Objective To explore the role of chemokines and ehemokine receptors in the etiopathog-enesis of diffuse proliferative lupus nephritis (LN). Methods ① Total RNA from the kidney tissues and peripheral blood cells of 12 patients with diffuse proliferative LN and 10 normal controls were prepared simultaneously and reverse transcribed into complementary DNA. Sybr green dye based real-time quantitative PCR method was used to compare the expression levels (indicated as-AACt value) of MCP-1, CCL19,CXCLg, CXCL10 and CCR2, CCR7, CXCR3. ② Immunofluoresceee labeling and immunohistochemical staining technique were used to observe the distribution of chemokines MCP-1, CCL19, CXCL9 and CXCL10 in normal and patients kidney tissues. Results The 4 chemokines genes (MCP-1, CCL19, CXCL9 and CXCL10) were consistently highly expressed in kidney tissues and peripheral blood ceils of diffuse proliferative LN patients compared with normal controls. The 2 chemokine receptors, CCR2 and CXCR3 were also overexpressed in peripheral blood cells of diffuse proliferative LN patients. There was nearly no expression of these 4 chemokine proteins in normal kidneys. But they were found in glomeruli of diffuse proliferative LN patients. Conclusion The expression of chemokines in the peripheral blood cells may be used as biomarkers for LN. Further study maybe lead to the development of specific drugs targeting at them for the treatment of systemic lupus erythematosus (SLE).

OBJECTIVE To explore the role of P38MAPK inhibitor on the soft palate reconstruction of the rats with chronic intermittent hypoxia. METHODS The animals were divided into normal control group, hypoxia control group and SB203580+hypoxia group (every group 20 rats). After 5 weeks, the expressions of p38MAPK and p-p38MAPK protein on the soft palate of the rats were detected with immunohistochemical techniques and western blot. RESULTS Compared with the normal control group, the soft palate tissue thickness of the hypoxia group were increased most obviously; Levels of p38MAPK were increased in hypoxia control group; Compared with the hypoxia control group, the levels of p-p38MAPK group were decreased in SB203580+hypoxia group. CONCLUSION p38MAPK may play important roles in the soft palate reconstruction of the rats with chronic intermittent hypoxia.

This study is to explore whether the Wnt/beta-catenin signaling pathway is involved in the process of tripchlorolide (T4) protecting against oligomeric Abeta(1-42)-induced neuronal apoptosis. Primary cultured cortical neurons were used for the experiments on day 6 or 7. The oligomeric Abeta(1-42) (5 micromol x L(-1) for 24 h) was applied to induce neuronal apoptosis. Prior to treatment with Abeta(1-42) for 24 h, the cultured neurons were pre-incubated with T4 (2.5, 10, and 40 nmol x L(-1)), Wnt3a (Wnt signaling agonists) and Dkk1 (inhibitors) for indicated time. Then the cell viability, neuronal apoptosis, and protein levels of Wnt, glycogen synthase kinase 3beta (GSK3beta), beta-catenin and phospho-beta-catenin were measured by MTT assay, TUNEL staining and Western blotting, respectively. The result demonstrated that oligomeric Abeta(1-42) induced apoptotic neuronal cell death in a time- and dose-dependent manner. Pretreatment with T4 significantly increased the neuronal cell survival and attenuated neuronal apoptosis. Moreover, oligomeric Abeta(1-42)-induced phosphorylation of beta-catenin and GSK3beta was markedly inhibited by T4. Additionally, T4 stabilized cytoplasmic beta-catenin. These results indicate that tripchlorolide protects against the neurotoxicity of Abeta by regulating Wnt/beta-catenin signaling pathway. This may provide insight into the clinical application of tripchlorolide to Alzheimer's disease.

Small interfering RNA (siRNA) is the initiator of RNA interference and inhibits gene expression by targeted degradation of specific messenger RNA. siRNA-mediated gene regulation has high efficiency and specificity and exhibits great significance in the treatment of diseases. However, the naked or unmodified siRNA has poor stability, easy to degrade by nuclease, short half-life, and low intracellular delivery. As an emerging non-viral nucleic acid delivery system, ionizable lipid nanoparticles play an important role in improving the druggability of siRNA. At present, one siRNA drug based on ionizable lipid nanoparticles has been approved for the treatment of rare disease. This review introduces the research progress in ionizable lipid nanoparticles for siRNA delivery, focusing on the effect of each component of lipid nanoparticles on the efficiency of siRNA-mediated gene silencing, which provides new references for the studies on ionizable lipid nanocarriers for siRNA delivery.

AIMTo describe an unusual symptom of benign prostatic hyperplasia (BPH).

METHODSA patient presented to our urology clinic having experienced post-coital gross hematuria for 2 years. He had not experienced lower urinary tract symptoms (LUTS). A series of examinations were performed to determine the source of bleeding.

RESULTSThe prostate was defined as the active bleeding source responsible for the patient's post-coital hematuria. Endoscopic fulguration did not alleviate the symptom. The use of dutasteride, a dual inhibitor of 5alpha-reductase, solved the problem.

CONCLUSIONThis study reports for the first time that post-coital gross hematuria is one of the clinical presentations of BPH, which can be successfully treated with 5alpha-reductase inhibitor.

