Study of the Characteristics and Comprehensive Fuzzy Assessment of Indoor Air Chemical Contamination in Public Buildings.

Quality-of-life is improving daily with continuous improvements in urban modernization, which necessitates more stringent requirements for indoor air quality. Fuzzy assessment enables us to obtain the grade of the evaluation object by compound calculation with the help of membership function and weight coefficient, overcoming the limitations of traditional methods applied to develop environmental quality indices. First, this study continuously measured SO2, O3, NO2, NO, CO, CO2, PM10, PM2.5, and other chemical pollutants during the daytime operating hours of a library and a canteen. We analyzed the concentration distributions of the particles in the air were discussed based on 31 different particle diameters. Finally, the experimental data in department store and waiting hall were analyzed by fuzzy evaluation, with the following results. (1) The library and canteen PM10 concentrations peaked at 07:45 in the morning and was elevated during the afternoon (48.9 and 59 µg/m3, respectively). (2) The Pearson correlation coefficient of the PM10 and PM2.5 concentrations in the library was 0.98. PM10 and SO2 in the canteen were negatively correlated, with a correlation coefficient of -0.65. PM2.5 and PM1 were always highly positively correlated. (3) The high concentration of particles in the library was associated with the small particle size range (0.25~0.45 µm). (4) By applying the fuzzy comprehensive evaluation method, the library grade evaluation was the highest level, and the waiting hall was the lowest. This study enhances our understanding of the indoor chemical contamination relationships for public buildings and highlights the urgent need for improving indoor air quality.

Ovarian preservation and prognosis in adnexal torsion surgery - a retrospective analysis.

OBJECTIVES: This study aims to analyze the conditions of ovarian preservation during adnexal torsion surgery, and safety of ovarian preservation. MATERIAL AND METHODS: A retrospective analysis of 130 patients, who underwent surgery for ovarian benign tumor pedicle torsion in Fujian Provincial Maternal and Child Health Hospital from June 2013 to June 2018, was conducted. This study analyses the possible risk factors affecting the operation method using multiple logistic regression and analyses the complications and the recovery of ovarian function after the treatment of the ovarian preservation. RESULTS: Among these patients, 58 received ovarian cystectomy, while 72 received ovariectomy. There was no significant difference in terms of age, preoperative blood, operation time and surgical bleeding volume between the two groups (p > 0.05). However, there was a significant difference in preoperative adnexal blood flow, abdominal pain to the surgical interval, and a collection of torsion cycles (p < 0.05). There was an increased risk of ovarian resection in patients whose blood flow of the annex disappeared, whose time of abdominal pain was long, and whose number of twists were significant. For the preservation group, there were no increases in postoperative complications. CONCLUSIONS: According to clinical indicators, such as preoperative adnexal blood flow, abdominal pain to the interval of surgery and the number of torsion cycles, it was determined whether it was feasible to keep the ovary. Retaining the ovary is safe, effective and feasible in adnexal torsion.

Effects of fine particulate matter (PM2.5) on ovarian function and embryo quality in mice.

Fine particulate matter (PM2.5) has an adverse effect on reproductive function, in particular causing reduced male reproductive function, but relatively few studies have directly targeted its effects on female reproduction. To investigate the effects of PM2.5 exposure on female reproduction, we exposed female mice to PM2.5 by intratracheal instillation for 28 days, and evaluated apoptosis of ovarian granulosa cells and oocytes and the quality embryos after insemination. Our results showed increased numbers of apoptotic granulosa cells and oocytes after exposure to elevated concentrations of PM2.5, which had adverse effects on female fertility via compromising embryo development and quality. We conclude that PM2.5 induced apoptosis of ovarian granulosa cells and oocytes leading to disrupted embryo development and female fertility in mice.

Effects of Prenatal PM10 Exposure on Fetal Cardiovascular Malformations in Fuzhou, China: A Retrospective Case-Control Study.

