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Biomedical subjects

X Shi

Publications and source records attributed to X Shi.

At least 181 records · Page 10Linked to original sources
PubMed2000

[Study on relationship between endometrium laminin expression and irregular uterine bleeding in Norplant users].

OBJECTIVE: To investigate the relationship between endometrium laminin (LN) expression and irregular uterine bleeding in Norplant users. METHODS: Eighteen endomerium samples obtained during day 10-14th from Norlant users for 1/2, 1 or > 2 years respectively with irregular bleeding were studied morphologically and immunohistochemically for LN expression. Six normal proliferative endometria and 18 connterpacts with regular bleeding were used as control. RESULTS: In Norplant users, endometrial glands decreased in numbers and asynchromized in appearance. The LN expression on basal lamina of glandular epithelium and vascular endothelium was lower in those with irregular bleeding as compared with regular bleeders (P < 0.05). CONCLUSION: The decline of LN expression may related to irregular bleeding in Norplant users.

Adult↗
PubMed2000

[An experimental study on physiotherapy for traumatic facial nerve injury].

OBJECTIVE: To investigate the effects of electric stimulation, iontophoresis and electric stimulation with iontophoresis therapy in treating traumatic facial nerve injury. METHODS: Fifty rabbits were used. All right buccal branch of facial nerve were injured. The rabbits were randomly divided into five groups and treated by different stimulation pattern: (a) electric stimulation group; (b) iontophoresis group; (c) iontophoresis with electric stimulation group; (d) routine therapy group; (e) control group. The histologic morphology, quantitative indices of nerve fibers and electroneurography(ENoG) indices were analyzed. RESULTS: (a) Iontophoresis with Vitamin B1 and Vitamin B12 improved the regeneration of facial nerve myelin sheath. And had the best effect among these groups. (b) Electric stimulation had great effect on axon regeneration. (c) The group of electric stimulation with iontophoresis therapy had the best comprehensive effect on the nerve injury. CONCLUSIONS: Both electric stimulation and iontophoresis have good effects on nerve regeneration, when they are used in combination, the best comprehensive effect will be expected.

Animals↗
PubMed2000

[The clinical significance of the change of blood testosterone in burned patients].

OBJECTIVE: To investigate the patterns and significance of the change in blood testosterone in burned patients. METHODS: The changes of blood testosterone and luteinizing hormone (LH) were dynamically monitored in 21 male patients with moderate burn injury. RESULTS: The blood testosterone levels in this group decreased persistently after burn, and the decrement degree was related to the burn severity. But LH exhibited no regular change and its change exerted no effects on the blood testosterone levels. CONCLUSION: Decrease in blood testosterone in burned patients was related to gonadal injury, which caused the shortage and insufficiency of anabolic hormone and also of protein synthesis. The correction of the shortage of testosterone might be beneficial to protein synthesis and to the restoration of positive nitrogen equilibrium in burned patients.

Adolescent↗
PubMed2000

[Effects of Salvia miltiorrhiza compound injection on serum endothelin, prostaglandin I2/thromboxane A2 ratio alteration following myocardial ischemia-reperfusion in patients undergoing intracardiac surgery].

OBJECTIVE: To investigate the effects of Salvia miltiorrhiza compound injection (SMCI) on serum endothelin (ET), prostaglandin I2(PGI2), thromboxane A2(TXA2), and PGI2/TXA2 ratio following myocardial ischemia-reperfusion in patients undergoing intracardiac surgery. METHODS: Twenty patients, scheduled for selective surgery, were randomly divided into the SMCI group (group A, 10 cases) and the control group (group B, 10 cases). SMCI 200 mg/kg was given intravenously in group A before starting the operation and at the time of rewarming respectively, and equivalent volumes of normal saline were administered to group B. The central venous blood samples were collected to measure the serum concentration of ET, PGI2, TXA2, and PGI2/TXA2 ratio. RESULTS: ET significantly reduced, while PGI2 and TXA2 obviously raised in both groups at the beginning (T1) of extracorporeal cardiopulmonary bypass (CPB) (P < 0.05). After cardiac ischemia-reperfusion, ET in group B increased rapidly and significantly (P < 0.05) and evidently higher than the corresponding value in group A 30 min after reperfusion (T3) till 24 hrs after reperfusion (T5). During reperfusion, PGI2 and TXA2 in group A decreased more rapidly than that of group B, while group A maintained higher PGI2/TXA2 ratio than that of group B. At T5, PGI2 and TXA2 in group A were significantly lower than those in group B, while PGI2/TXA2 ratio was higher than that in group B (P < 0.05). The serum ET level was obviously negatively correlated to PGI2/TXA2 ratio. The postoperative cardiac function recovered much better in group A than in that group B. CONCLUSION: SMCI can significantly reduce serum ET level, raise PGI2/TXA2 ratio, thus facilitate the postoperative cardiac function recovery following intracardiac surgery under CPB.

