Adult ; Cryptococcosis ; Cryptococcus neoformans ; Humans ; Lung Diseases, Fungal ; Male

Objective To observe the therapeutic effect of resveratrol (Rsv) on psoriasis like skin damage induced by imiquimod (IMQ) and study its mechanism.Methods BALB/c mice were randomly divided into four groups:control group,Rsv group,model (IMQ) group and Rsv treatment (IMQ + Rsv) group with six mice in each group.Psoriasis like skin model induced by smearing IMQ in the mice's ear for 8 d,20 mg Rsv cream were gave at the same time for treatment.Observe erythema and psoriasis degree,and measure ear thickness with vemier caliper.HE staining was used to observe tissue change,real time quantitative PCR (qRT-PCR) was used to detect K17,IL-17A,IL-19 and IL-23 mRNA and Western blotting were used to detected K17 protein expression in tissues.Results Compared with the model group,mice erythema area and the thickness of epidermal scale decreased significantly in Rsv treatment group;HE staining results showed that,Rsv significantly reduced ear marginal tissue epidermal thickness,and diminished severity of the psoriasis-like skin inflammation.qRT-PCR and Western blotting confirmed a Rsv dependent decrease of in K17,IL-17A and IL-19 in mRNA level and protein levels of K17.Conclusion Rsv improves psoriasis like skin damage by down-regulating expression of Keratinl 7.

Objective To investigate the associations of baseline serum uric acid, bilirubin levels with short-term outcome in patients with acute ischemic stroke. Methods The clinical data in successive patients with acute ischemic stroke were colected, including the serum levels of uric acid and bilirubin on admission, the National Institutes of Health Stroke Scale (NIHSS) score, and the modified Rankin scale (mRS) score at discharge or at day14 (mRS 0-2 was defined as good outcome, > 2 was defined as poor outcome). Results A total of 162 patients with ischemic stroke were enroled, including 114 in the good outcome group and 48 in the poor outcome group. There were significant differences in proportions of the patients with diabetes melitus (51. 75% vs. 75. 00% ; χ2 = 7. 526, P = 0. 006), previous history of stroke or transient ischemic attack (TIA) (18. 42% vs. 50. 00% ; χ2 = 17. 790, P = 0. 001), as wel as the baseline diastolic blood pressure (87. 061 ± 12. 245 mmHg vs. 82. 375 ± 10. 949 mmHg; t = 2. 293, P = 0. 023; 1 mmHg =0. 133 kPa), high-density lipoprotein cholesterol (1. 604 ± 0. 299 mmol/L vs. 1. 265 ± 0. 206 mmol/L; t =3. 227, P = 0. 002), fasting glucose (2. 875 ± 0. 438 mmol/L vs. 8. 160 ± 0. 592 mmol/L; t = - 4. 761, P <0. 001), uric acid (289. 365 ± 77. 168 μmol/L vs. 248. 206 ± 66. 206 μmol/L; t = 3. 111, P = 0. 002), total bilirubin (14. 673 ± 2. 213 μmol/L vs. 10. 395 ± 2. 714 μmol/L; t = 3. 779, P = 0. 001 ), direct bilirubin (6. 036 ± 1. 392 μmol/L vs. 4. 956 ± 1. 379 μmol/L; t = 2. 088, P = 0. 038), and indirect bilirubin (8. 634 ± 2. 307 μmol/L vs. 5. 439 ± 1. 223 μmol/L; t = 4. 219, P < 0. 001) levels between the 2 groups. Multivariate logistic regression analysis showed that the previous history of stroke or TIA (odds ratio [ OR ] 3. 751, 95% confidence interval [CI ] 1. 395-10. 091; P = 0. 009) and baseline NIHSS score (OR 2. 723, 95% CI 1. 093-6. 783; P = 0. 031) were the independent risk factors for poor outcome of ischemic stroke; while uric acid (OR 0. 357, 95% CI 0. 141-0. 900; P = 0. 029), high-density lipoprotein (OR 0. 262, 95% CI 0. 079-0. 870; P = 0. 029), and indirect bilirubin (OR 0. 117, 95% CI 0. 025-0. 539; P = 0. 006) were independently correlated with good outcome. Conclusions The increased baseline uric acid and indirect bilirubin levels are the favorable factors for good outcome in patients with acute ischemic stroke.

