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L S Chang

Publications and source records attributed to L S Chang.

At least 19 recordsLinked to original sources
PubMed2002

Involvement of L-arginine/nitric oxide pathway at the paraventricular nucleus of hypothalamus in central neural regulation of penile erection in the rat.

The objective of this study is to investigate whether the L-arginine/nitric oxide pathway is involved in the neurotransmission of paraventricular nucleus of hypothalamus (PVN) activation-induced penile erection in the rat. Male adult Sprague-Dawley rats anesthetized with pentobarbital were used. The femoral artery was cannulated to measure systemic and mean arterial pressure (SAP and MAP), and heart rate (HR). A 26-gauge needle was inserted into corpus cavernosum to measure the intracavernous pressure (ICP) simultaneously with SAP, MAP and HR on a polygraph. Four groups of study were arranged: (1) stereotaxically delivery of L-arginine (500 nmol/500 nl) into PVN; (2) administration of a mixture (1 microl) containing N(G)-Nitro-L-arginine methyl ester (L-NAME) 500 nmol and L-arginine 500 nmol into PVN; (3) microinjection of saline 500 nl into PVN as a vehicle control; and (4) intracavernous injection of L-arginine (100 nmol/50 microl). The ICP, SAP, MAP and HR were monitored for at least 2 h after each administration of the experimental agents. Upon administration of L-arginine into PVN, there was a significant increase of ICP from resting 9.6+/-2.5 mmHg to peaked at 64.4+/-9.8 mmHg after a latency of 3016.0+/-1749.7 s and with a duration of 27.6+/-15.8 min. There was no change of resting ICP after administration of the mixture of L-NAME and L-arginine into PVN. Application of saline to PVN and intracavernous injection of L-arginine failed to increase ICP. Based on elicitation of penile erection upon administration of L-arginine into PVN, and elimination of this L-arginine induced penile erection by co-administration of L-NAME with L-arginine, the results of this study suggest that L-arginine/nitric oxide pathway may be involved in the neurotransmission of PVN activation-induced penile erection in the rat.

Animals↗
PubMed2002

The correlation between pretreatment serum hormone levels and treatment outcome for patients with prostatic cancer and bony metastasis.

OBJECTIVE: To evaluate whether pretreatment serum hormone levels are a prognostic factor for prostatic cancer with bony metastasis under hormonal treatment. PATIENTS AND METHODS: Between 1980 and 1994, 96 patients with prostate cancer and bony metastasis were included for an evaluation by a retrospective review of their charts. All 96 had received hormonal treatment after a diagnosis of metastatic prostatic carcinoma. Serum testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin were assessed before treatment. The patients were divided into two groups according to their response during the follow-up. Group 1 (good response) had no change or resolution of metastatic lesion(s) on the bone scan and a declining prostate-specific antigen (PSA) level. Group 2 had increased PSA or progression of metastatic lesion(s) on the bone scan. Tumours were graded as low (2-4), intermediate (5-7) and high (8-10) using the Gleason score. RESULTS: There were 43 patients in group 1 and 53 in group 2; the overall mean (sd) age was 72.5 (6.8) years and the follow-up 29.5 (0.5) months. The respective mean (sd) levels of testosterone, LH, FSH and prolactin before treatment were 4.6 (1.6) ng/mL, 20.2 (13.3) mIU/mL, 19.6 (18.6) mIU/mL and 20.7 (12.1) ng/mL in group 1, and 2.6 (1.0) ng/mL, 27.3 (11.0) mIU/mL, 27.1 (9.8) mIU/mL and 41.3 (28.4) ng/mL in group 2. The level of testosterone was significantly higher in group 1 than in group 2, while LH, FSH and prolactin were significantly lower in group 1 than in group 2. When stratified by tumour grade, patients in group 1 still had significantly higher pretreatment testosterone and lower LH, FSH and prolactin than those in group 2. CONCLUSION: Higher testosterone and lower LH, FSH and prolactin levels were good prognostic factors for patients with metastatic prostatic cancer under hormonal treatment, irrespective of tumour grading.

Aged↗
PubMed2001

Oxidative damage to proteins and decrease of antioxidant capacity in patients with varicocele.