6-Ketoprostaglandin F1 alpha↗
PubMed2000

[Application of indigo disulphonate spectrophotometry on the determination of ozone in indoor air].

Spectrophotometric determination of ozone in indoor air by using indigo disulphonate was investigated. The results showed that the average recovery of ozone was 99% and the relative standard deviation was 2.3% when the concentration of indoor ozone was in the range of 0.2-1.0 microgram/ml. The lowest detection concentration was 0.009 mg/m3 (sampling 20 L) when the range of determination was 0.18-10.0 mg/10 ml.

Air Pollutants↗
PubMed2000

[Mutations in the connexin 26 gene in patients with nonsyndromic hearing impairment].

OBJECTIVE: To determine the prevalence and characteristics of deafness-causing mutations in Connexin 26(Cx26, GJB2) gene in Chinese with nonsyndromic hearing impairment(NSHI). METHODS: Study subjects are all Chinese including 16 infants with sporadic congenital deaf-mutism, 39 patients with autosomal recessive hereditary hearing loss, 30 patients with autosomal dominant hereditary hearing loss and 100 normal adults. The subjects were screened for base variations by single-strand conformational polymorphism (SSCP) analysis of the amplified products of polymerase chain reaction (PCR). Those who were found have abnormal conformational band were sequenced. RESULTS: Five kinds of polymorphism were found in 15 cases of controls and six kinds of polymorphism in 10 patients. No mutation was found in Cx26 gene in Chinese with autosomal recessive NSHI. Heterozygous deletion AT at position 299-300 of Cx26 cDNA, which results in premature chain termination, was found in a pedigree with autosomal dominant hereditary nonsyndromic hearing loss. CONCLUSION: The prevalence of deafness-causing mutations in Cx26 gene in Chinese with autosomal recessive NSHI maybe is lower than that of other ethnic groups. Heterozygous deletion AT at position 299-300 of Cx26 cDNA can lead to autosomal dominant hereditary hearing loss (DFNA3).

Asian People↗
PubMed2000

Treatment of sodium disorders after surgery of craniopharyngioma.

OBJECTIVE: To study the treatment of the patients with blood sodium disorder after craniopharyngioma surgery. METHOD: The blood sodium in 44 patients with craniopharyngiomas was daily examined from operative to post-operative days. Hypernatremia is defined as [Na] > 145 mmol/l, and hyponatremia as [Na] < 135 mml/L. RESULTS: Of the 44 patients, 36 developed sodium disorder. Among them, simple hyponatremia was 16 patients, simple hypernatremia was 9 patients, and alternative sodium disorder was 11 patients. CONCLUSION: The blood sodium disorder in patients with craniopharyngiomas after surgery appears to present complicated changes. Three types of blood sodium disorder could be determined as simple hyponatremia, simple hypernatremia, and alternative sodium disorder. Treatment of the sodium disorder in patients with after surgery could be carried in accordance with the above three types.

Adolescent↗
PubMed1999

Involvement of 5'-flanking kappaB-like sites within bcl-x gene in silica-induced Bcl-x expression.

The present study investigated the involvement of the transcription factor NF-kappaB in the expression of an anti-apoptotic gene, bcl-x, using a murine macrophage cell line and peritoneal macrophages from both wild type (p50(+/+)) and NF-kappaB p50 gene knockout (p50(-/-)) mice. Increased expression of Bcl-x protein was observed in native and silica-exposed p50(-/-) macrophages in which the NF-kappaB p65-containing complex was predominantly induced. Co-transfection experiment using a bcl-x promoter reporter construct and an expression vector for NF-kappaB p50 or p65 indicates that p65, but not p50, up-regulates the promoter activity of the bcl-x gene. DNA sequence analysis revealed that there are several kappaB-like sites within the 5'-flanking region of the bcl-x gene. Electrophoretic mobility shift assay suggested differences in binding of the NF-kappaB complexes to these putative NF-kappaB binding sites of the bcl-x gene.

Animals↗
PubMed1999

Role of reactive oxygen species and p53 in chromium(VI)-induced apoptosis.