BACKGROUND: Maternal exposure to ambient air pollution has been associated with an increased risk of congenital heart defects in offspring; however, the results are inconsistent. OBJECTIVES: We investigated whether there is an association between prenatal exposure to particulate matter with diameter ≤10µm (PM10) during early pregnancy and fetal cardiovascular malformations. METHODS: The gravidae from a hospital-based case­control study in Fuzhou, China, during 2007­2013 were assigned 10-d or 1-mo averages of daily PM10 using an air monitor­based inverse distance weighting method during early pregnancy. A total of 662 live-birth or selectively terminated cases and 3,972 live-birth controls were enrolled. The exposure was considered as a categorical variable. A multivariable logistic regression model was constructed to quantify the adjusted odds ratios (aORs) of the exposure to PM10 and the risks of fetal cardiovascular malformations. RESULTS: PM10 levels were positively associated with the risks of atrial septal defect (aORs ranging from 1.29 to 2.17), patent ductus arteriosus [aORs = 1.54, 1.63; 95% confidence intervals (CIs): 1.17, 2.23; 1.06, 3.24], overall fetal cardiovascular malformations (aOR = 1.28; 95% CI: 1.03, 1.61), ventricular septal defect (aOR = 1.19; 95% CI: 1.00, 1.43), and tetralogy of Fallot (aOR = 1.44; 95% CI: 1.01, 2.19) in the various observed periods scaled by 10 d or 1 mo in the first and second gestation months. The strongest associations were observed for exposure to PM10 in the second quartile, whereas the associations were attenuated when higher concentrations of PM10 in the third and fourth quartiles of the exposure were evaluated. No correlations of PM10 levels with these cardiovascular malformations in the other time periods of gestation were observed. CONCLUSIONS: Our findings suggest some positive associations between maternal exposure to ambient PM10 during the first two months of pregnancy and fetal cardiovascular malformations. https://doi.org/10.1289/EHP289.

Maternal exposure to ambient PM2.5 exaggerates fetal cardiovascular maldevelopment induced by homocysteine in rats.

Maternal exposure to airborne particulate matter with aerodynamic diameter <2.5 µm (PM2.5 ) during pregnancy and lactation periods is associated with filial congenital cardiovascular diseases. This study aimed to investigate the toxic effects of maternal exposure to ambient levels of PM2.5 on filial cardiovascular maldevelopment induced by homocysteine. Using a 2 × 2 factorial design, rats were randomized into four groups and were exposed to ambient PM2.5 or filtered air (FA) throughout the pregnancy and lactation periods coupled with the administration of either homocysteine (HCY) or normal saline (NS) daily from gestation days 8-10. Morphological changes in the heart, myocardial apoptosis, expressions of cardiac progenitor transcriptional factors, and levels of cytokines were investigated in the offspring. The apoptosis-like changes in the myocardium were seen in the FA plus HCY-treated group and more obviously in the PM2.5 plus HCY-treated group, which was in accordance with an increased myocardial apoptosis rate in the two groups. PM2.5 exposure resulted in significantly decreased Nkx2-5 protein level and GATA4 and Nkx2-5 mRNA expressions, and significantly increased TNF-α and IL-1ß levels. There were significant interactions between PM2.5 exposure and HCY-treatment that PM2.5 exposure reduced Nkx2-5 protein levels and GATA4 and Nkx2-5 mRNA expressions in the HCY-treated groups. These results suggest that maternal exposure to PM2.5 , even at the ambient levels in urban regions in China, exaggerates filial cardiovascular maldevelopment induced by HCY in a murine model, exacerbating structural abnormalities in the filial cardiac tissue, which is possibly associated with oxidative stress and reduced GATA4 and Nkx2-5 transcription factor expressions. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 877-889, 2017.

Suppression of placental metallothionein 1 and zinc transporter 1 mRNA expressions contributes to fetal heart malformations caused by maternal zinc deficiency.

