Desensitization, Immunologic ; methods ; Oligodeoxyribonucleotides ; therapeutic use ; Toll-Like Receptor 9 ; therapeutic use

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Cell Survival ; drug effects ; Cells, Cultured ; Cerebral Cortex ; cytology ; drug effects ; Dose-Response Relationship, Drug ; Neurons ; drug effects ; Nickel ; toxicity ; Rats ; Rats, Wistar

Bacteremia ; etiology ; Female ; Humans ; Infant, Newborn ; Listeria monocytogenes ; isolation & purification ; Male

Animals ; Dose-Response Relationship, Drug ; Male ; Mice ; Mice, Inbred Strains ; Nickel ; toxicity ; Oxidative Stress ; physiology ; Testis ; drug effects ; metabolism

BackgroundPterygium is an ocular surface disease of abnormal cell proliferative kind and angiogenesis plays an important role in its development and recurrence.Several anti-angiogenic therapies have been used to treat pterygium,but there very few studtes for the in vivo observation of the microvessles in pterygium.ObjectiveThis study was to observe angiogenesis in pterygium with a high-resolution confocal microscope in vivo and to perform immunohistochemical study in vitro.MethodsA prospective case-controlled study was designed.Twenty eyes of 20 consecutive patients with primary pterygia and 20 age- and sex-matched patients with inner eye diseases and strabismus with normal conjunctiva were enrolled in this study.An in vivo confocal microscopy imaging system (Heidelberg Retina Tomograph Ⅱ Rostock Cornea Module) was used to collect microvascular pictures from the anterior part of pterygia and normal nasal conjunctiva of controls,and then immunochemistry was performed to examine the expression of CD31 in microvessel in vitro.The vascular density values were compared between these two groups.The correlation of vascular density values between in vivo Heidelberg Retina Tomograph and in vitro immunohistochemistry was calculated.Written informed consent was obtained from pationts before any examination and surgery.ResultsUnder the in vivo confocal microscope,the microvessel density was (8929±2993) μm/mm2 and (4202 ±692)μm/mm2,respectively,in pterygium and the normal conjunctiva group with a statistically significant difference between them (t =6.881,P＜0.01 ).Immunochemistry revealed that the expression of CD31 to measure vascular density was ( 21.00 ± 4.06/400 × field ) and ( 6.07 ± 1.75/400 × field ) in pterygium and the normal conjunctiva group,showing significant difference (t =12.312,P＜0.01 ).Positive correlations were found in the vascular density values between in vivo corneal laser confocal microscopy examination and in vitro immunochemistry examination in both the pterygium group and normal conjunctiva group (pterygium group:r=0.649,P＜0.01 ;normal conjunctiva group: r=0.572,P＜0.01 ) ConclusionsIn vivo confocal microscopy imaging is superior to in vitro immunochemistry in evaluating the microvessel of pterygium.The results of this study offer a new way index for further investigation of the biological behavior of pterygium and its mechanism.

Different antiepileptic drugs (AEDs) may cause similar adverse effects, one of which is diplopia. However, the AEDs causing diplopia and the dose-response effect of each drug remains uncertain. In this study, we compared several second-generation AEDs to find out whether they would contribute to the risk of diplopia and their effect-causing dose. A meta-analysis was performed on 19 studies in agreement with our inclusion criteria. The results showed that eight commonly used second-generation AEDs (gabapentin, levetiracetam, oxcarbazepine, lamotrigine, pregabalin, topiramate, vigabatrin and zonisamide) could cause diplopia. The reported odds ratios (ORs) ranged from 1.406 to 7.996. Ranking risks from the highest to the lowest ORs of the eight AEDs of any dose resulted in the following order: use of oxcarbazepine (7.996), levetiracetam (7.472), lamotrigine (5.258), vigabatrin (3.562), pregabalin (3.048), topiramate (2.660), gabapentin (1.966), zonisamide (1.406). Taking into account the ORs above, we can conclude that second-generation AEDs of any dose may cause diplopia. However, the levetiracetam-caused diplopia needs to be further studied according to the data (OR, 7.472; 95% confidence interval, 0.375-148.772). These findings ask for better concerns about patients' quality of life when giving antiepileptic treatments.

Objective To investigate the protective and cure effects of dexamethasone on bleomycin-induced pulmonary fibrosis.Methods32 rats were randomly divided into the control group (C-group, n=8), injury group (I-group, n=12) and dexamethasone group (D-group, n=12). The acute pulmonary model was established by intratracheal injection of bleomycin with rats of the I-group and D-group; while rats of the C-group injected with distilled water. After that, rats of the D-group were injected with dexamethasone sodium phosphate in intraperitoneal every day, those of the C-group and I-group were injected with saline. The animals were killed on the 3rd, 7th, 14th, and 27th days after treatment, and tests of bronchoalveolar lavage fluid (BALF), total lung collagen content and lung tissue processing were performed.ResultsPathological evidence of the I-group rats demonstrated that the alveolar compartment companied with massive inflammatory cell invasion and a number of myofibroblast proliferation became more thick. However, lung injury in the D-group rats got better than that in the I-group. Neutrophil percentage achieved peak in both I-group and D-group on the 7th day. But the neutrophil ratio in the D-group was significantly lower than that of the I-group on the 7th day ( P<0.05) and the 14th day ( P<0.01). Total lung collagen content achieved peak on the 14th day both in I-group and D-group, but that of the I-group was significantly higher than that of the C-group ( P<0.01) and the D-group was significantly lower than the I-group ( P<0.01).ConclusionDexamethasone plays a protective and cure role in lung fibrosis by efficiently inhibiting the gather and invasion of neutropils and restraining the increase of collagen secreted by proliferous fibroblasts.

