ABSTRACT
<p><b>OBJECTIVE</b>To observe the therapeutic effect of local antibiotic injection into the female prostate on female urethral syndrome (FUS), and search for an effective treatment for this disease.</p><p><b>METHODS</b>This study included 163 FUS patients treated in the out-patient department between July 2009 and December 2010. According to the visiting order, the patients were randomly assigned to Groups A (n = 58), B (n = 55) and C (n = 50). All underwent routine treatment. Inaddition Group A received local injection of 2 ml of 80 000 U gentamycin + 2 ml of lidocaine, and Group B 2 ml of normal saline + 2 ml of lidocaine, both injected into the distal segment of the urethral back wall where the female prostate is located, twice a week for 3 weeks. The therapeutic effects were evaluated according to the changes of the patients' independent symptom scores at 2 and 4 weeks after the treatment. Disappearance of the symptoms was considered as "curative" , > 1/2 reduction in the symptom score as "obviously effective", 1/2 - > 1/4 reduction in the symptom score as "effective", and < 1/4 reduction or increase in the symptom score as "ineffective".</p><p><b>RESULTS</b>At 2 weeks after the treatment, the total effectiveness rate was significantly higher in Group A (77.5%) than in B (67.3%) and C (68.0%) (P < 0.05), but with no statistically significant difference between B and C (P > 0.05). At 4 weeks, the total effectiveness rate of Group A was slightly decreased, but still remarkably higher than that of group B or C (P < 0.05).</p><p><b>CONCLUSION</b>Local injection of gentamycin into the female prostate is effective for the treatment of female urethral syndrome.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Middle Aged , Young Adult , Administration, Topical , Gentamicins , Therapeutic Uses , Injections , Prospective Studies , Treatment Outcome , Urethral Diseases , Drug TherapyABSTRACT
<p><b>BACKGROUND</b>Vascular endothelial growth factor (VEGF) is well known as a hypoxia-induced protein. That it markedly increased expression of VEGF and improvement of rat motor function after spinal cord injury suggested that VEGF could play a neuroprotective role in ischaemic tolerance. This study investigated whether vascular endothelial growth factor has direct neuroprotective effects on rat spinal cord neurons.</p><p><b>METHODS</b>We employed primary cultures of embryonic rat spinal cord neurons, then administrated different concentrations of VEGF164 in the culture medium before hypoxia when the number of neurons was counted and the cell viability was detected by MTT. The neuronal apoptosis and expression of VEGF and its receptor genes were evaluated by terminal deoxynucleotidyl transferase mediated dUTP nick-end labelling (TUNEL) and immunohistochemistry. The VEGFR2/FLK-1 inhibitor, SU1498, was used to confirm whether the neuroprotective effect of VEGF was mediated through VEGFR2/Flk-1 receptors.</p><p><b>RESULT</b>In hypoxic conditions, the number and viability of neurons decreased progressively, while the number of TUNEL-positive cells increased along with the prolongation of hypoxic exposure. When the concentration of VEGF in cell culture medium reached 25 ng/ml, the cell viability increased 11% and neuronal apoptosis reduced to half, this effect was dose dependent and led to an approximately 25% increase in cell viability and about threefold decrease in TUNEL-positive cells at a maximally effective concentration of 100 ng/ml. In normal conditions, VEGF/Flk-1 but not VEGF/Flt-1 gene expressed at a low level: after hypoxia, the expression of VEGF/Flk-1, but not VEGF/Flt-1 was significantly increased. The protective effect of VEGF was blocked by the VEGFR2/Flk-1 receptor tyrosine kinase inhibitor, SU1498.</p><p><b>CONCLUSIONS</b>VEGF has direct neuroprotective effects on rat spinal cord neurons, which may be mediated in vitro through VEGFR2/Flk-1 receptors.</p>