Apoptosis is a programmed cell death mechanism to control cell number in tissues and to eliminate individual cells that may lead to disease states. The present study investigates chromium(VI) (Cr(VI))-induced apoptosis and the role of reactive oxygen species (ROS) and p53 in this response. Treatment of human lung epithelial cells (A549) with Cr(VI) caused apoptosis as measured by DNA fragmentation, mitochondria damage, and cell morphology. Cr(VI)-induced apoptosis is contributed to ROS generation, resulting from cellular reduction of Cr(VI) as measured by flow cytometric analysis of the stained cells, oxygen consumption, and electron spin resonance spin trapping. Scavengers of ROS, such as catalase, aspirin, and N-acetyl-L-cysteine, decreased Cr(VI)-induced apoptosis, whereas NADPH and glutathione reductase, enhancers of Cr(VI)-induced ROS generation, increased it. p53 is activated by Cr(VI), mostly by ROS-mediated free radical reactions. Cr(VI)-induced ROS generation occurred within a few minutes after Cr(VI) treatment of the cells, whereas p53 induction took at least 5 h. The level of Cr(VI)-induced apoptosis was similar in both p53-positive cells and p53-negative cells independent of p53 status in the early stage (0-3 h) of Cr(VI) treatment. However, at the later stage (3-24 h), the level of the apoptosis is higher in p53-positive cells than in p53-negative cells. These results suggest that ROS generated through Cr(VI) reduction is responsible to the early stage of apoptosis, whereas p53 contributes to the late stage of apoptosis and is responsible for the enhancement of Cr(VI)-induced apoptosis at this stage.

Apoptosis↗
PubMed1999

Freshly fractured crystalline silica induces activator protein-1 activation through ERKs and p38 MAPK.

The transcription factor activator protein-1 (AP-1) reportedly plays an important role in the induction of neoplastic transformation and multiple genes involved in cell proliferation, differentiation, and inflammation. To investigate the mechanisms of silica-induced carcinogenesis, AP-1-luciferase reporter transgenic mice were used as an in vivo model, whereas the JB6 mouse epidermal cell line and a rat lung epithelial cell line were employed as in vitro models to study the effects of silica at the molecular level. Freshly fractured silica caused an 8-fold increase in AP-1 activity in JB6 cells and a 2.5-fold increase in rat lung epithelial cells. The induction of AP-1 activity in cultured cell lines was time- and dose-dependent. Intratracheal administration of silica was also able to induce AP-1 transactivation in transgenic mice. AP-1 activation was first observed at 2 days after silica administration and reached its maximum at 3 days post-exposure of the mice to silica. The signal transduction pathways for AP-1 activation were also investigated using these cell lines. The results demonstrate that freshly fractured silica stimulates mitogen-activated protein kinase (MAPK) family members, as determined by the phosphorylation of p38 MAPK and extracellular signal-regulated protein kinases (ERKs). Inhibition of ERKs with PD98059 or of p38 with SB203580 significantly inhibited silica-induced AP-1 activation. These findings demonstrate for the first time that freshly fractured silica induces AP-1 activation, which may be mediated through p38 MAPK and ERK pathways. Unraveling the complex mechanisms associated with these events may provide insights into the initiation and progression of silica-induced carcinogenesis.

Animals↗
PubMed1999

Regulation of a cell type-specific silencer in the human interleukin-3 gene promoter by the transcription factor YY1 and an AP2 sequence-recognizing factor.

Negative regulation of cytokine gene transcription is an important mechanism in maintaining homeostasis of immune function. In this study, we characterized a silencer element in the human interleukin-3 gene promoter that is responsible for the cell-specific expression of interleukin-3. This silencer activity was proposed to be mediated by an unidentified nuclear inhibitory protein (NIP). In this study, we have identified two nuclear factors that are responsible for the silencer activity in T cells. The NIP element forms four specific DNA-protein complexes (designated as complexes A-D) with the Jurkat nuclear proteins. Complex A contains a nuclear protein that shares DNA-binding specificity with the transcription factor AP2 (designated as an AP2 sequence-recognizing factor (ASRF)). Formation of this ASRF complex is required for the NIP silencer function, as mutation of the ASRF-binding site abrogated the silencer activity. Complex B contains the nuclear factor YY1 (Yin-Yang 1), whose function is to down-regulate ASRF activity in the silencer. YY1 activity is supported by data from mutation and cotransfection analyses. Complexes C and D are formed by nonspecific binding proteins and do not express any regulatory activity in the NIP element. These data indicate that a cell type-specific silencer activity might be determined by a unique profile of ubiquitous transcription factors.

DNA-Binding Proteins↗
PubMed1999

Vanadate induction of NF-kappaB involves IkappaB kinase beta and SAPK/ERK kinase 1 in macrophages.

