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Xiao-Bing Fu

Publications and source records attributed to Xiao-Bing Fu.

At least 19 recordsLinked to original sources
PubMed2006

Angiotensin II regulates phosphoinositide 3 kinase/Akt cascade via a negative crosstalk between AT1 and AT2 receptors in skin fibroblasts of human hypertrophic scars.

Angiotensin II (Ang II) stimulation has been shown to regulate proliferation of skin fibroblasts and production of extracellular matrix, which are very important process in skin wound healing and scarring; however, the signaling pathways involved in this process, especially in humans, are less explored. In the present study, we used skin fibroblasts of human hypertrophic scar, which expressed both AT1 and AT2 receptors, and observed that Ang II increased Akt phosphorylation and phosphoinositide 3 kinase (PI 3-K) activity. In addition, the Ang II-induced Akt phosphorylation was blocked by wortmannin, a PI 3-K inhibitor. This Ang II-activated PI 3-K/Akt cascade was markedly inhibited by valsartan, an AT(1) receptor-specific blocker, whereas it was enhanced by PD123319, an AT(2) receptor antagonist. On the other hand, the Ang II- or EGF-induced activation of PI 3-K/Akt was strongly attenuated by AG1478, an inhibitor of epidermal growth factor (EGF) receptor kinase. Moreover, Ang II stimulated tyrosine phosphorylation of EGF receptor and p85alpha subunit of PI 3-K accompanied by an increase in their association, which was inhibited by valsartan, and enhanced by PD123319. The Ang II-induced transactivation of EGF receptor resulted in activation of extracellular signal-regulated kinase (ERK) that was also inhibited by valsartan, and enhanced by PD123319. Taken together, our results showed that AT(1) receptor-mediated activation of PI 3-K/Akt cascades occurs at least partially via the transactivation of EGF receptor, which is under a negative control by AT(2) receptor in hypertrophic scar fibroblasts. These findings contribute to understanding the molecular mechanism of human hypertrophic scar formation.

Angiotensin II↗
PubMed2006

Analysis of differentially expressed genes in fetal skin of scarless and scar-forming periods of gestational rats.

OBJECTIVE: To study the differences of gene expression between earlier gestational skin and later gestational skin of rats with the aids of single primer amplification (SPA) and high-density oligonucleotide DNA array to understand the molecular mechanism of scarless healing. METHODS: Total RNAs were isolated from fetal rat skin of the scarless (E15) and scar-forming (E18) periods of gestation (term = 21.5 days). The RNAs from earlier gestational skin (EGS) and later gestational skin (LGS) were both reversely transcribed to cDNAs, then labeled with the incorporation of fluorescent dCTP for preparing the hybridization probes by SPA method. The mixed probes were then hybridized to the oligonucleotide DNA arrays which contained 5,705 probes representing 5,705 rat genes. After highly stringent washing, these DNA arrays were scanned for fluorescent signals to display the differentially expressed genes between the 2 groups of skin. RESULTS: Among 5,705 rat genes, there were 53 genes (0.93 percent) with differentially expressed levels between EGS and LGS groups, 27 genes, including fibroblast growth factor 2 (FGF2) and follistatin were up-regulated (0.47%) and 26 genes were down-regulated (0.46%) in fetal skin during scarless period versus scar-forming period. Higher expressions of FGF2 and follistatin in EGS than those in LGS were also revealed by RT-PCR method. CONCLUSIONS: High-density oligonucleotide DNA array provided a powerful tool for investigating differential gene expression in earlier and later gestational fetal skins. This technology validates that the mechanism of fetal scarless healing is very complicate and the change of many gene expressions is associated with fetal scarless healing.

Animals↗
PubMed2005

Exogenous acid fibroblast growth factor inhibits ischemia-reperfusion-induced damage in intestinal epithelium via regulating P53 and P21WAF-1 expression.