Zinc has been implicated to have a protective role against heart malformations during fetal development. Metallothionein 1 (MT-1) and zinc transporter 1 (ZnT-1) are two major metabolic factors that are associated with zinc metabolism. The present work aimed to investigate the association of placental MT-1 and ZnT-1 expressions with fetal heart malformations resulting from maternal zinc deficiency. Sprague-Dawley female rats were randomly divided into five groups of extremely low-zinc, low-zinc, moderately low-zinc, marginally low-zinc and normal zinc (n = 9-12), and were fed diets with controlled zinc content at 1.0 ± 0.3, 8.4 ± 1.8, 15.4 ± 2.8, 22.4 ± 4.1 and 29.4 ± 5.3 [mean ± standard deviation (SD)] mg of zinc/kg, respectively, from day 25 of preconception until day 19 of gestation. The female rats were bred, their fetuses were harvested at day 19 of gestation after killing the dams, and fetal hearts were morphologically examined. Zinc concentration and alkaline phosphatase (ALP) activity in maternal venous blood sera were tested, and MT-1 and ZnT-1 mRNA expressions in the placenta were assayed. Zinc concentrations and ALP activities in the blood were low in all zinc-deficient diet groups in a dose-dependent fashion. The incidences of heart malformations were increased, and the levels of placental MT-1 and ZnT-1 mRNA expressions were decreased in the extremely low-zinc, low-zinc and moderately low-zinc groups compared with the normal zinc group. Specifically, mRNA levels of placental MT-1 or ZnT-1 were significantly decreased and were lower than the specific threshold values in the fetuses with heart malformations but not in the fetuses without heart malformations in all the groups. These data indicate that maternal zinc deficiency resulted in an elevated incidence of fetal heart malformations, which was associated with significant decreases in placental MT-1 and ZnT-1 mRNA expressions to the levels below the threshold values that may be a crucial factor to determine the presence of fetal heart malformations.

Identification of pathology from diesel exhaust particles in the bladder in a rat model by aspiration of particles from the pharynx.

To determine whether diesel exhaust particles (DEPs) could be a toxic agent to the bladder, rats were exposed to different concentrations of DEPs for one month or three months. When the rats were sacrificed, morphologic changes of the urothelium were investigated. The antioxidase activity and the levels of lipid peroxidation in the bladder were assayed. In the three-month group, DEPs at doses of 21.03 µg/µl insulted the structural integrity of surface glycosaminoglycans, widened the gap between urothelial cells, increased levels of lipid peroxidation, and decreased antioxidase activities in the urinary bladder (p<0.05). Furthermore, DEPs at a dose of 5.61 µg/µl decreased glutathione, catalase, and glutathione peroxidase activities (p<0.05). These results led to the conclusion that DEPs were a toxic agent in the bladder. The toxic effects might be attributed to oxidative damage mediated by pro-oxidant/antioxidant imbalance or excessive free radicals.

Maternal exposure to airborne particulate matter causes postnatal immunological dysfunction in mice offspring.

Evidence suggests that prenatal exposure to air pollution affects the ontogeny and development of the fetal immune system. The aim of this study was to investigate the effect of maternal exposure to airborne particulate matter (PM) on immune function in postnatal offspring. Pregnant female ICR mice were intralaryngopharyngeally administered with 30 µl of phosphate buffered solution (the control group) or resuspended PM of Standard Reference Material 1649a at 0.09 (low), 0.28 (medium), 1.85 (high) or 6.92 (overdose) µg/µl once every three days from day 0 to 18 of pregnancy (n=8-10). Offspring were sacrificed on postnatal day 30. Interleukin-4 and interferon-γ levels in plasma and splenocytes, splenic lymphocyte proliferation, and expressions of GATA-3 and T-bet mRNA in the spleen were tested. The spleen and thymus were histopathologically examined. The offspring of the medium, high and overdose PM-exposed dams showed significantly suppressed splenocyte proliferation. Decreased interferon-γ and increased interleukin-4 levels in the blood and splenocytes, and lowered T-bet and elevated GATA-3 mRNA expressions were found in the spleen in the medium, high and overdose groups when compared with the control or low dose group (P<0.05). Histopathology revealed prominent tissue damage in the spleen and thymus in the overdose group. These results suggest that exposure of pregnant mice to PM modulates the fetal immune system, resulting in postnatal immune dysfunction by exacerbation of Thl/Th2 deviation. This deviation is associated with altered T-bet and GATA-3 gene expressions.

[Effect of airborne particulate matter exposure on pregnancy and fetal development in female mice].

