded to the temporal bone were reviewed retrospectively and staged into three subgroups according to the University of Pittsburgh TNM Staging System. There were 3 patients with Stage I and II disease(tumor confined to auditory canal), 17 patients with Stage III (tumor involving the middle ear or mastoid), and 13 patients with Stage IV(more extensive disease). Two patients were treated by surgery alone. Eleven patients received irradiation only, and the remaining 20 patients underwent combined surgery and perioperative radiotherapy. The surgical intervention included sleeve resection for patients with Stage I and II lesions and mastoidectomy for all patients with Stage III and IV lesions except 1 who had subtotal temporal bone resection. The radiation dose delivered was in the range of 3500 approximately 10 000 cGy, with an average dose of 6560 cGy. RESULTS: The five-year survival rate for the whole series was 51.7% by the life-table analysis. After being staged into three subgroups (ie, Stage I + II, Stage III, and Stage IV), the estimated five-year survival rates were 100%, 68. 8%, and 19.6%, respectively (p = 0.04). Radiation alone yielded a 28. 7% five-year survival, while combined surgery and irradiation gave a result of 59.6% (p = 0.80). For patients treated with planned combined therapy, the actuarial five-year survival rates were 72.7% (8/11) for Stage III disease and 12.5% (1/8) for Stage IV disease (p = 0.02). Twelve patients who died of disease did so of local recurrence (10 cases), cervical metastases (1 case), and liver metastases (1 case), with 70% of succumbing to their diseases within two years. Complications include osteonecrosis (n = 1), osteitis (n = 3), radiation dermatitis (n = 2), facial nerve palsy (n = 2), and delayed healing (n = 2). Data on clinical presentation and treatment modality were also analyzed. CONCLUSION: The results of mastoidectomy with removal of all gross tumor, combined with planned perioperative irradiation therapy, seems to be a useful approach for SCC of the temporal bone. This gives at least as good, and possibly better, five-year survival than temporal bone resection. The mastoidectomy procedure creates less operative morbidity and mortality. To facilitate the development of more effective means of treating advanced disease, an accepted staging system and cooperative group investigation is necessary.

Adult↗

PubMed1999

Rapid colorimetric assay of urinary beta-galactosidase and N-acetyl-beta-D-glucosaminidase with Cobas Mire Auto-analyzer.

A rapid and simple colorimetric method for the assay of urinary beta-galactosidase (GAL) and N-acetyl-beta-D-glucosaminidase (NAG) using 4-nitrophenyl-glycosides as the substrates and a Cobas Mire Auto-analyzer is described. Optimal conditions for this method including substrate concentration, ionic strength, pH and incubation time were characterized. Endogenous substances in urine did not interfere with the assays. Incubation time could be shortened to 10 minutes. A small volume of an alkaline buffer to terminate the enzyme reaction achieved better sensitivity and accuracy. Buffer-substrate solutions were stable for at least one week at 4 degrees C. Normal values of the two urinary enzymes are also reported.

Acetylglucosaminidase↗

PubMed1999

PFG-omega1-filtered TOCSY experiments for the determination of long-range heteronuclear and homonuclear coupling constants and estimation of J-coupling "crosstalk" artifacts in 2-D omega1-filtered "E. COSY-style" spectra.

We present novel one- and two-dimensional versions of the omega1-filtered TOCSY experiment. These experiments utilize pulsed-field gradient techniques and INEPT-reverse INEPT magnetization transfer to generate heteronuclear filtering by means of coherence pathway selection. The major advantages of this approach are twofold: first, each experiment requires a reasonable number of transmitter pulses, gradient pulses, and delays to implement. Second, the use of z-axis gradients at the beginning and termination of the pulse sequences prevents the recovery of dephased magnetization prior to FID detection. This technique was incorporated into 1-D and 2-D omega1-filtered JXH- and JHH-TOCSY-style experiments. As demonstrated on 15N-enriched peptide samples, the use of the pulsed-field-gradient coherence selection scheme effectively filters out unwanted magnetization components, thereby improving the overall sensitivity of the experiments. In addition to this suite of pulse sequences, we also present a method for correcting the reduction in J-coupling that results from crosspeak shifting in 2-D omega1-filtered E. COSY-style spectra. This correction is applicable to both Lorentzian and Gaussian 2-D crosspeak lineshapes.

Humans↗

PubMed1999

A kinetic molecular model of the reversible unfolding and refolding of titin under force extension.