AIM: To detect the effect of acid fibroblast growth factor (aFGF) on P53 and P21WAF-1 expression in rat intestine after ischemia-reperfusion (I-R) injury in order to explore the protective mechanisms of aFGF. METHODS: Male rats were randomly divided into four groups, namely intestinal ischemia-reperfusion group (R), aFGF treatment group (A), intestinal ischemia group (I), and sham-operated control group (C). In group I, the animals were killed after 45 min of superior mesenteric artery (SMA) occlusion. In groups R and A, the rats sustained for 45 min of SMA occlusion and were treated with normal saline (0.15 mL) and aFGF (20 mug/kg, 0.15 mL), then sustained at various times for up to 48 h after reperfusion. In group C, SMA was separated, but without occlusion. Apoptosis in intestinal villi was determined with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling technique (TUNEL). Intestinal tissue samples were taken not only for RT-PCR to detect P53 and P21WAF-1 gene expression, but also for immunohistochemical analysis to detect P53 and P21WAF-1 protein expression and distribution. RESULTS: In histopathological study, ameliorated intestinal structures were observed at 2, 6, and 12 h after reperfusion in A group compared to R group. The apoptotic rates were (41.17+/-3.49)%, (42.83+/-5.23)%, and (53.33+/-6.92)% at 2, 6, and 12 h after reperfusion, respectively in A group, which were apparently lower than those in R group at their matched time points (50.67+/-6.95)%, (54.17+/-7.86)%, and (64.33+/-6.47)%, respectively, (P<0.05)). The protein contents of P53 and P21WAF-1 were both significantly decreased in A group compared to R group (P<0.05) at 2-12 h after reperfusion, while the mRNA levels of P53 and P21WAF-1 in A group were obviously lower than those in R group at 6-12 h after reperfusion (P<0.05). CONCLUSION: P53 and P21WAF-1 protein accumulations are associated with intestinal barrier injury induced by I-R insult, while intravenous aFGF can alleviate apoptosis of rat intestinal cells by inhibiting P53 and P21WAF-1 protein expression.

Animals↗
PubMed2005

Acid fibroblast growth factor reduces rat intestinal mucosal damage caused by ischemia-reperfusion insult.

AIM: To detect the effects of acid fibroblast growth factor (aFGF) on apoptosis and proliferation of intestinal epithelial cells in differentiation or proliferation status to explore the protective mechanisms of aFGF. METHODS: Wistar rats were randomly divided into sham-operated control group (C, n=6), intestinal ischemia group (I, n=6), aFGF treatment group (A, n=48) and intestinal ischemia-reperfusion group (R, n=48). Apoptosis of intestinal mucosal cells was determined with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) technique. Proliferating cell nuclear antigen (PCNA) protein expression and distribution were detected with immunohistochemical method. Plasma levels of D-lactate were determined with modified Brandts method. RESULTS: In A group, administration of exogenous aFGF could improve intestinal histological structure and decrease plasma D-lactate levels at 2-12 h after the reperfusion compared with R group. The apoptotic rates and PCNA protein expressions were not increased until 2 h after reperfusion and were maximal at 12 h. After reperfusion for 2-12 h, the apoptotic rates were gradually augmented along the length of jejunal crypt-villus units. Administration of aFGF could significantly reduce the apoptotic response at 2-12 h after reperfusion (P<0.05). Apoptosis rates in villus and crypt epithelial cells in A group at 12 h after reperfusion were (62.5+/-5.5)% and (73.2+/-18.6)% of those in R group, respectively. Treatment of aFGF could apparently induce protein expression of PCNA in intestinal mucosal cells of A group compared with R group during 2-12 h after reperfusion (P<0.05). There were approximately 1.3- and 1.5-times increments of PCNA expression levels in villus and crypt cells in A group at 12 h after reperfusion compared with R group, respectively. CONCLUSION: Intestinal I/R insult could lead to histological structure change and apoptotic rate increment. The protective effects of aFGF against ischemia/reperfusion in rat intestinal mucosa might be partially due to its ability to inhibit ischemia/reperfusion-induced apoptosis and to promote cell proliferation of crypt cells and villus epithelial cells.

Animals↗
PubMed2005

Protective effects of non-mitogenic human acidic fibroblast growth factor on hydrogen peroxide-induced damage to cardiomyocytes in vitro.