Objective To investigate the effect of ultraviolet A (UVA) radiation on the expression and secretion of cathepsin G (CatG) by human dermal fibroblasts.Methods Dermal fibroblasts were isolated from the foreskins of boys,and subjected to primary culture and subculture.After 10 or less passages,the fibroblasts were collected and divided into several groups to be irradiated with 10 J/cm2 UVA followed by 24,48 and 72 hours of additional culture,or be irradiated with 10,20 and 30 J/cm2 UVA followed by 24 hours of additional culture,with those receiving no treatment serving as the control group.Subsequently,cells and culture supernatant were collected,real time PCR and Western blot were performed to detect the expressions of CatG mRNA and protein respectively in these cells,and enzyme-linked immunosorbent assay (ELISA) was conducted to measure the expression of CatG protein in the culture supernatant of these cells.Results Compared with the control group,the fibroblasts irradiated with 10 J/cm2 UVA showed a significant increase at 24,48 and 72 hours in the expressions of CatG mRNA (0.376 ± 0.014 vs.0.183 ± 0.003,0.308 ± 0.022 vs.0.185 ± 0.005,0.296 ± 0.032 vs.0.182 ± 0.004,respectively,all P＜ 0.05) and protein (1.80 ± 0.12 vs.0.96 ± 0.06,1.41 ± 0.17 vs.0.95 ± 0.22,1.27 ± 0.09 vs.1.00 ± 0.14,respectively,all P ＜ 0.05),as well as in the supernatant level of CatG protein ((161.35 ± 7.55) vs.(122.45 ± 6.46) ng/L,(141.76 ± 2.95) vs.(124.17 ± 6.15) ng/L,(139.63 ± 3.04) vs.(121.72 ± 3.17) ng/L respectively,all P ＜0.05),with the strongest increase observed at 24 hours.At 24 hours after 10,20 and 30 J/cm2 of UVA radiation,the expression of CatG mRNA in irradiated fibroblasts was 1.90,2.51 and 3.04 times respectively (all P ＜ 0.05),the expression of CatG protein was 1.88,3.97 and 4.72 times respectively (P ＜ 0.05),and the supernatant level of CatG protein was 1.36,1.50 and 1.66 times respectively (P ＜ 0.05),that in the control group,and there was an increasing trend in all the above three parameters with increasing dose of UVA.Conclusion Acute UVA radiation can promote the expression and secretion of CatG by human dermal fibroblasts.