Molecular elasticity is a physicomechanical property that is associated with a select number of polypeptides and proteins, such as the giant muscle protein, titin, and the extracellular matrix protein, tenascin. Both proteins have been the subject of atomic force microscopy (AFM), laser tweezer, and other in vitro methods for examining the effects of force extension on the globular (FNIII/Ig-like) domains that comprise each protein. In this report we present a time-dependent method for simulating AFM force extension and its effect on FNIII/Ig domain unfolding and refolding. This method treats the unfolding and refolding process as a standard three-state protein folding model (U right arrow over left arrow T right arrow over left arrow F, where U is the unfolded state, T is the transition or intermediate state, and F is the fully folded state), and integrates this approach within the wormlike chain (WLC) concept. We simulated the effect of AFM tip extension on a hypothetical titin molecule comprised of 30 globular domains (Ig or FNIII) and 25% Pro-Glu-Val-Lys (PEVK) content, and analyzed the unfolding and refolding processes as a function of AFM tip extension, extension rate, and variation in PEVK content. In general, we find that the use of a three-state protein-folding kinetic-based model and the implicit inclusion of PEVK domains can accurately reproduce the experimental force-extension curves observed for both titin and tenascin proteins. Furthermore, our simulation data indicate that PEVK domains exhibit extensibility behavior, assist in the unfolding and refolding of FNIII/Ig domains in the titin molecule, and act as a force "buffer" for the FNIII/Ig domains, particularly at low and moderate extension forces.

Amino Acid Sequence↗

PubMed1999

Campestanol (24-methyl-5alpha-cholestan-3beta-ol) absorption and distribution in New Zealand White rabbits: effect of dietary sitostanol.

Campestanol (24-methyl-5alpha-cholestan-3beta-ol) is a naturally occurring plant stanol, structurally similar to cholesterol (5-cholesten-3beta-ol) and widely distributed in vegetable oils consumed in human diets. We measured the absorption and turnover of campestanol by the plasma dual-isotope ratio method and mathematical analysis of specific activity versus time decay curves after simultaneous oral and intravenous pulse-labeling with [3alpha-3H]- and [23-14C]-labeled campestanol, respectively, in New Zealand White (NZW) rabbits: six fed chow and six fed chow with 125 mg/d campestanol and 175 mg/d sitostanol (24-ethyl-5alpha-cholestan-3beta-ol). Plasma concentrations increased insignificantly from 0.08+/-0.01 to 0.09+/-0.01 mg/dL with dietary stanols. The percent campestanol absorption measured by the plasma dual-isotope ratio method after the rabbits were fasted for 6 hours yielded the percent absorption in the absence of competing intestinal sterols and stanols and declined insignificantly from 11.6%+/-3.5% in controls to 8.1%+/-3.7% in the treated rabbit groups. In contrast, the turnover, which measured actual absorption averaged over 24 hours, increased from 0.12+/-0.05 to 0.37+/-0.05 mg/d (P < .05) with campestanol and sitostanol added to the diet. However, the actual percent absorption declined from 3% to 0.3% of dietary intake with the campestanol and sitostanol-enriched diet. Campestanol pool sizes, although remaining small, increased slightly from 1.1+/-0.4 to 2.5+/-1.5 mg. The removal constant (KA) from pool A (MA) did not change significantly with added dietary campestanol and sitostanol (KA= -0.040+/-0.005 v -0.037+/-0.007 d(-1)). The results demonstrate small campestanol plasma concentrations and body pools even when the rabbits consumed substantial amounts because (1) intestinal absorption was limited and (2) was further reduced by competing dietary sitostanol, and (3) campestanol was removed rapidly from the body. Thus, campestanol, which shares the same basic structure and intestinal absorption pathway with cholesterol, does not accumulate when fed, and may be incorporated into the diet to block cholesterol absorption.

Administration, Oral↗

PubMed1999

Comparative regulation of hepatic sterol 27-hydroxylase and cholesterol 7alpha-hydroxylase activities in the rat, guinea pig, and rabbit: effects of cholesterol and bile acids.

