Investing on quality, quantity, neurophils and mucin test for 30 joint fluid samples collected from 30 patients with various arthral conditions, comparing to control subjects in Arthral-Skeletal Department of Bach Mai Hospital from Mar. 2002 to Jun. 2002. Results: There were changes in macroscopy: the volume of joint fluid was more than 5ml, light or dark yellow, lack of transparency, completely reduced viscosity. Test mucin was positive range from (++) to (+++), counts of white blood cell and neurophil increased. It was suggested that mucin and joint fluid cell studies can add for diagnosis of some arthral conditions.
Arthritis ; Immunophilins ; diagnosis

To investigate the effect of a novel p21-modulating protein WISp39 on proliferation, apoptosis and cell cycle of leukemia cells, the plasmid pLenti6/V5-WISp39 was constructed and transfected into the human myelocytic leukemia cell line-U937 cells. The expression of WISp39 was detected by real-time PCR at 48 hours after transfection, proliferation of U937 cells assayed by CCK-8, apoptosis and cell cycle were determined by flow cytometry. The results showed that plasmid pLenti6/V5-WISp39 could readily enhance the expression of WISp39 in U937 cells. A significant growth inhibition (37.6%) was observed in cells tranfected with pLenti6/V5-WISp39, while the control plasmid pLenti6/V5-lacZ showed little effect on U937 growth. Further analysis revealed that pLenti6/V5-WISp39 did not show obvious apoptosis induction effect, but it could really regulate U937 proliferation via cell cycle modulation. Compared with pLenti6/V5-lacZ, pLenti6/V5-WISp39 resulted in increase of cells in G(0)/G(1) phase by 10% at 48 hours after transfection. It is concluded that the WISp39 gene has no significant apoptosis induction effect on leukemic cells, but it can increase cells at G(0)/G(1) phase via effect on cell cycle, thus inhibiting the U937 proliferation. This result means WISp39 gene can act as a negative modulator on tumour cells.
Apoptosis ; genetics ; Cell Cycle ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p21 ; metabolism ; Humans ; Immunophilins ; metabolism ; RNA, Messenger ; metabolism ; Sincalide ; pharmacology ; Transfection ; U937 Cells

Advances in the neurobiology of growth factors, neural development, and prevention of cell death have resulted in a heightened clinical interest for the development of protective and regenerative neuromodulatory strategies for the cavernous nerves (CNs), as therapies for prostate cancer and other pelvic malignancies often result in neuronal damage and debilitating loss of sexual function. Nitric oxide released from the axonal end plates of these nerves within the corpora cavernosa causes relaxation of smooth muscle, initiating the haemodynamic changes of penile erection as well as contributing to maintained tumescence; the loss of CN function is primarily responsible for the development of erectile dysfunction (ED) after pelvic surgery and serves as the primary target for potential neuroprotective or regenerative strategies. Evidence from pre-clinical studies for select neuromodulatory approaches is reviewed, including neurotrophins, glial cell line-derived neurotrophic factors (GDNF), bone morphogenic proteins, immunophilin ligands, erythropoetin (EPO), and stem cells.
Animals ; Bone Morphogenetic Proteins ; therapeutic use ; Brain-Derived Neurotrophic Factor ; therapeutic use ; Erectile Dysfunction ; drug therapy ; etiology ; therapy ; Erythropoietin ; therapeutic use ; Glial Cell Line-Derived Neurotrophic Factor ; therapeutic use ; Growth Differentiation Factor 5 ; Humans ; Immunophilins ; Male ; Nerve Growth Factors ; therapeutic use ; Neurotransmitter Agents ; therapeutic use ; Penis ; innervation ; Peripheral Nerve Injuries ; Postoperative Complications ; Stem Cell Transplantation