Objective To investigate whether ultraviolet A UVA)-induced CatK expression is regulated by the mitogen-activated protein kinases (MAPK) signaling pathway in human dermal fibroblasts in vitro.Methods Human dermal fibroblasts were obtained from circumcised foreskin of children,and subjected to primary culture.After several passages of subculture,some fibroblasts were irradiated with UVA at a dose of 10 J/cm2.Western blot was performed to measure the expressions of total and phosphorylated JNK (t-and p-JNK) and P38 (t-and p-P38) at 0.75,1.5,3 and 6 hours after the irradiation.Some fibroblasts were divided into six groups:control group receiving no treatment,SP group treated with SP600125 of 800 nmol/L,SB group treated with SB203580 of 10 μmol/L,UVA group irradiated with UVA at a dose of 10 J/cm2,UVA-SP group treated with SP600125 for 1 hour before and for 1.5 or 48 hours after UVA irradiation at 10 J/cm2,UVA-SB group treated with SB203580 for 1 hour before and for 1.5 or 48 hours after UVA radiation at 10 J/cm2.Subsequently,Western blot was performed to determine the expressions of p-c-Jun and p-MAPKAPK2 in these groups at 1.5 hours after the UVA irradiation,and reverse transcription (RT)-PCR and Western blot to detect the mRNA and protein expressions of CatK at 48 hours after the UVA irradiation,respectively.Statistical analysis was carried out by t test,one way analysis of variance and least significant difference (LSD)-t test.Results The expression levels (gray values) of p-JNK and p-P38 were significantly increased at 0.75 hour (4.77 ± 0.19 and 2.44 ± 0.13 respectively,both P ＜ 0.05) and 1.5 hours (4.68 ± 0.09 and 2.30 ± 0.04 respectively,both P ＜ 0.05),but showed no significant changes at 3 hours (both P ＞ 0.05) and 6 hours (both P ＞ 0.05) after the UVA irradiation compared with those before the irradiation (3.2 ± 0.27 and 1.61 ± 0.08 respectively).A significant decrease was observed in the expression of p-c-Jun in the UVA-SP group and p-MAPKAPK2 in the UVA-SB group compared with the UVA group (p-c-Jun,2.55 ± 0.48 vs.4.85 ±0.96; p-MAPKAPK2,1.16 ± 0.12 vs.2.46 ± 0.09,both P ＜ 0.05).The CatK mRNA and protein expressions were attenuated by 61.1％ and 44.3％ respectively in the UVA-SP group (both P ＜ 0.05),and by 71.3％ and 50.4％ respectively in the UVA-SB group (both P ＜ 0.05) in comparison with the UVA group.The UVA-SP group also showed a significant reduction in CatK mRNA and protein expressions as compared with the UVA-SB group (both P ＜ 0.05).Conclusion Both JNK and P38 signaling pathways,especially the JNK pathway,may contribute to the upregulation of CatK expression in dermal fibroblasts induced by UVA irradiation.

OBJECTIVETo explore early clinical effect of acetabular cup in total hip replacement for the treatment of Crowe II developmental dysplasia of hip.

METHODSEighteen patients (18 hips) with Crowe type II developmental dysplasia of hip were treated with total hip replacement from September 2001 to July 2013. Among them,including 13 males and 5 females aged from 42 to 60 years old with an average of 47.6 years old; the courses of diseases ranged from 9 to 22 years with an average of 13.5 years. All the patients had hip joint pain, limb shortening and limited hip function before operation. Harris score of hip joint were used to evaluate recovery of function at 1 day and 12 months after operation. Prosthetic coverage of acetabular cup at 1 week after operation was observed by using radiography.

RESULTSEighteen patients (18 hips) were followed up from 12 to 24 months with an average 17 months. All incisions were healed at stage I. No deep vein thrombosis, hip dislocation, periprosthetic joint infection and prosthesis loosening were occurred. No revision surgery during follow-up period. Prosthetic coverage of acetabular cup was more than 80% at 1 week after operation. Harris score were increased from 42.67 ± 5.06 before operation to 94.79 ± 3.27 at 12 months after operation (t = -45.269, P < 0.001).

CONCLUSIONFor type Crowe II developmental dysplasia of hip patients, 15° face-changing acetabular cups in THR could obtain higher actebular component coverage rate and satisfactory early clinical effects.

Acetabulum ; surgery ; Adult ; Arthroplasty, Replacement, Hip ; instrumentation ; Female ; Follow-Up Studies ; Hip Dislocation, Congenital ; surgery ; Hip Joint ; surgery ; Hip Prosthesis ; Humans ; Male ; Middle Aged

objective To study the TCR gene mutation in peripheral blood lymphocytes induced by X-ray exposure using cultured lymphocytes cloning method.Methods Freshly isolated peripheral lymphocytes from healthy aduh donors were irradiated with X-ray in doses ranging from 0 to 8 Gy and cultured with interleukin2 and phytohemagglutinin for 7 days.The mutant frequencies of TCR gene(TCR MF)were detected by flow cytonletry and the dose response curves were fitted.Results TCR MF increased with the dose going up.An aquadratic polynomial dose response model was fitted.Conclusions TCR gene mutation could which serve as a potential biological dosimeter.It might be applied for the estimation of biological dose in emergency exposure.