To examine oxidative damage to blood proteins in the spermatic vein and seminal plasma antioxidant capacity of patients with varicocele, 30 young male patients with varicocele (group 1), 25 young male patients with subclinical varicocele (group 2), and 15 normal young males without varicocele (group 3) were recruited in this study. Varicocele and subclinical varicocele were confirmed by physical examination and Doppler ultrasonography. Blood samples were drawn from peripheral and spermatic veins before varicocelectomy. Plasma protein carbonyls were measured by a spectrophotometric assay after reacting with 2,4-dinitrophenylhydrazine. Protein thiols and ascorbic acid of seminal plasma were measured by spectrophotometric methods. We found that plasma protein carbonyls in the spermatic veins were significantly higher than those of corresponding peripheral veins in all 30 patients in group 1 and 12 patients in group 2 receiving varicocelectomy. Protein carbonyls in the spermatic veins of patients with varicocele (3.72 +/- 0.56 nmole/mg protein) and patients with subclinical varicocele (3.50 +/- 0.30 nmole/mg protein) were found to be higher than those of the control (2.35 +/- 0.33 nmole/mg protein). Protein thiols were 0.97 +/- 0.96, 1.50 +/- 0.89, and 3.49 +/- 0.81 nmole/ml, and ascorbic acid levels were 1.87 +/- 0.42, 2.13 +/- 0.24, and 2.38 +/- 0.07 mg/dl, in seminal plasma of the patients in groups 1, 2, and 3, respectively. Seminal plasma protein thiols and ascorbic acid levels in group 1 were significantly lower than those in groups 2 and 3, respectively. These results indicate that oxidative stress in the patients with varicocele and subclinical varicocele was higher than that of the control. We suggest that plasma protein carbonyls, and protein thiols and ascorbic acid of seminal plasma are useful markers for the assessment of oxidative stress in patients with varicocele and subclinical varicocele.

Adult↗
PubMed2001

Refolding of Taiwan cobra neurotoxin: intramolecular cross-link affects its refolding reaction.

In order to explore the effect of intramolecular cross-linking in the folding reaction of cobrotoxin from Naja naja atra (Taiwan cobra) venom, the toxin molecule was modified with glutaraldehyde (GA). The monomeric GA-modified cobrotoxin (mGA-cobrotoxin) was separated from the dimeric and trimeric derivatives using gel filtration. The results of electrophoretic and chromatographic analyses revealed that mGA-cobrotoxin comprised two modified derivatives, which contained modified Lys residues at positions 26 and 27 and at positions 26, 27, and 47, respectively. Moreover, an intramolecular cross-linking of loops II and III by Lys residues was noted with the monomeric derivative containing three modified Lys residues. In sharp contrast to cobrotoxin observations, the folding rate of mGA-cobrotoxin decreased in the presence of GSH/ GSSG, but notably increased in the absence of thiol compounds. Particularly, the accelerated effect of GSH/GSSG on the refolding reaction was affected by the presence of the intramolecular cross-link. Comparative analyses on cobrotoxin and mGA-cobrotoxin CD spectra revealed that modification with the GA reagent caused a change in the gross conformation of cobrotoxin. Fluorescence measurement revealed that the stability of the microenvironment around the single Trp-29 in mGA-cobrotoxin and unfolded mGA-cobrotoxin was appreciably higher than in cobrotoxin and unfolded toxin. Moreover, the ordered structure formation around Trp-29 in refolded mGA-cobrotoxin was faster than in refolded cobrotoxin as evidenced by fluorescence quenching studies. Taken together, these results suggest that the structural flexibility of unfolded cobrotoxin should be favorable for the thiol catalyst to exert its action in the refolding reaction after modification with GA.

Amino Acids↗
PubMed2001

Effects of hyperprolactinemia on testosterone production in rat Leydig cells.