OBJECTIVE: To investigate subacute exposure of airborne particulate matter (PM) on pregnancy and fetal development in female mice. METHODS: Forty female and forty male ICR adult mice were caged separately by 1:1 to get access to pregnancy. The pregnant mice were randomized into control group (A), small (B), middle (C), large (D) or overdose (E) PM challenge groups (n = 8-11), and were administered with 30 µl of phosphate buffered solution (A) or resuspended standard PM SRM 1649a at 0.09 (B), 0.52 (C), 1.85 (D) or 69.2 (E) µg/µl, once per trid from d 0 till d 19 of pregnancy via instillation onto the base of the tongue. Fetal mice were harvested by cesarean section at the time when spontaneous delivery occurred. Body weight of the pregnant mice, gestational days, intrauterine survival and growth, hepatic and pneumonic histopathological changes of the fetal mice were investigated. Lung/body and liver/body weight ratios were calculated. Expressions of mRNA and protein of CYP1A1 in the fetal lung and CYP1A2 in the fetal liver were assayed. RESULTS: (1) All of the pregnant mice survived pregnancy throughout the entire experiment. Body weight of the pregnant mice was not significantly different among all the groups at gestational d 1 and 7 (P > 0.05), but significantly lower in group E [(41.8 ± 5.8) and (48.9 ± 8.9) g] than in group A [(45.9 ± 1.8) and (56.2 ± 4.9) g] at gestational d 14 and 18 (P < 0.05). The gestational days were significantly decreased in group E [(19.3 ± 1.3) d] when compared with group A [(20.5 ± 0.7) d; P < 0.05] and were not significantly different among groups A, B, C and D (P > 0.05). Lung/body and liver/body weight ratios of the fetal mice were significantly increased in group E [(1.21 ± 0.18) and (4.68 ± 0.21)%] as compared with groups A, B, C and D (P < 0.05). (2) Mortality rates of the fetuses were significantly higher in group E (23.0%) than in groups A (0.8%), B (0.9%), C (1.7%) and D (3.7%) (P < 0.05), but were not significantly different among groups A, B, C and D (P > 0.05) despite of an increasing tendency. (3) Pathological changes in the liver and lung of the fetuses were conspicuous in group E. The fetal liver injury was histopathologically evidenced by deranged tissue structure, degenerated parenchyma of hepatic cells, and mildly stained cytoplasm. Adipose degeneration was represented by clear-boundary intracytoplasmic vacuoles in most of the liver cells, and cell pyknosis with heavily stained cytoplasm was observed in some of the liver cells. Inflammatory cell infiltration and focal necrosis were occasionally found in the hepatic tissue. The fetal lung exhibited bronchiole with narrow lumina, vascular engorgement in the submucosal layer, interstitial and alveolar edema, thickened alveolar septum, granulocyte and lymphocyte infiltrations within the pulmonary alveoli and around the bronchioles. The above pathological changes were lesser in groups C and D, and were not or least found in groups A and B. (4) Protein expressions of CYP1A1 in the fetal lung and CYP1A2 in the fetal liver were significantly increased in group E (1.20 ± 0.40 and 2.55 ± 0.89) when compared with group A (0.77 ± 0.36 and 2.08 ± 0.31) (P < 0.05). mRNA expressions of CYP1A1 in the fetal lung were significantly increased in groups C (0.36 ± 0.12), D (0.41 ± 0.08) and E (0.43 ± 0.11) compared with group A (0.21 ± 0.10), and significantly increased in groups D and E compared with group B (0.28 ± 0.10, P < 0.05). mRNA expressions of CYP1A2 in the fetal liver were significantly increased in groups C (0.37 ± 0.13), D (0.36 ± 0.14) and E (0.43 ± 0.16) compared with group A (0.21 ± 0.03), and significantly increased in group E compared with group B (0.24 ± 0.11, P < 0.05). CONCLUSIONS: PM elicited embryotoxigenicity and resulted in adverse pregnancy outcomes in mice by intrauterine exposure of overdose PM. The expressions of cancer-related genes CYP1A1 and CYP1A2 were up-regulated in organs after the middle- and large-dose subacute exposure of PM, which may have a potential role on the future development.

[Instillation of diesel exhaust particles on the posterior wall of pharynx on reproductive function in female mice].