AIM: To study the protective effect of non-mitogenic human acidic fibroblast growth factor (FGF) on cardiac oxidative injury in vivo. METHODS: Ventricular cardiomyocytes were isolated from 1- to 3-d-old neonatal SD mice and cultured in Dulbecco's minimum essential medium supplemented with 15% fetal bovine serum under an atmosphere of 50 mL/L CO2-95% air at 37 degrees, as well as assessed by immunocytochemical assay. We constructed the cardiomyocyte injury model by exposure to a certain concentration of H2O2. Cellular viability, superoxide dismutase (SOD) activity, leakage of maleic dialdehyde and anti-apoptosis effect were included to evaluate the cardiac protective effect of non-mitogenic human acidic FGF. RESULTS: Over 50% of the cardiomyocytes beat spontaneously on the 2nd d of culture and synchronously beat after being cultured for 3 d. Forty-eight hours after plating was completed, the purity of such cultures was 95% myocytes, assessed by an immunocytochemical assay. Cellular viability dramatically decreased with the increasing of the concentration of H2O2. Non-mitogenic human acidic FGF showed significant resistance to the toxic effect of H2O2, significantly increased the cellular viability as well as the activity of SOD, and dramatically decreased the leakage of maleic dialdehyde as well as the cellular apoptosis rate. CONCLUSION: Hydrogen peroxide shows strong cytotoxicity to the cultured cardiac myocytes, and non-mitogenic human acidic FGF shows strong cardio-protective effect when exposed to a certain concentration of H2O2.

Animals↗
PubMed2005

Intravenous acid fibroblast growth factor protects intestinal mucosal cells against ischemia-reperfusion injury via regulating Bcl-2/Bax expression.

AIM: To detect the effect of acid fibroblast growth factor (aFGF) on apoptosis and gene expression of bax and bcl-2 gene in rat intestine after ischemia/reperfusion (I/R) injury, and to explore the protective mechanisms of aFGF. METHODS: One hundred and eight Wistar rats were randomly divided into sham-operated control group (C) (n = 6), intestinal ischemia group (I) (n = 6), aFGF treatment group (A) (n = 48) and intestinal ischemia-reperfusion group (R) (n = 48). In group I, the animals were killed after 45 min of superior mesenteric artery (SMA) occlusion, while in groups R and A, the rats sustained 45 min of SMA occlusion and were then treated with normal saline and aFGF, respectively, sustained 15 min, 30 min, 1, 2, 6, 12, 24, or 48 h of reperfusion, respectively. In group C, SMA was separated, but without occlusion. Apoptosis in intestinal villus was determined with terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling technique (TUNEL). Intestinal tissue samples were taken not only for detection of bax and bcl-2 gene expression by RT-PCR, but also for detection of bax and bcl-2 protein expression and distribution by immunohistochemical analysis. RESULTS: The rat survival rates in aFGF treated group were higher than group R (P<0.05) and the improvement of intestinal histological structures was observed at 2, 6, and 12 h after the reperfusion in group A compared with group R. The apoptotic rates were (41.17+/-3.49)%, (42.83+/-5.23)% and (53.33+/-6.92)% at 2, 6 and 12 h after reperfusion, respectively in group A, apparently less than those of group R at matched time points (50.67+/-6.95, 54.17+/-7.86, 64.33+/-6.47, respectively) (P<0.05). The bax gene transcription and translation were significantly decreased in group A vs group R, while mRNA and protein contents of Bcl-2 in group A were obviously higher than those in group R during 2-12 h period after reperfusion. CONCLUSION: The changes in histological structure and the increment of apoptotic rate indicated that the intestinal barrier was damaged after intestinal I/R injury, whilst intravenous aFGF could alleviate apoptosis induced by ischemia and reperfusion in rat intestinal tissues, in which genes of bax and bcl-2 might play important roles.

Animals↗
PubMed2005

Inhibition of p38 mitogen-activated protein kinase may decrease intestinal epithelial cell apoptosis and improve intestinal epithelial barrier function after ischemia- reperfusion injury.