The pathogenesis of hyperprolactinemia (hyperPRL) induced hypogonadism has been suggested to be related with a dysfunction of hypothalamus-pituitary-testis axis. While the direct inhibitory effects of prolactin (PRL) on testosterone (T) release have been demonstrated, the mechanism is still unclear. Our previous study demonstrated a diminished T release in the testicular interstitial cells (TICs) from the anterior pituitary (AP)-grafted rats as compared with the control, and the pattern was in agreement with the in vivo model. However, TICs incubation cannot totally represent the response of the Leydig cells. Therefore, a Percoll gradient purified Leydig cell model was adopted to explore the response of T release under similar challenges in this study to investigate the effects of hyperPRL on the Leydig cells per se. HyperPRL in male rats was induced by grafting rat AP under the renal capsule. The control animals were grafted with rat brain cortex tissue (CX). Six weeks after grafting, the rats were sacrificed. Either TICs or Leydig cells were isolated, respectively, for in vitro incubation and challenge. Challenge drugs included human chorionic gonadotropin (hCG, 0.05 IU/ml), steroidogenic precursors (25-OH-cholesterol, 10(-6) M; pregnenolone, 10(-6) M), forskolin (an anenylyl cyclase activator, 10(-4) M) and 8-bromo-3':5' cyclic adenosine monophosphate (cAMP) (8-Br-cAMP 10(-4) M). T released by TICs or Leydig cells was determined by radioimmunoassay. The TICs from the AP-grafted rats showed lower levels of T release than the control group while the purified Leydig cells demonstrated a reverse pattern in response to challenges of hCG, steroidogenic precursors, forskolin and 8-Br-cAMP. In hyperPRL rats, a paradoxical pattern of T release between TICs and purified Leydig cells is observed. The purified Leydig cells from AP-grafted rats demonstrated a higher level amount of T release than the control after stimulation. The phenomenon can be attributed to the change of Leydig cell sensitivity to the stimulation after the effects of chronic hyperPRL. Moreover, another possibility is the role played by other interstitial cells to modulate steroidogenesis in Leydig cells.

Animals↗
PubMed2001

Oxytocinergic neurotransmission at the hippocampus in the central neural regulation of penile erection in the rat.

OBJECTIVES: To investigate whether there is an oxytocinergic neurotransmission at the hippocampus involved in the central regulation of penile erection in the rat. METHODS: Male adult Sprague-Dawley (n = 27) rats anesthetized with pentobarbital were used. A 26-gauge needle was inserted into the corpus cavernosum to measure the intracavernous pressure (ICP) and the systemic and mean arterial pressure and heart rate simultaneously. The following studies were performed: stereotaxic delivery of oxytocin acetate (3 pmol/100 nL) into the hippocampus; microinjection of a mixture of [d(CH(2))(5)-Tyr(Me)(2)-Orn(8)]-vasotocin (3 pmol/100 nL) and oxytocin (3 pmol/100 nL) into the hippocampus; injection of saline into the hippocampus; and intracavernous injection of oxytocin (3 pmol/100 microL). The ICP and hemodynamic parameters were monitored after each administration of the experimental agents. RESULTS: After administration of oxytocin into the hippocampus, a significant increase in the ICP occurred from resting (8.8 +/- 1.7 mm Hg) to a peak at 49.6 +/- 12.5 mm Hg and persisted for 18.6 +/- 9.4 minutes after an onset latency of 500.0 +/- 389.7 seconds. However, no change in the ICP occurred after administration of [d(CH(2))(5)-Tyr(Me)(2)-Orn(8)]-vasotocin plus oxytocin into the hippocampus. In addition, no elevation of ICP occurred after administration of saline to the hippocampus or after intracavernous injection of oxytocin. CONCLUSIONS: The results demonstrate that administration of oxytocin into the hippocampus induces penile erection in the rat. However, concomitant administration of oxytocin and its antagonist was ineffective in eliciting penile erection. These observations suggest that oxytocinergic neurotransmission at the hippocampus may be involved in the central neural regulation of the penile erection in the rat.

Animals↗
PubMed2001

High failure rate using allograft fascia lata in pubovaginal sling surgery for female stress urinary incontinence.

OBJECTIVES: To present our unfavorable experiences using allograft fascia lata. Allograft fascia lata is an attractive sling material providing less pain, a shorter operation time, and a reported effectiveness equal to autologous fascia. METHODS: A total of 18 women (mean age 51.7 years, range 37 to 76) underwent pubovaginal sling surgery for stress urinary incontinence between March 1999 and July 1999 and were enrolled in this study. Solvent dehydrated gamma-irradiated human fascia lata with a size of 7 x 2 cm was used as the sling. The results were collected with a questionnaire survey. RESULTS: All patients were followed up for a mean of 9.2 months (range 6.9 to 11.6). Thirteen patients considered the surgery successful or to have provided improvement, with a mean of 82.5% (range 50% to 100%) subjective improvement. Five patients (27.8%) had significant failure with full recurrence of incontinence within 3 to 6 months. CONCLUSIONS: Solvent dehydrated gamma-irradiated allograft fascia is not reliable in pubovaginal sling surgery. The high failure rates within a short period prohibit its use in the operative management of stress urinary incontinence.

