1.Combination of improved sex therapy and sildenafil for erectile dysfunction in Uigur men: retrospective analysis of 2505 cases.
Mu-la-jiang AI ; Er-ken AI ; Er-ban KU ; Mu-tu-la NI ; Er-mai-mai-ti NU ; Zhi-hua CAI ; A BU-DU-WAI-LI ; De-er KA ; Ke-bai-er AI ; Yi-er TA ; Si-hai-ti AI ; A DA-LI ; Qin XU
National Journal of Andrology 2010;16(3):261-263
OBJECTIVEThe sex therapy is not yet popularized at present. This study aimed to evaluate the effect of the combination of the improved sex therapy and oral sildenafil on erectile dysfunction (ED).
METHODSA total of 3130 Uigur cases of ED received in Xinjiang Bogda Hospital were divided into a control group (n=625) and a trial group (n=2505), the former treated with oral sildenafil alone, and the latter by the combination of the improved genital therapy and sildenafil, both for 3 months and followed up at 6 and 12 months after the treatment. The therapeutic effects were evaluated and compared using IIEF-5.
RESULTSThe IIEF-5 scores of the control group were 12.80 +/- 3.76 and 18.10 +/- 2.61 before and after the treatment, and 17.35 +/- 2.73 and 16.64 +/- 2.63 at 6 and 12 months, respectively, while those of the trial group were 12.73 +/- 3.52 and 19.06 +/- 4.07 before and af- ter the treatment, and 19.86 +/- 2.42 and 20.47 +/- 2.38 at 6 and 12 months, respectively, with statistically significant differences either between pre- and post-treatment (P < 0.05) or between the control and trial groups at 6 and 12 months (P < 0.05).
CONCLUSIONThe combination of the improved sex therapy and oral sildenafil is superior to sildenafil alone in the treatment of ED, and its efficacy is relatively stable at 12 months.
Adult ; Aged ; Asian Continental Ancestry Group ; Erectile Dysfunction ; drug therapy ; ethnology ; Humans ; Male ; Middle Aged ; Piperazines ; therapeutic use ; Purines ; therapeutic use ; Retrospective Studies ; Sildenafil Citrate ; Sulfones ; therapeutic use ; Treatment Outcome ; Young Adult
2.A genome sequence of novel SARS-CoV isolates: the genotype, GD-Ins29, leads to a hypothesis of viral transmission in South China.
E'de QIN ; Xionglei HE ; Wei TIAN ; Yong LIU ; Wei LI ; Jie WEN ; Jingqiang WANG ; Baochang FAN ; Qingfa WU ; Guohui CHANG ; Wuchun CAO ; Zuyuan XU ; Ruifu YANG ; Jing WANG ; Man YU ; Yan LI ; Jing XU ; Bingyin SI ; Yongwu HU ; Wenming PENG ; Lin TANG ; Tao JIANG ; Jianping SHI ; Jia JI ; Yu ZHANG ; Jia YE ; Cui'e WANG ; Yujun HAN ; Jun ZHOU ; Yajun DENG ; Xiaoyu LI ; Jianfei HU ; Caiping WANG ; Chunxia YAN ; Qingrun ZHANG ; Jingyue BAO ; Guoqing LI ; Weijun CHEN ; Lin FANG ; Changfeng LI ; Meng LEI ; Dawei LI ; Wei TONG ; Xiangjun TIAN ; Jin WANG ; Bo ZHANG ; Haiqing ZHANG ; Yilin ZHANG ; Hui ZHAO ; Xiaowei ZHANG ; Shuangli LI ; Xiaojie CHENG ; Xiuqing ZHANG ; Bin LIU ; Changqing ZENG ; Songgang LI ; Xuehai TAN ; Siqi LIU ; Wei DONG ; Jun WANG ; Gane Ka-Shu WONG ; Jun YU ; Jian WANG ; Qingyu ZHU ; Huanming YANG
Genomics, Proteomics & Bioinformatics 2003;1(2):101-107
We report a complete genomic sequence of rare isolates (minor genotype) of the SARS-CoV from SARS patients in Guangdong, China, where the first few cases emerged. The most striking discovery from the isolate is an extra 29-nucleotide sequence located at the nucleotide positions between 27,863 and 27,864 (referred to the complete sequence of BJ01) within an overlapped region composed of BGI-PUP5 (BGI-postulated uncharacterized protein 5) and BGI-PUP6 upstream of the N (nucleocapsid) protein. The discovery of this minor genotype, GD-Ins29, suggests a significant genetic event and differentiates it from the previously reported genotype, the dominant form among all sequenced SARS-CoV isolates. A 17-nt segment of this extra sequence is identical to a segment of the same size in two human mRNA sequences that may interfere with viral replication and transcription in the cytosol of the infected cells. It provides a new avenue for the exploration of the virus-host interaction in viral evolution, host pathogenesis, and vaccine development.
Base Sequence
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China
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Cluster Analysis
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Gene Components
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Genetic Variation
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Genome, Viral
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Genotype
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Molecular Sequence Data
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Phylogeny
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Reverse Transcriptase Polymerase Chain Reaction
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SARS Virus
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genetics
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Sequence Analysis, DNA
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Severe Acute Respiratory Syndrome
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genetics
3.PMExposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes.
Rong HU ; Xiao-Yuan XIE ; Si-Ka XU ; Ya-Ning WANG ; Ming JIANG ; Li-Rong WEN ; Wei LAI ; Lei GUAN
Chinese Medical Journal 2017;130(18):2205-2214
Background:PM(aerodynamic diameter ≤ 2.5 μm) is a dominant and ubiquitous air pollutant that has become a global concern as PMexposure has been linked to many adverse health effects including cardiovascular and pulmonary diseases. Emerging evidence supports a correlation between increased air PMlevels and skin disorders although reports on the underlying pathophysiological mechanisms are limited. Oxidative stress is the most common mechanism of PM-induced adverse health effects. This study aimed to investigate PM-induced oxidative damage and apoptosis in immortalized human keratinocyte (HaCaT) cells.
Methods:HaCaT cells were exposed to 0, 25, 50, 100, or 200 μg/ml PMfor 24 h. Reactive oxygen species (ROS) generation, lipid peroxidation products, antioxidant activity, DNA damage, apoptotic protein expression, and cell apoptosis were measured.
Results:PMexposure (0-200 μg/ml) for 24 h resulted in increased ROS levels (arbitrary unit: 201.00 ± 19.28, 264.50 ± 17.91, 305.05 ± 19.57, 427.95 ± 18.32, and 436.70 ± 17.77) and malondialdehyde production (0.54 ± 0.05 nmol/mg prot, 0.61 ± 0.06 nmol/mg prot, 0.68 ± 0.05 nmol/mg prot, 0.70 ± 0.05 nmol/mg prot, and 0.76 ± 0.05 nmol/mg prot), diminished superoxide dismutase activity (6.47 ± 0.28 NU/mg prot, 5.97 ± 0.30 NU/mg prot, 5.15 ± 0.42 NU/mg prot, 4.08 ± 0.20 NU/mg prot, and 3.76 ± 0.37 NU/mg prot), and increased DNA damage and apoptosis in a dose-dependent manner in HaCaT cells. Moreover, cytochrome-c, caspase-3, and caspase-9 expression also increased proportionately with PMdosing.
Conclusion:PMmight elicit oxidative stress and mitochondria-dependent apoptosis that likely manifests as skin irritation and damage.