OBJECTIVETo investigate the sexual function and the quality of sexual life in patients with chronic prostatitis (CP), and to analyze the correlated factors and their influence on the quality of life (QOL) of the CP patients.

METHODSWe randomly selected 148 CP patients as the CP group and 71 healthy men as controls, asked them to fill out a questionnaire on sexual function and the quality of sexual life, obtained their scores on NHI-CPSI, and comparatively analyzed the results. We also made analyses on the influence of age, disease course, CP symptom scores and EPS level on sexual function and the quality of sexual life, as well as the impact of CP symptoms, sexual dysfunction and sexual life quality on the QOL of the CP patients.

RESULTSNo retro-ejaculation was found in either of the two groups. The mean score on sexual function and sexual life quality was 38.1 +/- 7.9 and 47.8 +/- 3.1 in the CP and the control group, respectively, with statistically significant differences (P < 0.05). Compared with the controls, the CP patients showed significantly decreased scores on libido, erectile function, ejaculation, orgasm frequency, self-confidence in sexual life, sexual satisfaction, and the partners' orgasm frequency and sexual satisfaction (P < 0.05). The indexes of sexual function and the QOL score were significantly correlated with CP symptoms, but not with the disease course and the WBC and lecithin counts in the prostatic fluid. The age of the patients was significantly correlated with the score of libido but not with other indexes of sexual function. CP symptoms, including pain, micturition and reduced sexual function and sexual life quality, along with the decreased orgasm frequency and sexual satisfaction of the patients' spouses, remarkably influenced the patients' QOL.

CONCLUSIONCP symptoms significantly decrease the indexes of sexual function of the patients and, in turn, their sexual life quality and QOL. Sexual dysfunction and reduced sexual life quality of CP patients are significantly correlated with CP symptoms, but not with the course of the disease, the age of the patient and the results of EPS detection.

Adult ; Case-Control Studies ; Erectile Dysfunction ; etiology ; Humans ; Male ; Middle Aged ; Prostatitis ; physiopathology ; Quality of Life ; Sickness Impact Profile ; Spouses ; Surveys and Questionnaires ; Young Adult

OBJECTIVETo evaluate the safety and the clinical value of external use of jiuyi Powder (JP) in treating plasma cell mastitis using partial least-squares discriminant analysis (PLSDA).

METHODSTotally 50 patients with plasma cell mastitis treated by external use of JP were observed and biochemical examinations of blood and urine detected before application, at day 4 after application, at day 1 and 14 after discontinuation. Blood mercury and urinary mercury were detected before application, at day 1, 4, and 7 after application, at day 1 and 14 after discontinuation. Urinary mercury was also detected at 28 after discontinuation and 3 months after discontinuation. The information of wound, days of external application and the total dosage of external application were recorded before application, at day 1, 4, and 7 after application, as well as at day 1 after discontinuation. Then a discriminant model covering potential safety factors was set up by PLSDA after screening safety indices with important effects. The applicability of the model was assessed using area under ROC curve. Potential safety factors were assessed using variable importance in the projection (VIP).

RESULTSUrinary β2-microglobulin (β2-MG), urinary N-acetyl-β-D-glucosaminidase (NAG), 24 h urinary protein, and urinary α1-microglobulin (α1-MG) were greatly affected by external use of JP in treating plasma cell mastitis. The accuracy rate of PLSDA discriminate model was 74. 00%. The sensitivity, specificity, and the area under ROC curve was 0. 7826, 0. 7037, and 0. 8084, respectively. Three factors with greater effect on the potential safety were screened as follows: pre-application volume of the sore cavity, days of external application, and the total dosage of external application.

CONCLUSIONSPLSDA method could be used in analyzing bioinformation of clinical Chinese medicine. Urinary β2-MG and urinary NAG were two main safety monitoring indices. Days of external application and the total dosage of external application were main factors influencing blood mercury and urine mercury. A safety classification simulation model of treating plasma cell mastitis by external therapy of JP was established by the two factors, which could be used to assess the safety of external application of JP to some extent.

