Peyronie's disease is characterized by local fibrosis of the tunica albuginea and relatively rare clinically. Few relevant basic researches could be retrieved, which might be attributed to the absence of a robust animal model of the disease as well as to its rareness. At present, some animal models available for Peyronie's disease have their own merits and demerits. TGF-β1-induced and Fibrin-induced models are lack of penile curvature and calcification/ossification. A surgical model might be established for the acute phase of the disease. The characteristic of a widespread fibrotic process involving many organs in the spontaneous model is quite different from that of human Peyronie's disease. Therefore, choosing the right model is essential for researches. This paper presents an overview of the animal models of Peyronie's disease, meant to provide some reference for the basic research of the disease.
Animals ; Disease Models, Animal ; Fibrin ; Fibrosis ; Humans ; Male ; Penile Induration ; chemically induced ; pathology ; Penis ; pathology ; Transforming Growth Factor beta1

Colitis, Ulcerative ; complications ; drug therapy ; Humans ; Male ; Middle Aged ; Psoriasis ; complications ; drug therapy ; Pyoderma Gangrenosum ; drug therapy ; etiology

0.05).But GR number[sites/cell]and the expression of GR mRNA in PBMCs from PM/DM was significantly lower than those in healthy controls(P

Objective To investigate the expression of glucocorticoid receptor-alpha and beta(GR?and GR?)mRNA of peripheral blood mononuclear cells(PBMCs)in patients with dermatomyositis/polymyositis (DM/PM)and analyze their association with the pathogenesis and clinical response to glucocorticoid therapy. Methods The expression of GR?and GR?mRNA in PBMCs from 20 normal controls and 36(24 steroid- sensitive,12 steroid-resistant)patients with DM/PM were detected by reverse transcription polymerase chain reaction(RT-PCR).Results Compared to normal controls,the expression of GR?mRNA in the DM/PM was significantly decreased(P

Objective To investigate the mechanism of apoptosis induced by arsenic trioxide(As2O3) on MDCC-MSB1 cancer cell line in vitro. Methods MDCC-MSB1 cells were divided into 4 groups, treated with 0 (control group), 2, 4 or 8 μmoL/L of As2O3. At 48 h following the treatment, MTr assay was applied to detect the inhibitory effect of As2O3 on MDCC-MSB1. Morphological changes of apoptosis were observed by fluorescence microscopy. Apoptosis was examined by DNA Ladder. Changes of mitochondrial transmembrane potential were examined by Rhodamin 123 dye and flow cytometry. Results Inhibition ratio was 0, (5.34±3.02)%, (10.78± 0.55)% and (20.02±3.24)% respectively, along with the dosages of As2O3, the differences between the groups were statistically significant(P<0.01). Morphologic changes of apoptosis were observed by DNA ladder of agarose gel electrophoresis. Apoptosis rates were significandy increased from 3.200±0.459, 11.543±0.391, 17.206±0.636 to 21.343±0.620, and the differences between the groups were statistically significant(P<0.01). DNA ladder of experimental group was detected, Intact cell membrane, and mitochondrial transmembrane potential Pl-/Rh123- decreased apoptotic cells percentage was significantly increased from (1.06±0.14)%, (4.63±0.04)%, (9.62±0.07)% to (10.39±0.10)%, respective to doses of 0, 2,4, and 8 μmol of As2O3. The differences between the groups were statistically significant(P<0.01). Conclusions As2O3 can induce apoptosis in MDCC-MSB1 cells by decreasing the mitochondrial transmembrane potential.

Background: IMpower 133 trial first confirmed the efficacy and safety of adding atezolizumab or placebo to first-line treatment with chemotherapy in patients with extensive-stage small-cell lung cancer(SCLC).While,overprice limited its broad use in clinical.The aim of this study was to evaluate the cost-effectiveness of atezolizumab plus chemotherapy in treatment of extensive SCLC as first line in China.Methods: A Markov model was established by extracting data from the IMpower 133 trial with untreated extensive SCLC patients.Utility values were obtained from published studies,and the costs were acquired from real world and literature.Additionally,sensitivity analyses based on a willingness-to-pay(WTP)threshold were performed to identify the uncertain parameters of Markov model.Results: Total costs of atezolizumab group were $48,129,while cost of chemotherapy alone was just $12,920 in placebo group.The quality-adjusted life-years(QALYs)in atezolizumab group was just 0.072 higher than that in placebo group(0.858 QALYs vs.0.786 QALYs).The cost-effectiveness ratio between atezolizumab combination with chemotherapy and chemotherapy alone was$489,013/QAL Y in China.The net benefit of placebo group was significantly higher than atezolizumab group.One-way sensitivity analyses highlighted that utilities of the progression-free survival(PFS)and progression disease state in placebo group were the most influential parameter.Conclusions: Atezolizumab combination therapy was not more cost-effective than chemotherapy alone at a WTP threshold of $25,929/QALY in China.