5-alpha Reductase Inhibitors ; Azasteroids ; therapeutic use ; Coitus ; physiology ; Dutasteride ; Enzyme Inhibitors ; therapeutic use ; Hematuria ; drug therapy ; etiology ; physiopathology ; Humans ; Male ; Middle Aged ; Prostatic Hyperplasia ; complications ; diagnosis ; physiopathology ; Urinary Tract

Objective To investigate transcriptional expression and promoter CpG methylation status of A-kinase anchoring protein 12 (AKAP12) gene and analyze their correlation with clinical pathological stage in bladder transitional cell carcinoma. Methods AKAP12 mRNA expression level and promoter CpG metbylation status was measured by fluorescent quantitative RT-PCR (FQ-RT-PCR) and methylation specific PCR (MSP) in 30 bladder transitional cell carcinoma and adjacent normal tissues. The products of PCR were cloned and bisulfite sequenced. Results Decreased AKAP12 mRNA expression was demonstrated in 22 carcinomas (73. 3% ) and was significantly associated with turnout grade (P =0. 02).The frequency of promoter methylation of AKAP12 gene was 53. 3 % (16/30) and correlated with the tumor stage(r =0.52,Pn =0.03)and grade(r =0.61,Pn =0.01). Conclusion Aberrant promoter methylation of AKAP12 can result in the loss of gene expression and may association with bladder transitional cell carcinoma.

We describe an unusual complication of coital trauma in a 29-year-old man who presented with a 3-year history of hematospermia and post-coital gross hematuria. Using urethroscopy under a semi-tumescent penis, an isolated urethral injury with active bleeding was detected at the prostatic urethra. The patient was successfully treated with transurethral fulguration. We suggest that isolated posterior urethral injury is one of the causes of male coital trauma, which might be asymptomatic when the penis is flaccid but show symptomatic bleeding when the penis is erect.
Adult ; Coitus ; Ejaculation ; Female ; Hematuria ; Humans ; Male ; Urethra ; injuries ; Urethral Diseases ; etiology

OBJECTIVETo study influenza epidemic and analyze antigenic and genetic characterization of the predominant strains in Wuhan area in 2003.

METHODSEpidemiological data and specimens from influenza patients were collected from surveillance sites weekly. Viruses were isolated from the specimens. Three H3 isolates were chosen to do antigenic analysis by hemagglutination inhibition (HI) test and their HA1 region was sequenced.

RESULTSTotally 58 influenza viruses were isolated from 418 specimens, 57 of them were identified as H3 subtype and 1 of them was B subtype; both monthly positive rate and numbers of influenza like illness had two peaks of winter and summer, the highest peak appeared in July. The 3 new H3 isolates were antigenically different from vaccine strain A/Panama/2007/99, 14 amino acid changes have been found in HA1 domain of these 3 strains compared with A/Panama/2007/99, phylogenetic analysis also confirmed the difference in HA1 domain.

CONCLUSIONSInfluenza epidemic had two peaks in Wuhan area in 2003. The activity of H3 virus was strengthened remarkably. And they are antigenically and genetically different from the vaccine strain.

Amino Acid Sequence ; Antigens, Viral ; immunology ; China ; epidemiology ; Genes, Viral ; Glycosylation ; Hemagglutination Inhibition Tests ; Humans ; Influenza A Virus, H3N2 Subtype ; genetics ; immunology ; isolation & purification ; Influenza, Human ; epidemiology ; virology ; Molecular Sequence Data ; Phylogeny ; Sequence Analysis, Protein

Human defensin is a family of cationic antimicrobial peptides in human being. During the last two decades a series of endogenous alpha-and beta-human defensins have been discovered. They are important components of the first barrier in human's body against the invasion of various microorganisms, and they are thought to play an important role in linking the innate and adaptive defense system of human being. The recent advances in the research of human defensins were reviewed, including their discovery, molecular and genetic properties, expression regulation, and mechanisms of antimicrobial activity. The possibility to produce human defensins via genetic engineering was also discussed. And the application outlook of human defensins in medicine and curing patients infected with antibiotics-resistant microbials was presented.
Amino Acid Sequence ; Defensins ; chemistry ; genetics ; metabolism ; physiology ; Genetic Engineering ; Humans ; Molecular Sequence Data ; Sequence Homology, Amino Acid

BACKGROUNDMotor dysfunction is common in stroke patients. Clinical electrophysiological studies suggest that transsynaptic degeneration occurred in the lower motor neurons, while pathological evidence is lacked. This study aimed to combine the electrophysiological and pathological results to prove the existence of transsynaptic degeneration in the motor system after stroke.

METHODSModified neurologic severity score, electrophysiological, and pathological assessments were evaluated in rats before middle cerebral artery occlusion (MCAO), and at 24 hours, 7 days, and 14 days after MCAO. Paired and independent-sample t-tests were applied to assess the changes of electrophysiological and pathological data.

RESULTSCompound motor action potential amplitude in the paretic side was significantly lower than the nonparetic side at both 24 hours (61.9 ± 10.4 vs. 66.6 ± 8.9, P < 0.05) and 7 days (60.9 ± 8.4 vs. 67.3 ± 9.6, P < 0.05) after MCAO. Motor unit number estimation of the paretic side was significantly less than the nonparetic side (379.0 ± 84.6 vs. 445.0 ± 89.5, P < 0.05) at 7 days after MCAO. Until 14 days after stroke, the pathological loss of motor neurons was detected. Motor neurons in 14-day MCAO group were significantly decreased, compared with control group (5.3 ± 0.7 vs. 7.3 ± 1.8, P < 0.05).

CONCLUSIONSBoth electrophysiological and pathological studies showed transsynaptic degeneration after stroke. This study identified the asynchronization in changes of electrophysiology and pathology. The abnormal physiological changes and function impairment can be detected in the early stage and recovered quickly, while the pathological loss of motor neuron can be detected only in a later stage.

Animals ; Electrophysiology ; Infarction, Middle Cerebral Artery ; pathology ; physiopathology ; Male ; Motor Neurons ; pathology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; pathology ; physiopathology