Lumbar disc herniation is a common male disease. In the past, More academic attention was directed to its relationship with lumbago and leg pain than to its association with andrological diseases. Studies show that central lumber intervertebral disc herniation may cause cauda equina injury and result in premature ejaculation, erectile dysfunction, chronic pelvic pain syndrome, priapism, and emission. This article presents an overview on the correlation between central lumbar intervertebral disc herniation and andrological diseases, focusing on the aspects of etiology, pathology, and clinical progress, hoping to invite more attention from andrological and osteological clinicians.
Chronic Pain ; etiology ; Erectile Dysfunction ; etiology ; Humans ; Intervertebral Disc Displacement ; complications ; Lumbar Vertebrae ; Male ; Pelvic Pain ; etiology ; Polyradiculopathy ; etiology ; Premature Ejaculation ; etiology ; Priapism ; etiology

Humans ; Medicine, Chinese Traditional ; Qi ; Thymoma ; surgery ; therapy

Adolescent ; Cardiology ; methods ; trends ; Child ; Child, Preschool ; China ; Cost-Benefit Analysis ; methods ; Diagnostic Tests, Routine ; economics ; Female ; Humans ; Male ; Pediatrics ; methods ; trends ; Syncope, Vasovagal ; diagnosis

Animals ; Humans ; Hydrogen Sulfide ; Hypertension, Pulmonary ; etiology ; pathology ; physiopathology ; Pulmonary Artery ; physiopathology ; Pulmonary Circulation

Objective To investigate the effect of carbon monoxide(CO) on hydrogen sulfide(H_2S)/cystathionine-?-lyase system(CSE) in vascular smooth muscle cells(VSMC) of spontaneous hypertensive rats(SHR).Methods The SHR VSMC were divided into 2 groups:experimental group(hemin was added to the culture media at a concentration of 10 ?mol/L)and control group (dimethyl sulfoxide was added to the culture media at an equal volume).The content of H_2S in the cultrue media was measured by sulfide electrode method,and the CSEmRNA level was assayed by competitive reversed transcription-polymerase chain reaction(RT-PCR).Results Compared with control group,the content of H_2S in the culture media of hemin-treated SMCs was significantly lower[(16.03? 2.14) ?mol/L vs (13.31?1.74)?mol/L],and the CSEmRNA level in hemin-treated SMCs was decreased markedly(0.17?0.04 vs 0.13?0.03).Conclusion CO can down-regulate the H_2S/CSE system in SMC of SHR.

Objective To investigate the effect of nitric oxide on hydrogen sulfide/ cystathionine-?-lyase(CSE) system in the vascular smooth muscle cells of spontaneously hypertensive rats(SHR).Methods The SHR aortic smooth muscle cells(SMCs) were divided into 2 groups: sodium nitroprusside(SNP) group and control group.The content of hydrogen sulfide in the culture media was measured by sulfide electrode method,and the CSE mRNA level was assayed by competitive reversed transcription-polymerase chain reaction((RT-PCR)).Results Compared with control group,the content of hydrogen sulfide in the culture media of SNP group was significantly higher [(16.16?3.71) ?mol/L vs(22.71?4.84) ?mol/L],and the CSE mRNA level in SMCs in SNP group was lower than that of control group.Conclusion Nitric oxide exerted complicated effect on the hydrogen sulfide/CSE system in the SHR smooth muscle cells.J Appl Clin Pediatr,2006,21(3):140-141