AIM: To investigate the role of p38 mitogen-activated protein kinase in rat small intestine after ischemia-reperfusion (I/R) insult and the relationship between activation of p38 MAPK and apoptotic cell death of intestine. METHODS: Ninety Wistar rats were divided randomly into three groups, namely sham-operated group (C), I/R vehicle group (R) and SB203580 pre-treated group (S). In groups R and S, the superior mesenteric artery (SMA) was separated and occluded for 45 min, then released for reperfusion for 0.25, 0.5, 1, 2, 6, 12 and 24 h. In group C, SMA was separated without occlusion. Plasma D-lactate levels were examined and histological changes were observed under a light microscope. The activity of p38 MAPK was determined by Western immunoblotting and apoptotic cells were detected by the terminal deoxynucleotidyl transferase (TdT)-mediated dUDP-biotin nick end labeling (TUNEL). RESULTS: Intestinal ischemia followed by reperfusion activated p38 MAPK, and the maximal level of activation (7.3-fold vs sham-operated group) was reached 30 min after I/R. Treatment with SB 203580, a p38 MAPK inhibitor, reduced intestinal apoptosis (26.72+/-3.39% vs 62.50+/-3.08% in I/R vehicle, P<0.01) and decreased plasma D-lactate level (0.78+/-0.15 mmol/L in I/R vehicle vs 0.42+/-0.17 mmol/L in SB-treated group) and improved post-ischemic intestinal histological damage. CONCLUSION: p38 MAPK plays a crucial role in the signal transduction pathway mediating post-ischemic intestinal apoptosis, and inhibition of p38 MAPK may attenuate ischemia-reperfusion injury.

Animals↗
PubMed2005

Morphological and distribution characteristics of sweat glands in hypertrophic scar and their possible effects on sweat gland regeneration.

BACKGROUND: In hypertrophic scar tissue, no sweet gland and hair follicle exist usually because of the dermal and epidermal damage in extensive thermal skin injury, thus imparing regulation of body temperature. This study was designed to reveal the morphological and distributional characteristics of the sweat glands in normal skin and hypertrophic scar obtained from children and adults, and to study the possible interfering effects of the scar on regeneration of the sweat gland after burn injury. METHODS: Biopsies of hypertrophic scar were taken from four children (4 - 10 years) and four adults (35 - 51 years). Normal, uninjured full-thickness skin adjacent to the scar of each patient was used as control. Keratin 19 (K19) was used as the marker for epidermal stem cells and secretory portion of the sweat glands, and keratin 14 (K14) for the tube portion, respectively. Immunohistochemical and histological evaluations were performed. RESULTS: Histological and immunohistochemical staining of skin tissue sections from both the children and adults showed K19 positive cells in the basement membrane of epidermis of normal skin. These cells were seen only single layer and arranged regularly. The secretory or duct portion of the eccrine sweat glands was situated in the dermis and epidermal layer. However, in the scar tissue, K19 positive cells were scant in the basal layer, and the anatomic location of the secretory portion of sweat glands changed. They were located between the border of the scar and reticular layer of the dermis. These secretory portions of sweat glands were expanded and were organized irregularly. But a few K14 positive cells were scattered in the scar tissues in cyclic form. CONCLUSIONS: There are some residual sweat glands in scar tissues, in which the regeneration process of active sweat glands is present. Possibly the sweat glands could regenerate from adult epidermal stem cells or residual sweat glands in the wound bed after burn injury.

Adult↗
PubMed2005

Ontogeny of expression of basic fibroblast growth factor and its receptors in human fetal skin.