Adult↗
PubMed2001

Probing the structural diversities of long alpha-neurotoxins by fluorescence quenching studies.

Trp fluorescence of Ophiophagus hannah neurotoxins (Oh-4, Oh-6A, Oh-7, and Oh-8) and Bungarus multicinctus (alpha-bungarotoxin was quenched by acrylamide and iodide. Acrylamide quenching studies indicated that the degree of exposure of Trp residues in the neurotoxins followed the order Oh-8 > Oh-7 > Oh-6A > Oh-4 > alpha-bungarotoxin, as did the accessibility for iodide. These results reveal that the exposed degree of Trp residues and the microenvironment surrounding Trp residues in the neurotoxins differ, even though their Trp residues and positively charged residues are located at the same or homologous positions. In contrast to unfolded Oh-4, Oh-6A, Oh-7, and alpha-bungarotoxin, unfolding of Oh-8 by reduction and S-carboxymethylation caused a notable decrease in the susceptibility of their Trp residues for iodide. These observations support the view that the side chains of Trp residues and positively charged residues in their native structure do not point toward the same spatial positions. Computer models of the neurotoxins are in good agreement with this proposition. These results elucidate why the conserved Trp residues and cationic groups do not always play the same roles in the biological activities of the neurotoxins.

Acrylamide↗
PubMed2001

Expression of A chain and B chain of beta-bungarotoxin from taiwan banded krait: the functional implication of the interchain disulfide bond between A chain and B chain.

beta-Bungarotoxin (beta-Bgt), the main presynaptic neurotoxin purified from the venom of Bungarus multicinctus, consists of two dissimilar polypeptide chains, the A chain and B chain, cross-linked by an interchain disulfide bond. The A and B chain cDNAs were subcloned into expression vectors pT7-7 and pET20b(+), respectively, and transformed into Escherichia coli strain BL21(DE3). The expressed protein was isolated from the inclusion bodies of E. coli and subjected to refolding into its folded structure. The yields of the refolded A and B chains increased markedly by at least 100-fold after substituting Ser for Cys1S of A chain and Cys55 of B chain, which formed an interchain disulfide bond. Either the A(C15) chain or B(C55S) chain alone or in combination cannot exhibit the phospholipase A2 activity or synaptosome binding activity of beta-Bgt. Nevertheless, the results of competitive enzyme-linked immunoassay, CD spectra, and fluorescence measurement revealed that the A(C15S) chain and B(C55S) chain possessed a native-like structure like the subunits of native beta-Bgt. Moreover, the interfacial interaction between the A and B chains explored by glutaraldehyde cross-linking revealed the essential aspects of the intact interchain disulfide bond in this interaction. This suggests that the formation of the interchain disulfide bond should not be a crucial step for the formation of folded A and B chains in the venom glands, and that the integrity of the interchain disulfide linkage favors the subunit interaction that consequently fulfills the functional mechanism of beta-Bgt.

Amino Acid Sequence↗
PubMed2001

Glutaraldehyde cross-linking alters the environment around Trp(29) of cobrotoxin and the pathway for regaining its fine structure during refolding.

Cobrotoxin, purified from the venom of Naja naja atra (Taiwan cobra), was subjected to modification with glutaraldehyde in order to prepare intra- and intermolecule cross-linked derivatives. Monomeric and dimeric derivatives were separated from polymeric derivatives by gel filtration. The results of amino acid analysis and sequence determination revealed that only Lys residues were selectively modified by glutaraldehyde. Glutaraldehyde cross-linking was accompanied by a change in the gross conformation of cobrotoxin as revealed by circular dichroism spectra of the modified derivatives. Compared with cobrotoxin, Trp(29) of monomeric and dimeric derivatives was in an apolar microenvironment. This was in agreement with acrylamide quenching studies showing that the spatial position of the Trp indole ring became buried in the interior of the molecule after glutaraldehyde cross-linking. Moreover, the Trp of modified derivatives was less accessible for iodide than that observed with cobrotoxin. Notably, disulfide reduction could not completely unfold the structure of glutaraldehyde-modified derivatives as evidenced by the results of acrylamide quenching studies and enzyme-linked immunoassay. Study of the characteristic changes in Trp fluorescence after the initiation of refolding suggested that the fine structure around Trp(29) of cobrotoxin and glutaraldehyde-modified derivatives was formed differently. These results suggest that glutaraldehyde cross-linking leads to a change in the microenvironment of cobrotoxin Trp(29) and alters the pathway of its fine structure formation during the refolding of cobrotoxin.