The uracil in DNA comes from either the misincorporation of dUTP in place of dTTP or deamination of cytosine. In the latter case, it can result in a GC to AT transition mutation if the uracil is not removed before DNA replication. Base excision repair (BER) is a major pathway for removing DNA lesions arising from endogenous processes as well as those induced by exposure to exogenous chemicals or irradiation. BER is initiated by DNA glycosylases that excise aberrant bases from DNA by cleavage of the N-glycosidic bond linking to the base of its deoxyribose sugar. Uracil N-glycosylase (UNG) is the enzyme responsible for the first step in the BER pathway that specifically removes uracil from DNA. The UNG gene undergoes both temporal and spatial regulation mainly at the level of transcription. Normally cancer cells undergo over-proliferation and up-regulate their UNG during tumorigenesis. In this study we examine the correlation between UNG level and carcinogenesis, and explore the possibility of using UNG as a marker for cancer diagnosis. Human UNG gene was amplified from the total RNA of the human choriocarcinoma cell line, JEG-3, by RT-PCR. After purification, the 942bp full-length UNG cDNA coding sequence was digested with EcoR I and Sal I, and cloned into the digested pET-21 to construct a recombinant vector, pUNG. The UNG protein was expressed under the control of T7 promoter in E. coli BL21 (DE3) cells induced with IPTG. After ultrasonic treatment, the cell lysate and precipitate were analyzed by SDS-PAGE and a 39kD band was detected. The plasmid was serially diluted at appropriate concentrations and employed as standards in the subsequent quantification. Total RNAs were extracted from 18 pairs of clinical samples, each pair contains a sample of esophageal squamous cell carcinoma (ESCC) tissue and its surrounding normal esophageal epithelia. The copy numbers of UNG mRNA in these RNA samples were determined by real-time quantitative RT-PCR using a Lightcycler (Roche). UNG was present in 13 cases of ESCC (13/18, n = 18) but absent in all of the normal tissues. The results indicated that there was a correlation between high level of UNG expression and the carcinogenesis of ESCC.
Carcinoma, Squamous Cell ; genetics ; metabolism ; Cell Line, Tumor ; Cloning, Molecular ; Electrophoresis, Polyacrylamide Gel ; Esophageal Neoplasms ; genetics ; metabolism ; Humans ; In Vitro Techniques ; Reverse Transcriptase Polymerase Chain Reaction ; Uracil-DNA Glycosidase ; genetics ; metabolism

Anti-Arrhythmia Agents ; therapeutic use ; Cardiomyopathies ; drug therapy ; etiology ; Child, Preschool ; Female ; Humans ; Moricizine ; therapeutic use ; Tachycardia ; complications ; drug therapy ; Treatment Outcome

OBJECTIVETo investigate the mechanism that the formulas for activating blood and resolving stasis can regulate hemopoietic stem cell to produce new blood.

METHODRats were established animal model of acute cerebral infarction by referencing Olivette' method. They were randomly divided into model group, the group of the high, middle, low dose of the formulas for activating blood and resolving stasis. Each group and then wasrandomly divided into subgroups by 1, 3, 7, 14, 28 d. Xuesaitong capsule was formulated into 20, 40, 60 g x L(-1) with normal saline. The rats were given gavage drugs once a day until the experient ended, and the model group was administrated by intragastrical perfusion of normal saline. ELISA was used to detect the expression of SCF in peripheral blood and bone marrow among different groups at different time points. Flow cytometry was used to observe the changes of CD117 in blood and bone marrow.

RESULTThe CD117+ HSC and SCF concentration in peripheral blood and bone marrow of model group were increasing during 1-14 d,there was a peak on the 14th day, then the expression was reducing. CD117+ HSC and SCF concentration rising trend in the group of the high, middle dose of the formulas for activating blood and resolving stasis was preceded model group (P < 0.05).

CONCLUSIONActivating blood and resolving stasis can regulate hemopoietic stem cell to produce new blood, and it is through the regulation of CD117+ HSC number to achieve the purpose.

Animals ; Bone Marrow Cells ; drug effects ; metabolism ; Capsules ; Cerebral Infarction ; blood ; drug therapy ; genetics ; metabolism ; Chemistry, Pharmaceutical ; Drugs, Chinese Herbal ; administration & dosage ; Hematopoietic Stem Cells ; drug effects ; metabolism ; Humans ; Male ; Proto-Oncogene Proteins c-kit ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stem Cell Factor ; genetics ; metabolism

Objective To investigate whether recombinant human endostatin can create a time window of vascular normalization prior to vascular pruning to alleviate hypoxia in Lewis lung carcinoma in mice. Methods Kinetic changes in morphology of tumor vasculature in response to recombinant human endostatin were detected under a confocal microscope with immunofluorescent staining in Lewis lung carcinomas in mice. The hypoxic cell fraction of different time was assessed with immunohistochemical staining . Effects on tumor growth were monitored as indicated in the growth curve of tumors . Results Compared with the control group vascularity of the tumors was reduced over time by recombinant human endostatin treatment and significantly regressed for 9 days. During the treatment, pericyte coverage increased at day 3, increased markedly at day 5, and fell again at day 7. The vascular basement membrane was thin and closely associated with endothelial cells after recombinant human endostatin treatment, but appeared thickened, loosely associated with endothelial cells in control tumors. The decrease in hypoxic cell fraction at day 5 after treatment was also found. Tumor growth was not accelerated 5 days after recombinant human endostatin treatment. Conclusions Recombinant human endostatin can normalize tumor vasculature within day 3 to 7, leading to improved tumor oxygenation. The results provide important experimental basis for combining recombinant human endostatin with radiation therapy in human tumors.