Acetylglucosaminidase ; Alpha-Globulins ; Discriminant Analysis ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Least-Squares Analysis ; Mastitis ; drug therapy ; Plasma Cells ; ROC Curve ; Safety

BACKGROUNDSevoflurane and propofol are widely used anesthetics for surgery. Studies on the mechanisms of general anesthesia have focused on changes in protein expression properties and membrane lipid. MicroRNAs (miRNAs) regulate neural function by altering protein expression. We hypothesize that sevoflurane and propofol affect miRNA expression profiles in the brain, expect to understand the mechanism of anesthetic agents.

METHODSRats were randomly assigned to a 2% sevoflurane group, 600 μg·kg - 1·min - 1 propofol group, and a control group without anesthesia (n = 4, respectively). Treatment group was under anesthesia for 6 h, and all rats breathed spontaneously with continuous monitoring of respiration and blood gases. Changes in rat cortex miRNA expression profiles were analyzed by miRNA microarrays and validated by quantitative real-time polymerase chain reaction (qRT-PCR). Differential expression of miRNA using qRT-PCR among the control, sevoflurane, and propofol groups were compared using one-way analysis of variance (ANOVA).

RESULTSOf 677 preloaded rat miRNAs, the microarray detected the expression of 277 miRNAs in rat cortex (40.9%), of which 9 were regulated by propofol and (or) sevoflurane. Expression levels of three miRNAs (rno-miR-339-3p, rno-miR-448, rno-miR-466b-1FNx01) were significantly increased following sevoflurane and six (rno-miR-339-3p, rno-miR-347, rno-miR-378FNx01, rno-miR-412FNx01, rno-miR-702-3p, and rno-miR-7a-2FNx01) following propofol. Three miRNAs (rno-miR-466b-1FNx01, rno-miR-3584-5p and rno-miR-702-3p) were differentially expressed by the two anesthetic treatment groups.

CONCLUSIONSSevoflurane and propofol anesthesia induced distinct changes in brain miRNA expression patterns, suggesting differential regulation of protein expression. Determining the targets of these differentially expressed miRNAs may help reveal both the common and agent-specific actions of anesthetics on neurological and physiological function.

Anesthesia, General ; Animals ; Brain ; drug effects ; metabolism ; Male ; Methyl Ethers ; pharmacology ; MicroRNAs ; genetics ; Propofol ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction

Objective:To investigate the incidence of hypothyroxinemia in very low birth weight infant (VLBWI) and its effect on early postnatal feeding and weight gain.Methods:This retrospective study analyzed 164 cases of VLBWIs admitted to the Neonatal Intensive Care Unit of Peking University First Hospital from January 2017 to December 2018. According to the gestational age, these VLBWIs were divided into <30 weeks group ( n=85) or ≥30 weeks group ( n=79), and the basic data and thyroid function were compared. According to the levels of serum tetraiodothyronine and free tetraiodothyronine at the first thyroid function test, the subjects were further assigned into normal thyroxine group and hypothyroxinemia group. The risk factors of hypothyroxinemia identified at the first detection were analyzed by single and multiple-facter analysis. The results of the second detection of thyroxine were also analyzed. On the basis of the first detection and receiving treatment or not, the <30 weeks and ≥30 weeks groups were divided into normal thyroxine, hypothyroxinemia treated and hypothyroxinemia untreated subgroups, and differences in the tolerance of early feeding and weight gain were compared between different groups. Two independent samples/paired t-test, rank sum test, Chi-square test and logistic regression were used for statistical analysis. Results:Out of the 164 VLBWIs with the gestational age of (29.7±2.0) weeks and birth weight of (1 210±210) g, 27 cases (16.5%) were extremely low birth weight infants. The age at their first detection was (10.7±3.1) d and the incidence of hypothyroxinemia was 45.1% (74/164), including 71 mild and three severe cases, with a higher incidence in the ≥30 weeks group comparing to the <30 weeks group [55.7%(44/79) vs 35.5%(30/85), χ 2= 6.883, P=0.009]. All the three severe cases were in the ≥30 weeks group. The gestational age ( OR=1.413, 95% CI:1.044-1.912, P=0.025) and male infant ( OR=2.082, 95% CI: 1.047-4.143, P=0.037) were the risk factors of hypothyroxinemia. At the second detection, the incidence of hypothyroxinemia in VLBWIs with normal thyroid function at their first test was 47.6% (39/82), which is higher in the ≥30 weeks group than in the <30 weeks group [64.5%(20/31) vs 37.3%(19/51), χ 2= 5.745, P=0.017]. Among the infants with hypothyroxinemia at the first detection, those untreated had a significantly higher incidence of hypothyroxinemia at the second detection than those treated [81.3%(26/32) vs 38.7%(12/31), χ 2= 11.905, P=0.001]. The incidence of abdominal distension within 21 days, feeding volume on day 7, 14, and 21, and neonatal weight gain within 7, 14, and 21 days were similar between normal thyroxine, hypothyroxinemia treated and hypothyroxinemia untreated subgroups within the ≥30 weeks or the <30 weeks groups (all P>0.05). Conclusions:VLBWI is at high risk of hypothyroxinemia. Two times of postnatal thyroid function tests can help to detect the delayed hypothyroxinemia. Thyroxine level and receiving treatment or not may have no significant effect on the early postnatal feeding and weight gain.

Objective To observe the clinical efficacy and safety of sorafenib tablets combined with transcatheter arterial chemoembolization (TACE) in the treatment of unresectable liver cancer. Methods A total of 164 patients with unresectable liver cancer were randomly divided into control and treatment groups with 82 cases per group. Control group was treated with TACE alone, once every 4 weeks. Treatment group was given sorafenib tablets 400 mg per time from 5 d after TACE treatment, bid, orally, on the basis of control group. Two groups were treated for 12 weeks. The clinical efficacy, serum tumor markers, serum vascular endothelial growth factor (VEGF) , levels of basic fibroblast growth factor (bFGF) , and adverse drug reactions were compared between two groups.Results After treatment, the objective remission rates of treatment and control groups were 52. 44％ (43 cases/79 cases) and 28. 05％ (23 cases/79 cases) , the disease control rates were 87. 80％ (72 cases/79 cases) and 68. 29％ (56 cases/79 cases) , the progression free survival time were (15. 32 ± 2. 04) and (10. 83 ± 1. 43) months, the overall survival time were (15. 32 ± 2. 04) and (10. 83 ± 1. 43) months, the differences were statistically significant (all P < 0. 05) . After treatment, the alpha fetoprotein of treatment and control groups were (71. 38 ± 10. 04) and (152. 36 ± 20. 37) ng·m L-1, the carcinoembryonic antigen were (2. 02 ± 0. 27) and (2. 94 ± 0. 34) μg·L-1, the VEGF were (317. 87 ± 32. 76) and (442. 45 ± 35. 09) pg·m L-1, the differences were statistically significant (all P < 0. 05) . The adverse reactions of treatment group and the control group were nausea and vomiting (71. 95％ vs63. 41％) , diarrhea (35. 37％ vs 42. 68％) , myelosuppression (43. 90％ vs 40. 24％) and fever (84. 15％ vs90. 24％) , oral mucositis (32. 93％ vs 6. 10％) , hand-foot skin reaction (69. 51％ vs 2. 44％) , the differences were statistically significant (all P < 0. 05) . Conclusion Sorafenib tablets combined with TACE have a definitive clinical efficacy in the treatment of unresectable liver cancer, which can effectively inhibit the release of tumor markers, decrease the levels of serum VEGF and other cytokines. Although the incidence of adverse drug reactions is high, they can be controlled.