Animals↗
PubMed2000

Mannitol facilitates rabbit urinary bladder recovery from overdistension injury.

OBJECTIVES: To investigate the existence and functional significance of the enhanced lipid peroxidation in bladder overdistension injury and to explore the effect of mannitol, a free radical scavenger. METHODS: Overdistension of rabbit bladders was induced and maintained for 3 hours by infusing normal saline into the bladder while keeping the intravesical pressure at 30 cm H(2)O. The bladders were then emptied and decompressed. Intravenous 20% mannitol was initiated 5 minutes before decompressing the overdistension. Detrusor tissue was obtained from the following groups: control, at the end of the overdistension period, and 30 minutes, 2 hours, and 7 days after decompressing the bladder. The tissue level of adenosine triphosphate (ATP) and phosphocreatine (PCr) and the lipid peroxidation product malondialdehyde (MDA) was assayed. Detrusor contractility was assessed by the response of the detrusor strips to KCl and bethanechol. RESULTS: Decompressing the overdistended bladder led to a period of enhanced lipid peroxidation with an increase of MDA content from 225 to 384 pmol/mg protein 30 minutes after the decompression. Two hours later, the MDA content had recovered to the normal level. Mannitol abolished this period of enhanced lipid peroxidation. Overdistension impaired detrusor contractility and reduced the content of PCr (from 24.1 to 10.8 nmol/mg protein) and ATP (from 9.6 to 4.6 nmol/mg protein). Both detrusor contractility and the content of PCr and ATP further decreased 30 minutes after the decompression (PCr 5.4 nmol/mg, ATP 2.8 nmol/mg). They had recovered, but not fully, 7 days later. Mannitol prevented the further decrease in detrusor contractility and in the content of PCr and ATP during the initial decompression period (30 minutes after the decompression). In addition, the mannitol-treated group had quicker recovery in PCr and ATP levels, which returned to normal 7 days later. CONCLUSIONS: Decompressing an overdistended bladder leads to enhanced lipid peroxidation, which is associated with an additionally decreased energetic metabolism and a more impaired contractile function. Mannitol effectively prevents enhanced lipid peroxidation and facilitates functional recovery. These results show that reactive oxygen species play a significant role in bladder overdistension injury.

Adenosine Triphosphate↗
PubMed2000

Disruption of the actin cytoskeleton leads to inhibition of mitogen-induced cyclin E expression, Cdk2 phosphorylation, and nuclear accumulation of the retinoblastoma protein-related p107 protein.

The actin cytoskeleton has been found to be required for mitogen-stimulated cells to passage through the cell cycle checkpoint. Here we show that selective disruption of the actin cytoskeleton by dihydrocytochalasin B (H(2)CB) blocked the mitogenic effect in normal Swiss 3T3 cells, leading to cell cycle arrest at mid to late G(1) phase. Cells treated with H(2)CB remain tightly attached to the substratum and respond to mitogen-induced MAP kinase activation. Upon cytoskeleton disruption, however, growth factors fail to induce hyperphosphorylation of the retinoblastoma protein (pRb) and the pRb-related p107. While cyclin D1 induction and cdk4-associated kinase activity are not affected, induction of cyclin E expression and activation of cyclin E-cdk2 complexes are greatly inhibited in growth-stimulated cells treated with H(2)CB. The inhibition of cyclin E expression appears to be mediated at least in part at the RNA level and the inhibition of cdk2 kinase activity is also attributed to the decrease in cdk2 phosphorylation and proper subcellular localization. The expression patterns of cdk inhibitors p21 and p27 are similar in both untreated and H(2)CB-treated cells upon serum stimulation. In addition, the changes in subcellular localization of pRb and p107 appear to be linked to their phosphorylation states and disruption of normal actin structure affects nuclear migration of p107 during G(1)-to-S progression. Taken together, our results suggest that the actin cytoskeleton-dependent G(1) arrest is linked to the cyclin-cdk pathway. We hypothesize that normal actin structure may be important for proper localization of certain G(1) regulators, consequently modulating specific cyclin and kinase expression.

3T3 Cells↗
PubMed2000

p53 dependence of topoisomerase I recruitment in vivo.