The present studies investigated the signaling pathways of vanadate, a vanadium ion with +5 oxidation state, to activate NF-kappaB transcription factor, a pivotal regulator of inflammatory responses. Treatment of macrophages with vanadate results in the activation of both NF-kappaB and c-Jun N-terminal kinase (JNK). The activity of a recently identified cellular kinase, IkappaB kinase-beta (IKKbeta), was significantly elevated concomitant with the increased degradation of IkappaBalpha and enhanced NF-kappaB activity in cells exposed to vanadate. To determine whether the IKK pathway and JNK pathway are interconnected or bifurcate upon vanadate stimulation, cells were transfected with either a kinase inactive form of IKKbeta or a kinase inactive form of SAPK/ERK kinase 1 (SEK1). Inactive IKKbeta was able to block vanadate-induced degradation of IkappaBalpha, yet it was unable to influence the activation of JNK by vanadate. Conversely, blockage of JNK activation by transfection of a kinase-inactive form of SEK1 resulted in partially inhibition of vanadate-induced IkappaBalpha degradation. Both vanadate-induced degradation of IkappaBalpha and activation of JNK were potently inhibited by pretreatment of cells with N-acetylcysteine or dimercaprol. These results demonstrate that early activation of stress kinases or change of cellular redox states plays a key role in vanadate-induced activation of NF-kappaB and JNK.

Animals↗
PubMed1999

Reactive oxygen species in the aerobic decomposition of sodium hydroxymethanesulfinate.

Sodium hydroxymethanesulfinate, (HOCH2SO2Na, HMS) is relatively stable in aqueous alkaline environments, but rapidly decomposes in acidic medium to give a variety of products that include sulfur dioxide. A detailed kinetic and mechanistic study of the decomposition of HMS in slightly acidic medium has shown a process that produces dithionite, S2O2-4, which is preceded by an induction period which persists for as long as molecular oxygen is present in the reaction solution. The complete consumption of molecular oxygen is a prerequisite for the formation of S2O2-4. Among some of the intermediates detected in the decomposition of HMS is the sulfite radical, SO-3. Comparisons are made between the decomposition mechanisms of thiourea dioxide (aminoiminomethanesulfinic acid) and HMS.

Catalase↗
PubMed1999

New generation dopaminergic agents. 6. Structure-activity relationship studies of a series of 4-(aminoethoxy)indole and 4-(aminoethoxy)indolone derivatives based on the newly discovered 3-hydroxyphenoxyethylamine D2 template.

A series of 4-(aminoethoxy)indoles 7 and a related series of 4-(aminoethoxy)indolones 8 were synthesized and evaluated for their affinity for both the high- and low-affinity agonist states (D2High and D2Low, respectively) of the dopamine (DA) D2 receptor. The 4-aminoethoxy derivatives (i.e., 7 and 8) were designed as bioisosteric analogues based on the phenol prototype 4. The indolones 8 were observed to have high affinity for the D2High receptor. Comparison of their previously reported chroman analogues with the more flexible 4-(aminoethoxy)indoles revealed the chroman analogues to be more potent, whereas little loss in D2High affinity was observed when comparing the 4-(aminoethoxy)indolones with their respective chroman analogues. Several regions of the phenoxyethylamine framework were modified and recognized as potential sites to modulate the level of intrinsic activity. A conformational analysis was performed and a putative bioactive conformation was proposed which fulfilled the D2 agonist pharmacophore criteria based on the McDermed model. Structure-activity relationships gained from these studies have aided in the synthesis of D2 partial agonists of varying intrinsic activity levels. These agents should be of therapeutic value in treating disorders resulting from hypo- and hyperdopaminergic activity, without the side effects associated with complete D2 agonism or antagonism.

Animals↗
PubMed1999

Cr(IV) causes activation of nuclear transcription factor-kappa B, DNA strand breaks and dG hydroxylation via free radical reactions.