AIM:To observe the changes of autophagy-related indexes during endoplasmic reticulum stress (ERS) induced by dithiothreitol (DTT) and its effect on apoptosis in human normal hepatocytes.METHODS:LO2 cells were treated with DTT at 2.0 mmol/L for 0, 6, 12 and 24 h to induce ERS.The expression of glucose-regulated protein 78 (GRP78) , protein kinase R-like endoplasmic reticulum kinase (PERK) , activating transcription factor 4 (ATF4) , C/EBP homologous protein (CHOP) , autophagy-related gene 12 (Atg12) , autophagy-related gene 5 (Atg5) and microtubule-associated protein 1 light chain 3 (LC3) at mRNA and protein levels was determined by real-time PCR and Western blot.The apoptosis was analyzed by flow cytometry.The formation of autophagosomes was observed under transmission electron microscope.After the LO2 cells were pretreated with rapamycin at 400 nmol/L for 1 h and treated with DTT at 2.0mmol/L for 24 h, the effect of rapamycin pretreatment on the apoptosis was analyzed by flow cytometry.RESULTS:After treatment with DTT at 2.0 mmol/L for 6, 12 and 24 h, the mRNA and protein levels of GRP78, PERK, ATF4, CHOP, Atg12, Atg5 and LC3 in the LO2 cells were significantly higher than those in 0 h group (P<0.05).At the same time, the ratio of LC3Ⅱ/LC3Ⅰwas also increased after DTT treatment (P<0.05).Observation under transmission electron microscope showed that autophagosomes were found in the LO2 cells treated with DTT for 6, 12 and 24 h.After DTT treatment for 6, 12 and 24 h, the apoptosis rate of LO2 cells was significantly higher than that in DTT 0 h group, while the apoptosis induced by DTT was significantly decreased after rapamycin pretreatment (P<0.05).CONCLUSION:ERS induces autophagy and rapamycin pretreatment alleviates the apoptosis of LO2 cells to some extent.

AIM:To investigate the effect of SET7/9 (SET domain containing 7/9) -mediated endoplasmic reticulum stress (ERS) on protein kinase R-like endoplasmic reticulum kinase (PERK) signaling pathway, and to explore the mechanisms of arsenic-induced hepatocyte apoptosis.METHODS:Human liver LO2 cells were divided into control group, arsenic poisoning model group, negative transfection group and SET7/9 siRNA transfection group.The apoptosis of the LO2 cells in each group was analyzed by flow cytometry.The protein levels of SET7/9, glucose-regulated protein 78 (GRP78) , PERK and p-PERK in the LO2 cells of each group were observed by Western blot.RESULTS:Inhibition of SET7/9 expression reduced the apoptotic rate of arsenic-induced LO2 cells.Arsenic exposure increased the expression of SET7/9 in the LO2 cells.Arsenic exposure increased the protein levels of GRP78 and p-PERK in the LO2 cells, but decreased the protein levels of GRP78 and p-PERK after transfection with SET7/9 siRNA (P<0.05).CONCLUSION:Arsenic exposure induces hepatocyte apoptosis by increasing SET7/9 to activate ERS by PERK signaling pathway.

AIM:To investigate the effect of suberoylanilide hydroxamic acid ( SAHA) on the proliferation and apoptosis of human hepatocellular carcinoma HepG 2 cells and to explore its possible mechanism .METHODS: HepG2 cells were treated with SAHA at different concentrations for 48 h.The proliferation of HepG2 cells was detected by real-time cellular analysis.The protein levels of acetylated histones H3K9 and H3K27, glucose-regulated protein 78 (GRP78), protein kinase R-like endoplasmic reticulum kinase ( PERK ) and p-PERK were determined by Western blot .The cell apoptosis was analyzed by flow cytometry .RESULTS:Compared with control group , treatment with SAHA at 0.1μmol/L and 1 μmol/L for 48 h showed no significant inhibitory effect on the proliferation of HepG 2 cells, while SAHA at 6 μmol/L and 12 μmol/L significantly inhibited the proliferation of HepG 2 cells (P<0.05).The results of Western blot showed that the protein levels of acH3K9, acH3K27, GRP78 and p-PERK increased significantly after treated with SAHA at diffe-rent concentrations for 48 h, while the protein level of PERK was decreased significantly (P<0.05).The results of flow cytometry analysis showed that the apoptotic rates of the HepG 2 cells increased with the increase in SAHA concentration . CONCLUSION:SAHA up-regulates the acetylation of H3K9 and H3K27 in the HepG2 cells and induces apoptosis of HepG2 cells by activating the endoplasmic reticulum stress-related apoptosis pathway .