OBJECTIVE: To investigate the expression characteristics of basic fibroblast growth factor (bFGF) and its receptors, flg (FGFR1) and bek (FGFR2), in fetal skin at different gestational ages underlying the relevance of these 3 proteins to skin development and the mechanisms underlying the phenotypic transition from scarless to scar-forming healing. METHODS: Eighteen specimens of fetal skin biopsies of human embryo were obtained from spontaneous abortions at different gestational ages of 13-32 weeks. Gene expression of bFGF, bek and flg was examined with reverse transcription-polymerase chain reaction (RT-PCR). The dynamic expression and distribution of these 3 proteins were detected with streptavidin peroxidase (SP) immunohistochemical staining method. RESULTS: In the early gestational fetal skin, genes of bFGF and flg were strongly expressed and more protein contents of these 2 proteins were found as compared with the genes at late gestation fetal skin (2.446+/-0.116 and 2.066+/-0.152 versus 2.157+/-0.101 and 1.818+/-0.086, respectively, P<0.05). On the contrary, the levels of gene expression and protein content of bek were not differently expressed in the early gestational fetal skin versus the late ones. Protein particles of bFGF were mainly distributed in the epidermal cells and some fibroblasts. Bek was mainly located in the cell membrane and cytoplasm of epidermal cells while flg protein was principally located in the epidermal cells, endothelial cells and some fibroblasts. CONCLUSIONS: The endogenous bFGF and their receptors might be involved in the cutaneous development at fetal stage. The differently expressing levels of bFGF and flg during gestation may be related to scarless or scar-forming repair during gestation.

Journal Article↗
PubMed2004

Enhanced anti-apoptosis and gut epithelium protection function of acidic fibroblast growth factor after cancelling of its mitogenic activity.

AIM: Mitogenic and non-mitogenic activities of fibroblast growth factor (FGF) are coupled to a range of biological functions, from cell proliferation and differentiation to the onset of many diseases. Recent reports have shown that acidic fibroblast growth factor (aFGF) has a powerful anti-apoptosis function, which may have potentially therapeutical effect on gut ischemia and reperfusion injuries. However, whether this function depends on its mitogenic or non-mitogenic activity remains unclear. In this study, we identified the source of its anti-apoptosis function with a mutant, aFGF28-154 and observed its effect on reducing gut ischemia and reperfusion injury. METHODS: aFGF28-154 was generated by amplification of appropriate DNA fragments followed by subcloning the products into pET-3c vectors, then they were expressed in BL21 (DE3) cells and purified on an M2 agarose affinity column. This mutant aFGF28-154 maintained its non-mitogenic activity and lost its mitogenic activity. With a dexamethasone (DEX)-induced mouse thymocyte apoptosis model in vitro and in vivo, we studied the anti-apoptotic function of aFGF28-154. Also, in vivo study was performed to further confirm whether aFGF28-154 could significantly reduce apoptosis in gut epithelium after gut ischemia-reperfusion injury in rats. Based on these studies, the possible signal transduction pathways involved were studied. RESULTS: With a dexamethasone (DEX)-induced mouse thymocyte apoptosis model in vitro and in vivo, we found that the anti-apoptotic function of aFGF28-154 was significantly enhanced when compared with the wild type aFGF. In vivo study further confirmed that aFGF28-154 significantly reduced apoptosis in gut epithelium after gut ischemia-reperfusion injury in rats. The mechanisms of anti-apoptosis function of aFGF28-154 did not depend on its mitogenic activity and were mainly associated with its non-mitogenic activities, including the intracellular calcium ion balance protection, ERK1/2 activation sustaining and cell cycle balance. CONCLUSION: These findings emphasize the importance of non-mitogenic effects of aFGF, and have implications for its therapeutic use in preventing apoptosis and other injuries in tissues and internal organs triggered by ischemia-reperfusion injury.

Animals↗
PubMed2004

[The pathogenesis of discogenic low back pain].

OBJECTIVE: To study the pathogenesis of the pain of discography and the discogenic low back pain. METHODS: 19 specimens of lumbar intervertebral discs from 17 patients with discogenic low back pain during posterior lumbar interbody fusion, and 12 physiologically aging discs and 10 normal control discs were collected to investigate the morphologic features and innervation containing neuropeptides substance P (SP), neural filament (NF), and vasoactive-intestinal peptide (VIP). RESULTS: The distinct morphologic characteristic of the disc from the patient with discogenic low back pain was the formation of the strip zone of vascularized granulation tissue from the nucleus pulposus to the outer part of the annulus fibrosus in which there was one or several fissures. The structure of annulus fibrosus beyond the strip zone of granulation tissue was basically normal. The structures of the aging discs and the control discs showed the age-related changes. The innervation of SP, NF and VIP immunoreactive nerve fibers in the painful discs was more extensive compared with the aging discs and the control discs. The nerve in growth deep into annulus fibrosus and nucleus pulposus was observed mainly along the strip zone of granulation tissue in the painful discs. CONCLUSIONS: Findings indicate that the strip zone of granulation tissue with extensive innervation in the posterior part of the painful disc is the original site of the pain of discography and the discogenic low back pain. The strip zone of granulation tissue might originate from the injury and subsequent reparation of the margin of annulus fibrosus. The difference of the aging disc and painful disc which can not be differed each other on MRI is the formation of the strip zone of granulation tissue along tear histologically in posterior part of the painful disc.