To explore the main clinical manifestation (lower back pain and ischialgia) of LDH with immunologic method and study the relationship and clinical significance of the cardinal symptom (pain) and immune comple (IC), macrophage (MP),interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor (TNF), prostaglandin E2 (PGE2), phosphatidase A2 (PLA2), nitrogen monoxidum (NO) expressing, finding a new way in order to prevention and cure of LDH. We will review immunologic theory of LDH pain.
Cytokines ; metabolism ; Humans ; Intervertebral Disc Displacement ; complications ; immunology ; metabolism ; Lumbar Vertebrae ; pathology ; Nitric Oxide ; metabolism ; Pain ; etiology ; immunology ; metabolism ; Phospholipases A2 ; metabolism

OBJECTIVETo evaluate current diagnosis and therapeutic effect and outcome of diffuse axonal injury (DAI) in 169 patients.

METHODSThe data of 169 DAI patients treated in the Second, Sixth, Eighth and Ninth Hospitals of Shenzhen and Shekou Hospital from January 2001 to January 2005 were collected. The imaging features, classification, GCS (Glasgow coma scale), treatment and outcome of the 169 patients were retrospectively analyzed.

RESULTSThe simpler the imaging features, the closer the focus of DAI to the periphery of hemisphere and the higher the GCS score, the better the prognoses of DAI patients will be.

CONCLUSIONSThe prognoses of DAI patients are closely related to the imaging features and classification, GCS and clinical treatment.

OBJECTIVETo investigate the effects of rapamycin on cholesterol homeostasis and secretory function of 3T3-L1 cells.

METHODSThe in vitro cultured 3T3-L1 cells (preadipocytes) were divided into control group, rapamycin 50 nmol/L group, rapamycin 100 nmol/L group, and rapamycin 200 nmol/L group. Intracellular cholesterol level was measured by oil red O staining and high performance liquid chromatography. The secretion levels of leptin and adiponectin were assayed by enzyme-linked immunosorbent assay. The mRNA and protein expressions of peroxisome proliferator-activated receptor (PPARgamma) were assayed by quantitative real-time polymerase chain reaction and Western blot.

RESULTSOil red O staining showed rapamycin down-regulated 3T3-L1 cells differentiation and lipid accumulation. Quantitative measurement of cholesterol with high performance liquid chromatography showed that the concentrations of free cholesterol in rapamycin treatment groups had a significant reduction. The concentrations of free cholesterol in the control group, rapamycin 50 nmol/L group, rapamycin 100 nmol/L group, and rapamycin 200 nmol/L group were (12.89 +/- 0.16), (9.84 +/- 0.45), (9.39 +/- 0.46), and (8.61 +/- 0.34) mg/ml, respectively (P < 0.05), and the concentrations of total cholesterol were (12.91 +/- 0.50), (9.94 +/- 0.96), (10.45 +/- 2.51), and (9.53 +/- 0.63) mg/ml, respectively. The leptin concentrations in the control group, rapamycin 50 nmol/L group, rapamycin 100 nmol/L group, and rapamycin 200 nmol/L group were (19.02 +/- 0.52), (16.98 +/- 0.11), (15.62 +/- 0.01), and (13.84 +/- 0.66) ng/ml, respectively. The mRNA expressions of PPARgamma in the rapamycin 50 nmol/L group, rapamycin 100 nmol/L group, and rapamycin 200 nmol/L group were significantly lower than that in control group (P < 0.05). The protein expressions of PPARgamma in the rapamycin 50 nmol/L group, rapamycin 100 nmol/L group, and rapamycin 200 nmol/L group were 80%, 74%, and 61% of that in control group (P < 0.05). After the cells were treated with rapamycin 100 nmol/L, PPARgamma blocking agent GW9662 10 micromol/L, and PPARgamma agonist troglitazone 10 micromol/L, respectively, for 96 hours, the mRNA expression of PPARgamma was (0.60 +/- 0.14), (0.67 +/- 0.03), and (1.30 +/- 0.14) of that in control group (P < 0.05). The protein expression showed a similar trend with mRNA expression (P < 0.05). After the cells were treated with rapamycin 100 nmol/L, PPARgamma blocking agent GW9662 10 micromol/L, and PPARgamma agonist troglitazone 10 micromol/L, respectively, for 96 hours, the expression of leptin in the control group, rapamycin 50 nmol/L group, rapamycin 100 nmol/L group, and rapamycin 200 nmol/L group was (19.02 +/- 0.52), (15.62 +/- 0.10), and (14.45 +/- 1.01) and (18.07 +/- 0.66) ng/ml, respectively (P < 0.05 compared with the control group).

CONCLUSIONSBy downregulating the expression of PPARgamma, rapamycin can decrease cholesterol accumulation in 3T3-L1 cells and inhibit its leptin-secreting capability. This finding may provide a possible explanation for rapamycin-induced hyperlipidemia in clinical practice.

3T3-L1 Cells ; Adipocytes ; drug effects ; metabolism ; Animals ; Cholesterol ; metabolism ; Leptin ; metabolism ; Mice ; PPAR gamma ; genetics ; metabolism ; Sirolimus ; pharmacology