Objectives To investigate preparation of gemcitabine albumin nanoparticles, and its property of slow-release, the cytotoxic effect on pancreatic cancer cells (PANC1) in vitro, for improving the effect of regional intra-arterial infusion chemotherapy in pancreatic cancer with new medicament in the future. Methods The gemcitabine albumin nanoparticles were prepared with bovine serum albumin and gemcitabine with the desolvation-crosslink method, the concentration of gemcitabine was detected by high performance liquid chromatography (HPLC). The cytotoxic effect on pancreatic cancer cells in vitro were detected with MTT colorimetric assay. Results The mean diameter of gemcitabine albumin nanoparticles was (156.2±2.2) nm, and Zeta potential was (-20.4±1.41)mV, drug loading was 10.8%, drug release time in virto was 3 hours respectively. Gemcitabine albumin nanoparticles (0.01～50 μg/ml) had a 31%～44% inhibitory rate on PANC1 cell, which was similar to the inhibitory rate of same concentration of gemcitabine (26%～47%). Conclusions The new preparation of gemcitabine albumin nanoparticles had obvious drug slow-release effect, which may help improve the effect of regional intra-arterial infusion chemotherapy for pancreatic cancer.

Objective To observe the consistency of T-cell receptor (TCR) genes mutation in lymphocytes in rats after irradiation in vivo and in vitro.Methods A total of 48 female rats were randomly divided into 6 equal groups.Peripheral blood samples from them were collected to separate the lymphocytes and then irradiated to X-ray irradiation with the dose rate of 200 cGy/min at the doses of 0,0.5,0.75,1.0,2.0,and 3.0 Gy,respectively.Then all the lymphocyte samples were cultured for 7 days.Flow cytometry with direct immunofluorescence was used to detect the TCR gene mutation.The levels of TCR gene mutant frequency (TCRMF) of different groups were calculated.Results The TCRMF levels of different groups after irradiation in vivo and in vitro all displayed a dose-dependent manner and there were no significant differences in the TCRMF between different dose irradiation groups(t = -1.1-0.3 ,P ＞0.05).Conclusions A consistency of TCRMF after irradiation in vivo and in vitro is proven.The results of TCRMF of peripheral blood lymphocytes irradiated in vitro by flow cytometry can precisely reflect the TCR genes mutation after whole-body irradiation.

The aim of this study is to investigate the therapeutic effect of RegIII-proinsulin-pBudCE4.1 plasmid on streptozotocin (STZ)-induced type 1 diabetes mellitus and its underlying mechanisms. The model of type 1 diabetes mellitus was established by intraperitoneal injections of STZ (40 mg kg(-1)) to Balb/c mice for five consecutive days. Then, ten type 1 diabetic mice were intramuscularly injected with 100 microg RegIII-proinsulin-pBudCE4.1 plasmid for 4 weeks (one time/week) and the blood glucose levels were monitored every week; whereas another ten diabetic mice served as negative control group were injected with pBudCE4.1 vector at the same dose. Normal control and model control mice were treated with normal saline at identical volume under the same way. Western blotting, MTT assay, ELISA, HE staining and Tunel assay were applied to explore the underlying mechanisms. Results showed that RegIII-proinsulin-pBudCE4.1 plasmid ameliorated the hyperglycemia symptoms in diabetic mouse remarkably. It induced an immunological tolerance state in type 1 diabetic mice by inhibiting the proliferation of splenic lymphocytes and recovering Th1/Th2 balance evidenced by MTT and ELISA analysis. Furthermore, it elevated insulin concentration in the serum of type 1 diabetic mice and promoted the regeneration of beta cells supported by the results of HE staining and Tunel assay. In conclusion, RegIII-proinsulin-pBudCE4.1 plasmid possesses powerful anti-diabetic ability, which may be involved in the inducing of immunological tolerance and enhancing beta cells recovery.