Adult↗
PubMed2004

[Enhancing the repair quality of skin injury on porcine after autografting with the bone marrow mesenchymal stem cells].

OBJECTIVE: To explore the effects of bone marrow mesenchymal stem cells (MSCs) on the quality of healing of porcine skin wounds after burn injury so as to provide a new method for clinical skin repair in the future. METHODS: Seventy-two deep-partial thickness burn wounds were produced on the back of 6 minipigs and then the pigs were randomly divided into 6 groups: saline control, MSCs treatment, MSCs plus basic fibroblast growth factor (bFGF) treatment, MSCs plus epidermal growth factor (EGF) treatment, bFGF treatment or EGF treatment only. MSCs were isolated from porcine marrow and cultured in vitro. After labeling with BrdU, MSCs were autografted onto the skin wounds. 7, 14, 21 and 42 days after the injury, the area of the wounds were measured and the histological examination was performed to evaluate the velocity and quality of wound healing.1, 2 and 4 weeks after transplantation, immunohistochemical examinations were carried out to detect the positive staining of BrdU, cytokeratin and S-100 to evaluate the wound healing quality. RESULTS: The area of wounds was decreased at day 7 and most of these wounds were healed on day 21 after injury. Although there was no significant statistical difference in the contraction rate among these six groups, however, the reduced wound areas in the MSCs plus bFGF treatment group was 15% to 20% more than that in the other 5 groups. Histological examination and semi-quantitative analysis demonstrated that the number of vessels and the expression density of S-100 in the MSCs plus bFGF treatment wounds were significantly enhanced than that in the other groups. CONCLUSION: MSCs autografting may benefit to enhance the wound healing quality in porcine skin, which may open a new way to reach a "perfect repair" after skin injury.

Animals↗
PubMed2004

[Gene expression of angiogenesis-related factors in fetal skin at different developmental stages and childhood skin].

OBJECTIVE: To explore the change in gene expression of angiogenesis-related factors vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1), acid fibroblast growth factor (aFGF) and basic fibroblast growth factor (bFGF), in fetal skin at different developmental stages and children skin and their potential biological significances. METHODS: Fetal skin samples of human embryo were obtained from spontaneous abortion at different gestational ages ranging from 13 to 32 weeks, and children skin specimens were collected from child patients (4-12 years) undergoing plastic surgery. After morphological characteristics of skin at different developmental stages were defined histologically gene expressions of VEGF, Ang-1, aFGF and bFGF were examined with reverse transcription-polymerase chain reaction analysis (RT-PCR). RESULTS: The trend of changes in gene expression of VEGF, Ang-1, aFGF and bFGF was not same for different skin specimens at various developmental stages. In early gestational fetal skin, genes of VEGF and Ang-1 were strongly expressed, while in late gestational and childhood skins, gene expressions of VEGF and Ang-1 were apparently decreased. In skin of middle gestational stage, the level of aFGF gene expression was highest, and then it was progressively reduced. In childhood skin, this gene was weakly expressed. In marked contrast, the contents of transcripts of bFGF showed no substantial change in fetal skin at different developmental stages, whilst the mRNA content of bFGF was significantly decreased in childhood skin. CONCLUSION: VEGF, Ang-1, aFGF and bFGF might be involved in regulating angiogenesis in skin from fetuses of different gestational stages and children. The relative increase in gene transcription of VEGF and Ang-1 in younger fetal skin might be one of the reasons why cutaneous cells proliferate rapidly and the wounds heal without scar.