Interferon gamma-inducible protein 10, a member of the family of CXC chemokines, is secreted by interferon gamma-stimulated, monocytes, endothelial cells and keratinocytes. Interferon gamma-inducible protein 10 plays an important role in recruiting activated T cells into sites of tissue inflammation. In this experiment, PCR products of Interferon gamma-inducible protein 10 were cloned into prokaryote expression vector pET 32(a) to generate recombinant pET-IP10 with S-Tag at the N-terminus, and expressed successfully in E. coli BL21 (DE3). The total expressed products amounted to 25.3% in all bacterion proteins. pET-IP10 mainly formed inclusion body in E. coli. Soluble recombinant protein accounted for 20% among IP-10 fusion protein. The soluble recombinant proteins were purified by using S-Tag affinity chromatography effectively with purity of over 90%. The chemotaxis biological activity of purified Interferon gamma-inducible protein 10 could specifically exhibit the directional migration of stimulated T cells at concentration of 100 ng/ml. The results indicated that the strategy we used in this experiment was effective for recombinant Interferon gamma-inducible protein 10 production with biological activity.
Chemokine CXCL10 ; biosynthesis ; Escherichia coli ; metabolism ; Genetic Vectors ; Humans ; Recombinant Proteins ; biosynthesis ; T-Lymphocytes ; cytology ; Thioredoxins ; biosynthesis

Objective The purpose of the present study was to identify the relationship between the plasma level of adiponectin and in-stent restenosis of patients with coronary heart disease after coronary stenting. Method The study population comprised 119 individuals (92 men ) who underwent stent implantation, including 65 subjects without in-stent restenosis (group A ) and 54 patients with in-stent restenosis (group B). The level of plasma adiponectin was measured using ELISA. Coronary angiography was performed immediately before and after implanting stent and 9-12 months later. Results Baseline characteristics including drug use after PCI were similar between the groups. The rate of implanting bare metal stent is 8(12. 31% ) and 6(11.11% ), TAXUS drug-eluting stent is 11 (16. 92% ) and 10(18.52%) and CYPHER drug-eluting stent is 46 ( 70. 77% ) and 38 ( 70. 37% ) respectively ( all P > 0. 05 ). Plasma level of adiponectin in patient of group A was significantly higher than that in group B [ ( 15. 16±5.02 )mg/L vs. ( 10. 01±4. 93 ) mg/L, P < 0. 05 ]. The quantitative coronary angiography ( QCA ) showed that lesion length was similar between groups [ ( 15.82±: 6. 67 ) mm vs. ( 13.40±4. 20 )mm, P > 0. 05 ], minimum lumen diameter(MLD) and stenosis rate were also similar before and after implanting stent ( P > 0. 05 ) and acute gain was ( 1.48±0. 65 ) mm vs. ( 1.19±0. 37 ) mm ( P > 0. 05 ). MLD was higher in group A than that in group B [(2.55±0.53)mm vs. (0.57±0.60)mm, P<0.01] at 9-12 months follow up. Restenosis rate [(24.2±11.2)% vs. (81.0±19.1)%,P<0.01] and late lumen loss [(0.50±0.34)mm vs.( 1.60± 0. 54)mm, P < 0. 01 ] were lower in group A than in group B. Conclusions The lower plasma adiponectin level might be associated with in-stent restenosis after coronary stenting.