OBJECTIVE: The present work aims to investigate the effects of subacute exposure to diesel exhaust particles (DEP) on reproductive function in female mice. METHODS: A total of 168 ICR (Institute of Cancer Research) mice were randomly divided into four groups by numeration table method, including the low (B), middle (C), high (D) dose DEP exposure groups and the control group (A). Each group consisted of 42 mice. Mice were inoculated with 30 µl DEP suspension at 0.8 (B), 3.0 (C), 12.0 (D) µg/µl, respectively, or the same volume of phosphate-buffered saline (A) on pharynx posterior wall per triduum for 4 times. The body weight and ovary weight were tested and ovary weight/body weight ratios were calculated. Rates of survival, germinal vesicle breakdown, extrusion of the first polar body, in-vitro fertilization and quantity of mitochondrial DNA for the oocytes were investigated. Ultrastructural changes of the oocytes were observed. RESULTS: The ovary weight/body weight ratios were (15.4 ± 7.3) × 10(-5), (14.1 ± 6.8) × 10(-5), (8.2 ± 0.7) × 10(-5) and (7.2 ± 2.5) × 10(-5) in groups A, B, C and D (F = 3.841, P < 0.05). In groups A, B, C and D at 48 h post-insemination, rates of oocyte survival were 64.3%, 56.8%, 39.5% and 32.9% (χ(2) = 21.575, P < 0.05), rates of extrusion of the first polar body were 75.5%, 65.3%, 37.0% and 27.1% (χ(2) = 52.772, P < 0.05), rates of 2-cell embryos were 27.9%, 39.1%, 17.6% and 12.5% (χ(2) = 20.148, P < 0.05), and rates of embryos over 2 cells were 45.3%, 32.2%, 12.5% and 13.9% (χ(2) = 32.135, P < 0.05), respectively, and were significantly lower in groups C and D compared with group A (P < 0.05). Logarithmic values of mitochondrial DNA copy numbers were 6.54 ± 0.13, 6.48 ± 0.09, 5.57 ± 0.15 and 5.41 ± 0.07 in groups A, B, C and D, respectively, and were significantly lower in groups C and D compared with group A or B (F = 89.241, P < 0.05). A number of mitochondria of the oocytes exhibited tremendous tumescence and vacuolization in groups C and D, which was contrast to a roughly normal appearance in groups A and B. CONCLUSIONS: DEP is noxious to murine female reproduction. Subacute exposure to DEP injures the ovary and oocyte resulting in compromised ovarian function and fertilizability of the oocyte.

The assessment of voluntary pelvic floor muscle contraction by three-dimensional transperineal ultrasonography.

INTRODUCTION AND HYPOTHESIS: The assessment of the levator function by ultrasound has not been fully studied. This study aims to test the validity of ultrasound parameters in the assessment of levator function in women presenting with different pelvic floor structural changes. METHODS: One hundred and three patients, 36 pelvic organ prolapse women, 36 stress urinary incontinence women and 31 normal controls, were recruited. The images of the midsagittal field and volume datasets at rest and during contraction were acquired. The intra-observer reliability of ultrasound measurements was determined by intraclass correlation coefficients and their 95% CI. Displacement of the bladder neck, sagittal hiatal diameter, levator hiatal angle and levator hiatus area were considered in the assessment. One-way ANOVA was used to determine the significance of differences of the parameters among the three groups. RESULTS: Ninety-six datasets were analyzed. The parameters measured at rest and during contraction were found to be significantly different, while the parameters representing changes in levator hiatus opening dimensions and displacement of the bladder neck during pelvic floor muscle contraction were found to be not significantly different. CONCLUSIONS: Ultrasound parameters representing changes in levator hiatus opening dimensions and displacement of the bladder neck during pelvic floor muscle contraction may not be sensitive enough to distinguish the state of the pelvic floor muscle function.

Intracerebral transplantation of mesenchymal stem cells derived from human umbilical cord blood alleviates hypoxic ischemic brain injury in rat neonates.

AIMS: Fetal hypoxic-ischemic brain injury (HIBI) is a severe condition for which no effective therapy exists. In this study mesenchymal stem cells (MSCs) from human umbilical cord blood (UCB) of full-term newborns were isolated and intracerebrally transplanted into rat neonates after HIBI induction. Nerve function was assessed by the modified neurological severity scores (mNSS) to establish if MSCs could alleviate nerve injury. RESULTS: Immunostaining showed the transplanted MSCs migrated to the hippocampus. Rats receiving MSCs treatment showed significant improvement in the mNSS when compared with controls. Also, histochemical study showed alleviation of brain tissue injury after MSCs treatment. Differentiation of MSCs to astrocytes, but not neurons, was observed. CONCLUSIONS: The results indicate a beneficial effect of intracerebral transplantation of MSCs on the functional recovery of rat neonates with HIBI.

Diesel exhaust exposure induces angiogenesis.