DNA damage is attended by rapid recruitment of endogenous type I topoisomerase (topo I) into covalent cleavage complexes with genomic DNA in vivo. In contrast, endogenous topoisomerase II alpha and beta are not stimulated by DNA damage. We show that topo I and p53 are able to associate at arrested topo I-genomic DNA covalent complexes in vivo, suggesting that p53 directly stimulates topo I activity and damage to the genome of the afflicted cell. Moreover, cells that express wild-type p53 are most proficient at recruiting topo I after DNA damage; however, the p53 dependence is conditional because topo I recruitment after DNA damage can be restored if p53 mutant cells (containing a single mutant allele) are artificially held in G1. In contrast, p53 null mutants do not recruit topo I after DNA damage under any conditions (although camptothecin-dependent topo I/DNA complexes readily form in the nulls). These results show that topo I activation after DNA damage depends on the p53 status of the cell. It also depends upon the cell cycle in a way that is very different from that observed with DNA replication-dependent, camptothecin-mediated DNA breaks. The data suggest a model where p53 activates topo I, which inflicts additional genomic damage after the initial UV damage events. Topoisomerases therefore contribute to the p53 commitment to apoptosis, and topo I might assist in elimination of DNA-damaged cells as part of the cellular proofreading function inherent in the p53 pathway.

Antigens, Neoplasm↗
PubMed2000

The multiplicity of cardiotoxins from Naja naja atra (Taiwan cobra) venom.

Four novel cardiotoxins were isolated from Naja naja atra (Taiwan cobra) venom by successive separation on a SP-Sephadex C-25 column and a reverse phase column. Amino acid sequences of the cardiotoxins were determined by Edman degradation and carboxypeptidase digestion. It shows that these cardiotoxins comprise 60 amino acid residues. Comparative analyses on the amino acid sequences of cardiotoxins from the venoms of N. naja atra and other Naja species indicated that amino acid substitutions of cardiotoxin isoforms frequently occurred at positions 7-11, 27-32 and 45-47. The hypervariable segments encoded by the second and third exon of cardiotoxin genes are located at or near the tips of loop structure of cardiotoxin molecules. These results, together with the suggestions that the residues at the tips of cardiotoxins' loop structure were involved in the manifestation of the biological activities of cardiotoxins, reflect that the preferential mutations may contribute to alterations in the function of cardiotoxin molecules. Analysis on the secondary structure of pre-mRNAs of N. naja atra cardiotoxin 4 gene and N. naja sputatrix cardiotoxin 3 gene has shown that the hypervariable regions of the exon 2 pertain to form intra-exon pairings and are not involved in the formation of intron-exon pairings. Since the pairings of splice sites and gene architecture were supposed to be associated with intron-exon recognition, it is likely that the preferred loci of mutations occurring with the evolution of cardiotoxin genes would not affect the processing of cardiotoxin precursors.

Amino Acid Sequence↗
PubMed2000

Mitochondrial DNA deletion of the human detrusor after partial bladder outlet obstruction-correlation with urodynamic analysis.

OBJECTIVES: To investigate mitochondrial DNA (mtDNA) mutations in human detrusor after partial bladder outlet obstruction (BOO) and correlate the findings with the results of urodynamic studies. METHODS: Sixty-two male patients with and without BOO were recruited and assessed by the International Prostate Symptom Score, a quality-of-life assessment index, and sonography. The severity of partial BOO was determined by pressure-flow study with an International Continence Society (ICS) nomogram. Random detrusor biopsies obtained cystoscopically were analyzed by polymerase chain reaction (PCR) techniques to detect possible mtDNA deletions. Primer-shift PCR and DNA sequencing were then performed to characterize specific mtDNA deletions. A semiquantitative PCR method was used to determine the proportion of the deleted mtDNA in detrusor. Finally, the mtDNA deletion and the urodynamic results were compared statistically. RESULTS: A 4977-bp mtDNA deletion was identified in the human detrusor. Its incidence and proportion were found to increase after partial BOO (P = 0.005 and 0.012, respectively). The incidence of the mtDNA deletion was 4.2% (1 of 24) in the unobstructed group, 27.8% (5 of 18) in the equivocal group, and 40% (8 of 20) in the obstructed group. The mean proportion of the 4977-bp deleted mtDNA was 23.7 and 12.7 times higher in the obstructed and equivocal groups, respectively, compared with that of the unobstructed group. CONCLUSIONS: We found mtDNA with the 4977-bp deletion in human detrusor and an increase of this deletion after partial BOO. This molecular change might account for the previous observations of mitochondrial functional impairment and voiding dysfunction after partial BOO.

Aged↗