The regulation of the classic and alternative bile acid synthetic pathways by key hepatic enzyme activities (microsomal cholesterol 7alpha-hydroxylase and mitochondrial sterol 27-hydroxylase, respectively) was examined in bile acid depletion and replacement and cholesterol-feeding experiments with rats, guinea pigs, and rabbits. The bile acid pool was depleted by creating a bile fistula (BF) and collecting bile for 2 to 5 days, and it was replaced by intraduodenal infusion of the major biliary bile acids (taurocholic acid [TCA], glycochenodeoxycholic acid [GCDCA], and glycocholic acid [GCA] in the rat, guinea pig, and rabbit, respectively) at rates equivalent to the measured hepatic flux of the bile acids. To study the effects of cholesterol, the animals were fed for 7 days on a basal diet with and without 2% cholesterol. Cholesterol 7alpha-hydroxylase and sterol 27-hydroxylase activities, measured by isotope incorporation assays, were related to bile acid output and composition and hepatic cholesterol concentrations. Intraduodenal infusion of bile acids increased the output of the tested bile acids, but did not significantly change hepatic cholesterol concentrations and had no effect on sterol 27-hydroxylase activity. Neither bile acid depletion nor replacement affected sterol 27-hydroxylase activity when three different substrates (cholesterol, 5beta-cholestane-3alpha,7alpha-diol, and 5beta-cholestane-3alpha,7alpha,12alpha-triol) were tested. In contrast, feeding 2% cholesterol increased hepatic cholesterol concentrations in rats, guinea pigs, and rabbits threefold, twofold, and eightfold, respectively, and increased hepatic mitochondrial sterol 27-hydroxylase activity (conversion of cholesterol to 27-hydroxycholesterol) in all three animal models. The stimulation and feedback inhibition of cholesterol 7alpha-hydroxylase activity by bile acid depletion and replacement were observed in all three animal models, whereas the effect of cholesterol feeding was species-dependent (cholesterol 7alpha-hydroxylase activity increased in the rat, did not change in the guinea pig, and was inhibited in the rabbit). Thus, in contrast to sterol 27-hydroxylase, which was upregulated by cholesterol but not affected by bile acid depletion and replacement in all three animal models, cholesterol 7alpha-hydroxylase activity was controlled consistently and inversely by the hepatic flux of bile acids, but was species-dependent in its response to a 1-week feeding with 2% cholesterol.

Animals↗

PubMed1999

Effect of pentoxifylline on early proliferation and phenotypic modulation of fibrogenic cells in two rat models of liver fibrosis and on cultured hepatic stellate cells.

BACKGROUND/AIMS: During liver fibrosis, different fibroblastic cells, i.e. hepatic stellate cells (HSCs) or portal fibroblasts, are involved in the development of lesions, and acquire myofibroblastic differentiation. We investigated, in the rat, whether pentoxifylline can influence the early phase of fibrogenesis in two animal models of fibrosis induced by either carbon tetrachloride (CCl4) plus acetone (given twice) or bile duct ligation. METHODS: The fibroproliferative response and myofibroblastic phenotypic modulation were evaluated by PCNA and alpha-smooth muscle (alpha-SM) actin immunohistochemistry, respectively, in livers taken 24 h after the last CCl4 treatment or 72 h after bile duct ligation. Desmin expression was also measured, and inflammation was evaluated by ED-1 staining. Furthermore, proliferation and alpha-SM actin expression were studied in cultured HSCs after pentoxifylline treatment. RESULTS: In the CCl4-acetone groups, pretreatment with pentoxifylline decreased the proliferative response and expression of alpha-SM actin in the HSCs. Similarly, pentoxifylline reduced the proliferation and myofibroblastic differentiation of portal fibroblasts after bile duct ligation. Pentoxifylline reduced ED-1 expression, particularly in the CCl4 model, where there was significant inflammation. In cultured pentoxifylline-treated HSCs, both proliferation and alpha-SM actin expression were decreased. CONCLUSIONS: In both animal models of fibrosis, during the early stages of tissue injury, pentoxifylline was able to reduce fibroproliferation and myofibroblastic differentiation and to reduce hepatocellular damage and the inflammatory response, particularly in the toxin-induced model. In culture, alpha-SM actin expression decreased in both growing and quiescent HSCs treated with pentoxifylline, indicating that the drug may also exert a direct effect on hepatic fibrogenic cells.

Acetone↗

PubMed1999

Rapid cross-linking of proteins by 4-ketoaldehydes and 4-hydroxy-2-alkenals does not arise from the lysine-derived monoalkylpyrroles.