Our aim was to test the hypothesis that exposure to whole diesel exhaust (WDE) would enhance angiogenesis/vasculogenesis. Male apolipoprotein E-deficient mice, with either scaffold implantation subcutaneously or hindlimb ischemia, were exposed to either WDE (containing diesel exhaust particle [DEP] at a concentration of about 1mg/m(3)) or filtered air 6 h/day, 5 days/week in a whole body exposure chamber for 2, 5, or 8 weeks, respectively. WDE exposure significantly increased total cell counts in the scaffolds, aortic, and perivascular fat tissues. Macrophage infiltration was enhanced and CD31 expression increased in the scaffolds, which was coupled by increased alpha-smooth muscle actin (alpha-SMA) expression. WDE exposure led to increased CD31 expression, while decreasing endothelial nitric oxide synthase in the aortic wall. The vessel volume measured by micro-CT was increased in ischemic and non-ischemic hindlimbs in response to WDE exposure. DEP exposure induced capillary-like tube formation in endothelial cells in vitro, and caused capillary sprouting from aortic rings ex vivo. In addition, WDE exposure significantly increased mRNA expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF)-1alpha, while decreasing prolylhydroxylase (PHD) 2 expression. WDE exposure increases inflammatory cell infiltration, enhances the vessel volume/flow, and increases capillary tube formation and sprouting, thereby inducing angiogenesis and vasculogenesis. The angiogenic effects may occur through increasing HIF-1alpha and VEGF while decreasing PHD2 expression.

Zinc antagonizes homocysteine-induced fetal heart defects in rats.

It has been suggested that zinc may have a protective role against heart defects during fetal development. We investigated the effects of zinc on the development of fetal cardiac malformations induced by homocysteine. Pregnant Sprague-Dawley rats were randomized into one of five groups: control (C), homocysteine (H), homocysteine + zinc (Z), homocysteine + folic acid (F), or homocysteine + zinc + folic acid (ZF) (each n = 8). Homocysteine (8 nmol/day) was administered intraperitoneally in the H, Z, F, and ZF groups on gestation days (GD) 8, 9, and 10. Zinc (30 mg/kg day), folic acid (30 mg/kg day), or both (30 mg/kg day each) were administered intragastrically daily in the Z, F, and ZF groups, respectively, throughout the pregnancy. In each group, two fetuses were removed on GD 13, 15, 17, and 19 and examined for cardiac malformations; maternal copper/zinc-containing-superoxide dismutase (Cu/Zn-SOD) activity and metallothionein type I (MT-1) mRNA expression were measured simultaneously. The prevalence of cardiac malformations was significantly higher in group H than in group C, and significantly lower in group Z than in group H at the studied time points. Cu/Zn-SOD activity and MT-1 mRNA levels were significantly lower in group H than in group C, and significantly higher in group Z than in group H. Our data suggest that zinc antagonizes homocysteine-induced teratogenic effects on the fetal heart, possibly via the inhibition of excessive peroxidation.

Changes in levator ani muscle after vaginal hysterectomy and prolapse repair using the Total Prolift procedure.

OBJECTIVE: To assess changes in the levator plate angle (LPA), anteroposterior length of the levator hiatus (H-line), and pelvic floor descent (M-line) after vaginal hysterectomy and prolapse repair using the Gynecare Prolift Total Pelvic Floor Repair System. METHODS: Before and after the intervention, 20 women with pelvic floor prolapse underwent dynamic magnetic resonance imaging in supine position during the Valsalva maneuver to measure the LPA, H-line, and M-line. Paired t tests were performed and Pearson correlation coefficients calculated from values obtained using the pelvic organ prolapse quantification system. RESULTS: After the intervention the LPA was smaller (46.92 degrees vs 55.39 degrees, P<0.05), the H-line was shorter (53.70 cm vs 60.46 cm, P<0.05), and the M-line was shorter (19.58 cm vs 25.27 cm, P<0.05). CONCLUSION: These changes suggest an efficient reconstruction and reinforcement of the pelvic floor after the surgery.

Role of vasoactive intestinal peptide and pituitary adenylate cyclase activating polypeptide in the vaginal wall of women with stress urinary incontinence and pelvic organ prolapse.