Angiogenic Proteins↗
PubMed2004

[Evaluation of a pilot study on needle and syringe exchange program among injecting drug users in a community in Guangdong, China].

OBJECTIVE: To evaluate the feasibility and effectiveness of needle and syringe exchange program among a community of injecting drug users (IDUs) on AIDS prevention. METHODS: A quasi-experiment design was used in a controlled community intervention study. Needle and syringe exchange program was implemented for 10 months in IDUs of an intervention community, including peer education and health education, provision of free needles and syringes, and collecting back of used needles and syringes by trained peer educators and local health workers, whereas no intervention measure in a control community was instituted. Interviews with IDUs were conducted before and after intervention with a snowballing strategy to evaluate its effectiveness. RESULTS: A total of 428 and 429 IDUs were interviewed with structured questionnaire before and after intervention in intervention and control communities, respectively. Results revealed that awareness of HIV-related knowledge increased from 29.4% to 58.7% in the intervention community. Multivariate logistic regression analysis showed that awareness of HIV-related knowledge was higher in those who had read health education materials (OR = 2.93, 95% CI 2.12 - 4.04). As compared with the baseline data, frequency of sharing needles and syringes in past 30 days in the intervention community decreased from 48.9% to 20.4% in before intervention community (chi(2) = 41.02, P = 0.001), whereas there was no significant change in the control community. The causes of sharing needles and syringes in the intervention community included 'disable to get needle and syringe during the night', 'lack of needle and syringe when injecting at friend's home', 'not daring to buy needle and syringe for fear of being arrested' and 'no money to buy needle and syringe', declined markedly. CONCLUSIONS: Needle and syringe exchange program was feasible and effective in reducing their risky drug injecting behavior among IDUs in communities. Such strategy should be adopted in the country to reduce rapid spread of HIV.

Adult↗
PubMed2003

Rapid mitogen-activated protein kinase by basic fibroblast growth factor in rat intestine after ischemia/reperfusion injury.

AIM: Previous studies showed that exogenous basic fibroblast growth factor (bFGF or FGF-2) could improve physiological dysfunction after intestinal ischemia/ reperfusion (I/R) injury. However, the mechanisms of this protective effect of bFGF are still unclear. The present study was to detect the effect of bFGF on the activities of mitogen-activated protein kinase (MAPK) signaling pathway in rat intestine after I/R injury, and to investigate the protective mechanisms of bFGF on intestinal ischemia injury. METHODS: Rat intestinal I/R injury was produced by clamping the superior mesenteric artery (SMA) for 45 minutes and followed by reperfusion for 48 hours. Seventy-eight Wistar rats were used and divided randomly into sham-operated group (A), normal saline control group (B), bFGF antibody pre-treated group (C), and bFGF treated group (D). In group A, SMA was separated without occlusion. In groups B, C and D, SMA was separated and occluded for 45 minutes, then, released for reperfusion for 48 hours. After the animals were sacrificed, blood and tissue samples were taken from the intestine 45 minutes after ischemia in group A and 2, 6, 24, and 48 hours after reperfusion in the other groups. Phosphorylated forms of p42/p44 MAPK, p38 MAPK and stress activated protein kinase/C-Jun N-terminal kinase (SAPK/JNK) were measured by immunohistochemistry. Plasma levels of D-lactate were examined and histological changes were observed under the light microscope. RESULTS: Intestinal I/R injury induced the expression of p42/p44 MAPK, p38 MAPK, and SAPK/JNK pathways and exogenous bFGF stimulated the early activation of p42/p44 MAPK and p38 MAPK pathways. The expression of phosphorylated forms of p42/p44 MAPK was primarily localized in the nuclei of crypt cells and in the cytoplasm and nuclei of villus cells. The positive expression of p38 MAPK was localized mainly in the nuclei of crypt cells, very few in villus cells. The activities of p42/p44 MAPK and p38 MAPK peaked 6 hours after reperfusion in groups B and C, while SAPK/JNK peaked 24 hours after reperfusion. The activities of p42/p44 MAPK and p38 MAPK peaked 2 hours after reperfusion in group D and those of SAPK/JNK were not changed in group B. D-lactate levels and HE staining showed that the intestinal barrier was damaged severely 6 hours after reperfusion; however, histological structures were much improved 48 hours after reperfusion in group D than in the other groups. CONCLUSION: The results indicate that intestinal I/R injury stimulates the activities of MAPK pathways, and that p42/p44 MAPK and p38MAPK activities are necessary for the protective effect of exogenous bFGF on intestinal I/R injury. The protective effect of bFGF on intestinal dysfunction may be mediated by the early activation of p42/p44 MAPK and p38 MAPK signaling pathways.

