Xiangfu Zhou

Increased severity of inflammation correlates with elevated expression of TRPV1 nerve fibers and nerve growth factor on interstitial cystitis/bladder pain syndrome.

Objectives: Although evidence supports a role for inflammation in interstitial cystitis/bladder pain syndrome (IC/BPS), the mechanism remains unknown. We determined whether inflammation causes an elevated expression of nerve growth factor (NGF) and transient receptor potential vanilloid receptor subtype 1 (TRPV1) and correlated them with the symptoms. Methods: Bladder biopsies were obtained from 53 IC/BPS patients and 27 controls, and hematoxylin and eosin staining, immunostaining and Western blotting were performed to detect inflammation, TRPV1-immunoreactive and PGP9.5-immunoreactive nerve fibers, and NGF, respectively. Symptoms were assessed using the Pelvic Pain/Urgency/Frequency (PUF) questionnaire and pain visual analogue scale scores. Suburothelial nerve fiber density was quantified and correlated with PUF scores. Results: Increased severity of inflammation was correlated with a higher TRPV1-immunoreactive nerve fiber density (r = 0.4113, p = 0.0024) and higher NGF levels (r = 0.3775, p = 0.0052). Suburothelial TRPV1-immunoreactive nerve fiber density was significantly correlated with pain scores and urgency scores (r = 0.3320, p = 0.0145 and r = 0.3823, p = 0.0039, respectively). PGP9.5-immunoreactive nerve fibers were significantly increased in IC/BPS (p = 0.0193) and had a positive relationship with inflammation severity (r = 0.6138, p < 0.0001). Conclusions: Our study revealed increased severity of inflammation correlated with a higher expression of TRPV1-immunoreactive nerve fibers and NGF in IC/BPS and correlated with clinical symptoms.

Gp120 in the pathogenesis of human immunodeficiency virus-associated pain

Chronic pain is a common neurological comorbidity of human immunodeficiency virus (HIV)‐1 infection, but the etiological cause remains elusive. The objective of this study was to identify the HIV‐1 causal factor that critically contributes to the pathogenesis of HIV‐associated pain.

Adding a sexual dysfunction domain to UPOINT system improves association with symptoms in women with interstitial cystitis and bladder pain syndrome.

OBJECTIVE To examine whether adding a sexual dysfunction domain to urinary, psychosocial, organ specific, infection, neurologic or systemic, and tenderness (UPOINT) system improves the association with interstitial cystitis and bladder pain syndrome (IC-BPS) symptom severity due to a high prevalence of sexual dysfunction in women. METHODS A total of 90 Chinese women with IC-BPS were prospectively collected and classified in each domain of the UPOINT system. Symptom severity was measured using the Interstitial Cystitis Symptom Index (ICSI). The sexual function was evaluated using the Female Sexual Function Index (FSFI). Clinically relevant associations were calculated. RESULTS The percentage of patients positive for each domain were 90 of 90 (100%), 33 of 90 (37%), 88 of 90 (98%), 21 of 90 (23%), 36 of 90 (40%), 38 of 90 (42%), 62 of 90 (69%) for the urinary, psychosocial, organ specific, infection, neurologic or systemic, tenderness, and sexual dysfunction, respectively. There were significant associations between the number of domains and ICSI (Spearman r = 0.386; P <.05) and FSFI (Spearman r = 0.614; P <.001) scores. After adding a sexual dysfunction domain to create a modified UPOINTS system, the association between the number of domains and symptom severity was improved (correlation coefficient r changed from 0.386 to 0.572; P <.001). The presence of sexual dysfunction had a significant impact on the ICSI scores (P = .032), pain scores (P = .042), and quality of life index scores (P = .035). Significantly reduced FSFI scores were found in patients who had positive psychosocial, organ specific, and tenderness domains (all P values <.05). CONCLUSION Our study demonstrated sexual dysfunction was an important component of IC-BPS phenotype, and adding a sexual dysfunction domain to the UPOINT system improved the association with IC-BPS symptom severity.

Supine lithotomy versus prone position in minimally invasive percutaneous nephrolithotomy for upper urinary tract calculi.

Objective: To compare operative time, safety and effectiveness of minimally invasive percutaneous nephrolithotomy (MPCNL) in the supine lithotomy versus prone position. Methods: Between January 2008 and December 2010, a total of 109 consecutive patients with upper urinary tract calculi were enrolled and randomly divided into group A (53 patients, supine lithotomy position) and group B (56 patients, prone position). The MPCNL procedures were performed under the guidance of real-time grayscale ultrasound system. The preoperative characteristics, intraoperative and postoperative parameters were analyzed and compared. Results: All patients were successfully operated. There was no significant difference between the two groups in stone-free rate (group A 90.1 vs. group B 87.5%, p = 0.45), mean blood loss, number of access tracts, calyx puncture, mean hospital stay (group A 6 ± 1.1 vs. group B 6 ± 1.5 days, p = 0.38) and complications. But the operative time was significantly shortened in supine lithotomy position (group A 56 ± 15 vs. group B 86 ± 23 min, p < 0.001). Conclusions: The effectiveness and safety of the supine lithotomy position for MPCNL were similar to the prone position. However, the supine lithotomy position has an important advantage of reducing the operative time. The supine lithotomy position could be a good choice to perform MPCNL.