Exposure of proteins to 4-hydroxy-2-nonenal (HNE) results in conversion of lysines in part to 2-pentylpyrroles that can be formed in higher yield by exposure to the isomeric 4-oxononanal. Since both HNE and 4-oxononanal cause protein cross-linking, and since pyrrolation of proteins by gamma-diketones is also known to result in protein cross-linking, it has been considered that the initially formed 2-pentylpyrroles are responsible for the protein cross-linking seen for HNE and 4-oxononanal. Here we show that protein-bound 2-alkylpyrrole products associated with modification by 4-hydroxy-2-alkenals and 4-oxoalkanals, possessing only monoalkyl substitution, induce undetectable levels of autoxidation-mediated protein cross-linking over time periods where the parent aldehydes effect extensive protein cross-linking, which then must be occurring through alternative mechanisms. Finally, using both RNase and BSA, our finding that reductive methylation of lysines blocks protein cross-linking induced by either HNE or 4-oxononanal (and development of fluorescence in the case of HNE) implicates the obligatory role of lysines in the cross-linking reactions.

Aldehydes↗

PubMed1999

Structural elucidation of a 2:2 4-ketoaldehyde-amine adduct as a model for lysine-directed cross-linking of proteins by 4-ketoaldehydes.

4-Ketoaldehydes react with lysine-based amines to form the same pyrroles that form in low yield by treatment of proteins with 4-hydroxy-2-alkenals generated endogenously during lipid peroxidation. Since pyrroles are susceptible to oxidative coupling, it has been presumed that the cross-linking of proteins observed for 4-ketoaldehydes involves the intermediacy of the corresponding lysine-derived pyrroles. However, the monoalkylpyrroles generated from simple 4-ketoaldehydes do not exhibit oxidative coupling within the time frame that 4-ketoaldehydes induce substantial protein cross-linking. Model studies have revealed that a side reaction competes with the formation of pyrroles from 4-ketoaldehydes and amines. In this paper, we show that this side reaction involves a non-redox aldol-like condensation process resulting in 2:2 adducts, which have been structurally characterized as isomeric pyrrolo[3.2. 1]azabicyclooctanes. Formation of these 2:2 adducts in competition with pyrrole formation is proposed to represent the major pathway for rapid lysine-dependent cross-linking of proteins by simple 4-ketoaldehydes.

Aldehydes↗

PubMed1999

Apoptosis and p53 gene expression in male reproductive tissues of cadmium exposed rats.

Reverse transcription (RT) PCR technique was used to investigate the mechanism of apoptosis induced by Cd and the change of its related genes in testes and prostate of rats. Adult male rats were given a single (s.c.) injection of CdCl2 0, 2.5, 5.0, 10 mumol/kg. 48 h and 72 h after administration of Cd, animals were sacrificed. The results indicated that Cd can induce apoptosis in testes via p53-independent pathway. No apoptosis occurred in prostate in any of the Cd-exposed groups. There was a clearly negative relationship in testes between p53 gene expression and Cd exposure and this dose-response relationship was observed both at 48 h and 72 h. There was a very small increase of this gene expression in the dorsolateral lobe of the prostate in Cd exposed groups. The other apoptosis related gene, bcl-x, was not detectable in either control or Cd-exposed group in testes and dorsal prostate. Although the MT-I gene was expressed in testes or dorsal prostate both in control and exposed groups, no overexpression of MT-I gene was found after administration of Cd. The expression of MT-I in the ventral prostate was not detected in the control group, but a weak expression was found after Cd exposure. Since p53 is a tumor suppressor gene which can inhibit tumorigenesis, the consequence of a Cd-induced decrease of p53 in testes may have a relation to the known risk of Cd tumorigenesis in this tissue.

Animals↗

PubMed1999

Gender comparisons of medical students' psychosocial profiles.

OBJECTIVES: This study was designed to compare male and female medical students on selected personality attributes that could influence their academic attainment and personal success. DESIGN: Participants were 1157 medical students (743 men, 414 women) who completed a set of psychosocial questionnaires measuring intensity and chronicity of loneliness, general anxiety, test anxiety, neuroticism, depression, extraversion, self-esteem, locus of control, perceptions of parents, general health and appraisals of stressful life events. Data were analysed by employing multivariate and univariate analysis of variance and chi-square analysis. SETTING: Jefferson Medical College. SUBJECTS: Medical students. RESULTS: Men scored significantly higher on the intensity of loneliness, and women scored higher on general anxiety, test anxiety and neuroticism scales, but the magnitudes of the effect size estimates were not large. No significant gender difference was observed on measures of chronicity of loneliness, depression, extraversion, self-esteem, external locus of control, perception of general health and perceptions of the mother and the father. Women who experienced stressful life events, such as death in the family or personal illness, appraised these events more negatively than did their male counterparts. CONCLUSIONS: Implications of the findings for medical education and practice are discussed.

Adult↗