Animals↗
PubMed2003

Activation of phosphorylating-p38 mitogen-activated protein kinase and its relationship with localization of intestinal stem cells in rats after ischemia-reperfusion injury.

AIM: To investigate the expression of phosphorylating p38 mitogen-activated protein kinase (MAPK) in rat small intestine after ischemia-reperfusion (I/R) insult and its relationship with the localization of intestinal stem cells. METHODS: Forty-eight Wistar rats were divided randomly into three groups, namely intestinal ischemia-reperfusion group (R), intestinal ischemia group (I) and sham-operated control group (C). In group I, the animals were killed 45 minutes after superior mesenteric artery (SMA) occlusion, while in group R the rats sustained SMA occlusion for 45 minutes and reperfusion for 2, 6, 12 or 24 hours respectively. In sham-operated control group, SMA was separated, but without occlusion. The activity of plasma diamine oxidase (DAO) was determined. Intestinal tissue samples were also taken for histological analysis and immunohistochemical analysis of MAPK p38 detection and intestinal stem cell localization. RESULTS: The changes in histological structure and plasma DAO levels indicated that the intestinal barrier was damaged after intestinal I/R injury. In group C and I, each crypt contained 5-6 p38 MAPK positive cells, which were mainly located in the lower region of the crypts. This was consistent with the distribution of intestinal stem cells. The presence of positive cells in crypts increased with the time of reperfusion and reached its peak at 12 hours after reperfusion (35.6 %). CONCLUSION: After intestinal I/R injury, the expression of phosphorylating-p38 MAPK in small intestine increased with the duration of reperfusion, and its distribution coincided with that of intestinal stem cells and their daughter cells, indicating that phosphorylating-p38 might be a possible marker of intestinal stem cells.

Animals↗
PubMed2003

[Study on the location and the expression characteristics of epidermal stem cells in normal adult skin and scar tissue].

OBJECTIVE: To investigate the different location and the expression characteristics of epidermal stem cells in normal adult skin and scar tissue. METHODS: Skin tissue specimens were harvested from the corresponding sites from 6 healthy volunteers and from scar tissue of 6 patients 1 year after major deep burn. beta1 integrin and keratin 19 (K19) were employed as the biochemical markers for stem cells and transit amplifying cells identification and keratin 14 (K14) and keratin 10 (K10) as markers for post-mitotic cells and terminally differentiated cells respectively. Integrin and keratin were determined by Elivision two-step immunohistochemistry. RESULTS: The expression of beta1 integrin and the K19 positive cell count in the epithelial basal layers of scar tissue were evidently decreased and weakened than those in normal adult healthy skin. Furthermore, the positive cells expressing K14 in epidermis of scar tissue were only located in 2 - 3 layers of basal epidermis, and their number was much less than that in normal adult skin. Whereas the cells positively expressing K10 were distributed wider in area than that in normal healthy skin. The epidermal stem cells and transit amplifying cells in scar epidermis were much less in number than that in normal skin. The differentiation process of scar epidermal stem cells was different from that of normal skin. And the proportions of post-mitotic cells and terminally differentiated cells were abnormal. CONCLUSION: The results indicated that the self-renewal ability of the scar epidermis was decreased, and the differentiation process of it was in disorder, which may be a reason for the abnormality of structure and function of the epidermis in scar, and a reason for the decreased ability of wound healing of scar tissue.

Adult↗