Pelvic floor connective tissue degeneration is closely associated with retrogradation of its dominating nerve fibers. We hypothesized that some neuropeptides from pelvic floor tissue might be involved in the pathological progress of stress urinary incontinence (SUI) and pelvic organ prolapse (POP) in women. Thirty premenopausal and 31 postmenopausal patients participated in the study. The morphological appearance in the vaginal tissue was examined. The vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating polypeptide-38 (PACAP) immunoreactivities (ir-VIP, ir-PACAP) were tested by immunohistochemistry and radioimmunoassay. We found that the VIP and PACAP immunostainings were weaker and sparser, and ir-VIP and ir-PACAP levels were significantly decreased in the anterior vaginal wall in the premenopausal and postmenopausal SUI or POP patients. Ir-VIP and ir-PACAP levels were reversely correlated with the age and menopausal status in the SUI or POP patients. Our data suggest that VIP and PACAP may participate in the pathophysiological process of SUI and POP.

Changes of collagen type III and decorin in paraurethral connective tissue from women with stress urinary incontinence and prolapse.

Thirteen premenopausal women with stress urinary incontinence (SUI), 6 with SUI and prolapse, 9 with prolapse, and 19 without prolapse were enrolled to observe the content change of collagen type III and the expression of decorin mRNA in paraurethral connective tissues. Collagen type III from transvaginal biopsies was assayed by immunohistochemical staining and decorin mRNA was detected by real-time PCR. Premenopausal women with SUI had a significantly decreased level of collagen type III. Decorin mRNA expression was significantly increased in both premenopausal SUI+prolapse group and premenopausal prolapse group reflected by the decrease of DeltaCt value compared to their corresponding controls. The results suggest that a high level of decorin mRNA might be associated with the reduced content of collagen type III, resulting in a less flexible form of extracellular matrix in the connective tissue in SUI and prolapse patients.

[Changes and significance of orphanin and serotonin in patients with postpartum depression].

OBJECTIVE: To study the changes of orphanin (OFQ) and serotonin (5-HT) in the patients with postpartum depression (PPD). METHODS: Twenty one patients with postpartum depression (PPD group) and 25 healthy lying-in women (control group) were studied. The concentrations of plasma OFQ were measured by radioimmunoassay. The levels of 5-HT were measured with high-pressure liquid chromatography with electrochemical detector. RESULTS: (1) The levels of plasma OFQ in PPD group were (28.5 +/- 5.8) ng/L, in control group, the levels of OFQ was (10.4 +/- 3.7) ng/L, the levels of OFQ in PPD group were significantly higher than that in the control group (P < 0.01). (2) The levels of plasma 5-HT in PPD group and control group were (1.0 +/- 0.3) micro mol/L and (1.4 +/- 0.4) micro mol/L respectively, the levels of 5-HT in PPD group decreased significantly (P < 0.05). (3) In the PPD group, there was a significant negative correlation between the OFQ and 5-HT level (P < 0.05). CONCLUSION: The PPD was associated with OFQ and 5-HT, the changes of OFQ levels may play an important role in the pathogenesis of the PPD.

[Changes of hypothalamus and peripheral orphanin in fetal rats with intrauterine ischemia and hypoxia].

OBJECTIVE: To evaluate the role of orphanin in the perinatal ischemia-hypoxia. METHODS: The concentration of hypothalamus and peripheral orphanin were measured by radioimmunoassay. Animal model of perinatal ischemia-hypoxia was set up by ligating uterine vessels. All the rats were delivered by cesarean section and scored according to respiration, heart beat, skin color, muscle tone and reflex after delivery. RESULTS: (1) The levels of orphanin in hypothalamus and peripheral blood in group B were (114 +/- 21) pg/g and (58 +/- 11) ng/L respectively. In group A, the were (71 +/- 14) pg/g and (31 +/- 7) ng/L respectively, the levels of orphanin in group B increased significantly when compared with the group A (P < 0.05). In control group, the levels of orphanin were (48 +/- 9) pg/g and (19 +/- 4) ng/L. The levels of orphanin in group A and B were significantly higher than those in the control group (P < 0.01, P < 0.05). (2) The Apgar scores in groups A and B were significantly decreased than that in control group (P < 0.01). The group A pups had significantly better scores than the group B (P < 0.05). CONCLUSION: The perinatal ischemia and hypoxia was associated with orphanin, the changes of orphanin levels may play an important role in the pathophysiological changes in perinatal ischemia and hypoxia.