As an important synthetic antibacterial drug, sulfonamides play an important role in the anti-infection field. Based on the research and development status of sulfonamides, this paper broke the classical structure of sulfanilamide, and designed and synthesized a series of acetyl-contained sulfanilamide tertiary amine thiol azole compounds and sulfanilamide tertiary amine amino azole compounds. The structures were confirmed by ¹H NMR, ¹³C NMR and HRMS. The antimicrobial activity of synthesized compounds in vitro was tested. The antimicrobial activity of amino triazole compound 7a gave stronger activity against Pseudomonas aeruginosa than that of positive control drug norfloxacin, and its inhibitory activity against Staphylococcus aureus was close to that of norfloxacin. The interaction between compound 7a and calf thymus DNA was studied, and the docking experiment between this compound and DNA was also researched.

OBJECTIVETo study the mechanism of male reproductive toxicity of metadoxine (MTDX) on mice and rats.

METHODSMouse multiple endpoints assay and Hershberger assay were employed to evaluate the potential estrogenic and/or antiandrogenic effects of MTDX. In mouse multiple endpoints assay, MTDX (0, 640, 1500 and 4000 mg/kg, respectively) were administered once daily p.o. for 5 days in sexually matured and ovariectomied female NIH mice. Five endpoints evaluated as markers of estrogenicity included the ratio of uterine weight to body weight, incidence and extent of uterine fluid imbibition (hydrometra), vaginal epithelial cornification during estrous cycle (estrinization) and thickness of uterine epithelial cell and stroma cell. In Hershberger assay, MTDX (0, 600 and 1500 mg/kg, respectively) was administered once daily p.o. for 10 days to castrated male SD rats with or without testosterone propionate (TP, 12.5 mg/kg, i.p. for 10 days) substitution. Relative weight of androgen dependent issues was measured.

RESULTSIn mouse multiple endpoints assay, ratio of uterine weight to body weight was 1.33, 1.38 and 1.31 x 10(-4) in MTDX 640, 1500 and 4000 mg/kg groups, respectively, without significant difference from that in control group (1.22 x 10(-4)). Thickness of uterine uterine epithelial cell (0.90 and 1.03 microm) and stroma cell (3.38 and 3.25 microm) in MTDX 1500 and 4000 mg/kg groups was not significantly different from the control group (0.85 microm and 2.77 microm, respectively). In Hershberger assay, relative weight of prostate plus seminal vesicle, levator ani muscle and bulbocavernous muscle was 1.13, 0.17 and 0.42, respectively, in the 1500 mg/kg group, significantly decreased as compared with those in the control group (1.46, 0.24 and 0.70, respectively) (P < 0.01). Relative weight of prostate plus seminal vesicle (1.29) in the MTDX 600 mg/kg group reduced slightly, with statistical significance (P < 0.05), as compared with that in the control group (1.46).

CONCLUSIONSIn the present study, MTDX did not exhibit any estrogenic effect in mice in vivo. However, it had antiandrogenic activity in castrated male SD rats, indicating that its antiandrogenic effect may be involved in it's male reproductive toxicity.

Androgen Antagonists ; toxicity ; Animals ; Drug Combinations ; Endpoint Determination ; Female ; Genitalia, Male ; drug effects ; pathology ; Male ; Mice ; Orchiectomy ; Ovariectomy ; Pyridoxine ; toxicity ; Pyrrolidonecarboxylic Acid ; toxicity ; Rats

OBJECTIVETo study the mechanism of the genital system damage by nickel sulfate in male rats in order to provide the laboratory theoretical evidence for the prevention and cure of nickel genital toxicity.

METHODSThree groups of rats were injected intraperitoneally with nickel sulfate at dose of 1.25, 2.50, 5.00 mg/kg respectively for two weeks. The content of testicle nickel and blood serum testosterone (T), follicle-stimulating hormone (FSH), luteinizing hormone (LH) were assessed with atomic absorption spectrum and radioimmuno-assay, meanwhile the activity of nitric oxide synthase (NOS) and the content of nitric oxide (NO) were measured by enzyme method.

RESULTSThe contents of testicle nickel [(0.22 +/- 0.03), (0.34 +/- 0.04), (0.41 +/- 0.02) micro g/g respectively] were increased, but the content of T, TSH, LH in blood serum were reduced; the activities of NOS in testicle tissue [(33.65 +/- 2.93), (26.53 +/- 9.52), (10.20 +/- 2.74) U/g respectively] were inhibited by nickel sulfate and the contents of NO [(0.26 +/- 0.03), (0.18 +/- 0.05), (0.15 +/- 0.02) mmol/g respectively] were decreased (P < 0.01).

CONCLUSIONNickel-induced genital system injury of male rats may be related to the decrease in the contents of T, TSH, LH, and the inhibition on NOS, as well as the fall of NO content.

Animals ; Follicle Stimulating Hormone ; blood ; Genitalia, Male ; drug effects ; metabolism ; pathology ; Luteinizing Hormone ; blood ; Male ; Nickel ; toxicity ; Nitric Oxide ; analysis ; Nitric Oxide Synthase ; analysis ; Radioimmunoassay ; Random Allocation ; Rats ; Rats, Wistar ; Testosterone ; blood