Analysis of the absence of the detrusor muscle in initial transurethral resected specimens and the presence of residual tumor tissue.

Objective: To investigate the relationship between surgeon’s experience, tumor characteristics, absent detrusor muscle (DM) tissue in resected specimens, and residual tumor after an initial transurethral resection. Patients and Methods: We conducted an analysis of 216 patients from two centers over a 3-year period. Patients with primary bladder tumors that were judged to have been completely resected were recruited. The data included tumor characteristics, surgeon category, and DM status. Logistic regression multivariate analyses were conducted. Results: Large tumors, lateral/dome/anterior wall tumors, and surgery performed by junior surgeons were independently associated with absent DM. Large tumors, dome/anterior wall tumors, T1 and absent DM were independently associated with residual disease. The absence and presence of the DM were associated with residual tumor rates of 51.8 and 20.9%, respectively (OR 15.537). Resection by senior surgeons was associated with the presence of DM and clean resection (OR 0.274 and 0.141, respectively). Conclusions: Absent DM and residual tumor were more likely to occur in cases involving large tumors that were located in the lateral/dome/anterior wall, especially when the surgery was performed by a junior surgeon. Absent DM appears to be a surrogate marker for residual disease.

Spinal astrocytic activation contributes to mechanical allodynia in a rat model of cyclophosphamide-induced cystitis

Background Previous studies have demonstrated that glial cells play an important role in the generation and maintenance of neuropathic pain. Activated glial cells produce numerous mediators such as proinflammatory cytokines that facilitate neuronal activity and synaptic plasticity. Similarly, bladder pain syndrome/interstitial cystitis shares many characteristics of neuropathic pain. However, related report on the involvement of spinal glia in bladder pain syndrome/interstitial cystitis-associated pathological pain and the underlying mechanisms are still lacking. The present study investigated spinal glial activation and underlying molecular mechanisms in a rat model of bladder pain syndrome/interstitial cystitis. Results A rat model of bladder pain syndrome/interstitial cystitis was established via systemic injection with cyclophosphamide. Mechanical allodynia was tested with von Frey monofilaments and up-down method. Moreover, Western blots and double immunofluorescence were used to detect the expression and location of glial fibrillary acidic protein, OX42/Iba1, P-P38, NeuN, interleukin (IL)-1β, phosphorylation of N-methyl-D-aspartate receptor 1 (P-NR1), and IL-1 receptor I (IL-1RI) in the L6-S1 spinal cord. We found that glial fibrillary acidic protein rather than OX42/Iba1 or P-P38 was significantly increased in the spinal cord of cyclophosphamide-induced cystitis. L-alpha-aminoadipate but not minocycline markedly attenuated the allodynia. Furthermore, we found that spinal IL-1β was dramatically increased in cyclophosphamide-induced cystitis, and activated astrocytes were the only source of IL-1β release, which contributed to allodynia in cystitis rats. Besides, spinal P-NR1 was statistically increased in cyclophosphamide-induced cystitis and only localized in IL-1RI positive neurons in spinal dorsal horn. Additionally, NR antagonist significantly attenuated the cystitis-induced pain. Interestingly, the time course of the P-NR1 expression paralleled to that of IL-1β or glial fibrillary acidic protein. Conclusions Our results demonstrated that astrocytic activation but not microglial activation contributed to the allodynia in cyclophosphamide-induced cystitis and IL-1β released from astrocytes might bind to its endogenous receptor on the neurons inducing the phosphorylation of NR1 subunit, leading to sensory neuronal hyperexcitability and pathological pain.

Gp120 in the pathogenesis of human HIV-associated pain

Chronic pain is a common neurological comorbidity of human immunodeficiency virus (HIV)‐1 infection, but the etiological cause remains elusive. The objective of this study was to identify the HIV‐1 causal factor that critically contributes to the pathogenesis of HIV‐associated pain.

Gp120 in the pathogenesis of human immunodeficiency virus-associated pain: Gp120 in HIV-Associated Pain

Chronic pain is a common neurological comorbidity of human immunodeficiency virus (HIV)‐1 infection, but the etiological cause remains elusive. The objective of this study was to identify the HIV‐1 causal factor that critically contributes to the pathogenesis of HIV‐associated pain.