Electrophoretic mobility shift, DNA strand breakage assays and electron spin resonance (ESR) spin trapping were used to investigate the activation of nuclear transcription factor (NF)-kappa B, DNA strand breakage and 2'-deoxyguanosine hydroxylation induced by Cr(IV), as well the role of free radical reactions in these processes. Incubation of synthesized Cr(IV)-glutathione complex with cultured Jurkat cells resulted in activation of DNA binding activity of NF-kappa B. Cr(VI) is also able to induce NF-kappa B activation through Cr(V) and Cr(IV) intermediates generated during the reduction of Cr(VI) by the cells. Cr(III) did not cause observable NF-kappa B activation due to its inability to cross cell membranes. Cr(IV)-induced NF-kappa B activation is dose-dependent. Catalase inhibited the activation while superoxide dismutase enhanced it. The metal chelator, deferoxamine, and hydroxyl (.OH) radical scavengers, sodium formate and aspirin, also inhibited the NF-kappa B activation. Electrophoretic assays using lambda Hind III linear DNA showed that, in the presence of H2O2, Cr(IV) is capable of causing DNA strand breaks. Deferoxamine, sodium formate and aspirin inhibited the DNA strand breaks. HPLC measurements also show that .OH radical generated by the Cr(IV)-mediated reaction with H2O2 was capable of causing 2'-deoxyguanosine (dG) hydroxylation to generate 8-hydroxyguanosine (8-OHdG). The relative magnitude of 8-OHdG formation correlated with the generation of .OH radicals. ESR spin trapping measurements showed that reaction of Cr(IV) with H2O2 generated .OH radicals, which were inhibited by deferoxamine, sodium formate and aspirin. The results show that Cr(IV) can cause NF-kappa B activation, DNA strand breaks and dG hydroxylation through .OH radical-initiated reactions. This reactive chromium intermediate may play an important role in the mechanism of Cr(VI)-induced carcinogenesis. The results also suggest that the Cr(IV)-glutathione complex may be used as a model compound to study the role of Cr(IV) in Cr(VI) carcinogenicity.

Antioxidants↗
PubMed1999

Smad1 interacts with homeobox DNA-binding proteins in bone morphogenetic protein signaling.

Bone morphogenetic proteins (BMP) transduce their signals into the cell through a family of mediator proteins known as Smads. Upon phosphorylation by the BMP receptors, Smad1 interacts with Smad4 and translocates into the nucleus where the complex recruits DNA-binding protein(s) to activate specific gene transcription. However, the DNA-binding protein(s) involved in BMP signaling has not been identified. Using a yeast two-hybrid approach, we found that Smad1 interacts with Hoxc-8, a homeodomain transcription factor. The interaction between Smad1 and Hoxc-8 was confirmed by a "pull-down" assay and a co-immunoprecipitation experiment in COS-1 cells. Interestingly, purified Smad1 inhibited Hoxc-8 binding to the osteopontin Hoxc-8 site in a concentration-dependent manner. Transient transfection studies showed that native osteopontin promoter activity was elevated upon BMP stimulation. Consistent with the gel shift assay, overexpression of Hoxc-8 abolished the BMP stimulation. When a wild type or mutant Hoxc-8 binding element was linked to an SV40 promoter-driven reporter gene, the wild type but not the mutant Hoxc-8 binding site responded to BMP stimulation. Again, overexpression of Hoxc-8 suppressed the BMP-induced activity of the wild type reporter construct. Our findings suggest that Smad1 interaction with Hoxc-8 dislodges Hoxc-8 from its DNA binding element, resulting in the induction of gene expression.

Animals↗
PubMed1999

Chronic haloperidol alters dopamine receptors: effects of cocaine exposure during the preweaning period.

The effect of cocaine exposure during the preweaning period on the function of the central dopaminergic systems was determined in adult rats. The present study investigated the alterations in dopamine receptors in 93-day-old male and female rats treated with cocaine (50 mg kg(-1) day(-1)), 1-[2-[bis(4-fluorophenyl)methoxyl]-4-[3-phenylpropyl]piperazine (GBR 12909) (50 mg kg(-1) every other day) or water during postnatal days 11-20. Haloperidol (2 mg kg(-1) day) or saline was injected during postnatal days 76-90 and the rats were killed on postnatal day 93. Quantitative receptor autoradiography with [3H]R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-b enzazepine ([3H]SCH 23390) for the dopamine D1 receptor and [3H]raclopride for the dopamine D2 receptor was carried out. The results show that haloperidol increased [3H]raclopride binding in many forebrain regions. Preweaning cocaine treatment in males increased the area showing this effect. Males generally were more responsive to haloperidol than females. However, in GBR 12909-treated females, raclopride binding showed widespread increases following haloperidol injection. For SCH 23390 binding, most regions showed a significant interaction between haloperidol, sex and preweaning treatment group. This was due primarily to the GBR 12909-treated males, which showed elevated basal dopamine D1 receptor binding levels and a haloperidol-induced reduction in dopamine D1 receptor binding in most regions evaluated. These data suggest that inhibition of the dopamine transporter during ontogeny produces long-term alterations in dopamine receptor regulation but that selective inhibitors of the dopamine transporter produced greater effects than cocaine on both raclopride and SCH 23390 binding following chronic haloperidol injection.

Animals↗