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Biomedical subjects

S Qian

Publications and source records attributed to S Qian.

At least 19 recordsLinked to original sources
PubMed2007

Hepatitis B virus (HBV) antigen-pulsed monocyte-derived dendritic cells from HBV-associated hepatocellular carcinoma patients significantly enhance specific T cell responses in vitro.

To investigate whether hepatitis B virus (HBV) antigen-pulsed monocyte-derived dendritic cells (MoDC) could mount a T cell response in hepatocellular carcinoma (HCC) patients associated with chronic HBV infection, peripheral blood mononuclear cells (PBMCs) from 36 HBV-associated HCC patients were induced into MoDC and pulsed with hepatitis B core antigen (HBcAg) and hepatitis B surface antigen (HBsAg), alone and in combination. Co-stimulatory molecules CD80, CD86 and CD40, as well as human leucocyte antigens D-related (HLA-DR) were found to express at the highest level on MoDC pulsed with HBcAg or HBsAg + HBcAg, at a median level on MoDC pulsed with HBcAg or HBsAg alone, and at the lowest level on non-antigen-pulsed MoDC. Interleukin (IL)-10 and IL-12 cytokines were released by antigen-pulsed MoDC at increased levels in the order: no-antigen < HBsAg < HBcAg < HBcAg + HBsAg. MoDC pulsed with HBcAg or HBsAg + HBcAg also had the strongest ability to stimulate autologous T cell proliferation and intracellular interferon (IFN)-gamma production. HBcAg- or HBsAg + HBcAg-pulsed MoDC could also induce HBV core peptide-specific CD8(+) T cell proliferation determined by tetramer staining. In addition, the antigen-pulsed MoDC were found to have a stronger capacity to produce IL-12 and induce T cell response in vitro for patients with higher alanine transaminase (ALT) levels than those with lower ALT levels, indicating that antigen pulse could substantially reverse the impaired function of MoDC in primary HCC patients with active chronic hepatitis B. In conclusion, HBV antigen-pulsed MoDC from HCC patients with chronic hepatitis B could induce HBV-specific T cell response in vitro.

Adult↗
PubMed2006

Treatment persistence: a comparison among patients with schizophrenia who were initiated on atypical antipsychotic agents.

BACKGROUND: Although clinical trials have demonstrated the efficacy of atypical antipsychotic agents in reducing symptoms of schizophrenia, the likelihood of sustaining control of schizophrenic symptoms may depend on treatment persistence. OBJECTIVE: In this study, we compared treatment persistence between patients who were initiated on risperidone or olanzapine, the two most widely prescribed atypical antipsychotic agents. METHOD: We identified patients with schizophrenia by ICD-9-CM codes (> or =1 inpatient or > or =2 outpatient ICD-9-CM codes > or =7 days apart) between 1 July 1998 and 30 June 1999. We further selected those who were prescribed the target drug during 1 April 1999 through 31 March 2000 provided that they were not on any antipsychotic agents during the prior 6 months. Using event history analysis, we compared the treatment persistence in terms of hazard ratio between olanzapine and risperidone initiators, adjusting for patient's sociodemographic and clinical characteristics. RESULTS: Following the initiation of the target drug, more patients switched from risperidone to olanzapine than vice versa. However, among patients with schizophrenia who had comorbid diabetes, there were more patients who made a switch from olanzapine to risperidone; whereas among those who used anxiolytics, there were more patients who switched from risperidone to olanzapine. Finally, olanzapine initiators had decreased hazards of discontinuation by 14% (unadjusted; P < 0.001) and 12% (adjusted; P = 0.002), respectively, than risperidone initiators. CONCLUSIONS: Compared with risperidone, olanzapine seems to be better tolerated by patients as indicated by better treatment persistence. As such, initiation of olanzapine may increase the likelihood of sustaining control of symptoms of schizophrenia. Future research needs to provide a more comprehensive assessment of treatment persistence by considering other antipsychotic agents in the study and developing models to assess treatment persistence and switching as two interdependent competing risks.

Adolescent↗
PubMed2005

Visual dysfunction in Parkinson disease without dementia.

OBJECTIVE: To determine the profiles of visual dysfunction and their relationship to motor and cognitive dysfunction and to disability in mild to moderate Parkinson disease (PD) without dementia. METHODS: Seventy-six independently living participants with mild to moderate PD and 161 neurologically normal older adults were studied using a comprehensive battery to assess visual acuity, contrast sensitivity (CS), visual speed of processing and attention, spatial and motion perception, visual and verbal memory, visuoconstructional abilities, executive functions, depression, and motor function. RESULTS: Participants with PD scored significantly worse on all tests of vision and cognition compared with normal elderly persons. Reduced CS contributed to deficits on tests of spatial and motion perception and attention in participants with PD. Impairments in visual attention and spatial perception predicted worse cognitive function. Worse performances on tests of visual speed of processing and attention, spatial and motion perception, visual construction, and executive functions correlated with measures of postural instability and gait difficulty (in the Motor section of the Unified Parkinson's Disease Rating Scale). Impairments in motor function, visual memory, mood, and executive functions predicted worse disability as measured by Schwab-England Activities of Daily Living Scale. CONCLUSIONS: Patients with mild to moderate Parkinson disease showed impaired visual perception and cognition compared with elderly control subjects. Visual dysfunction contributes to parkinsonian disability through its influences on cognition and locomotion.

Aged↗
PubMed2005

Adjunctive use of atypical antipsychotics and anticholinergic drugs among patients with schizophrenia.

BACKGROUND: Treatment of schizophrenia with antipsychotics is often associated with extrapyramidal symptoms (EPS), a disorder involving involuntary muscle movement. Because EPS are often associated with the use of antipsychotics, anticholinergic agents are often indicated. OBJECTIVE: In this observational, retrospective study, we examined whether the initiation of olanzapine or risperidone, the two most widely prescribed atypical antipsychotics, is related to the adjunctive use of anticholinergic agents. METHOD: We identified patients with schizophrenia from outpatient clinics in the Veterans Health Administration (VA) and defined initiation of olanzapine or risperidone as patients who were not on any antipsychotics for 6 months and subsequently initiated on the target drug between 1/4/1999 and 31/3/2000. The data were analysed using tests of means or chi-square tests. RESULTS: The study yielded two major findings. First, compared with risperidone initiators, there were significantly fewer olanzapine initiators who used at least one anticholinergic agent adjunctively. Secondly, among olanzapine or risperidone initiators, patients who used at least one anticholinergic agent adjunctively tended to stay on the target drug significantly longer than those who did not use any anticholinergic agent adjunctively with the target drug. CONCLUSION: As the use of anticholinergics is a proxy for the presence of EPS, these findings suggest that risperidone may be more associated with EPS than olanzapine. However, to assess the benefits and side effects associated with olanzapine or risperidone, future research needs to examine various patient outcomes resulting from the initiation of each drug.

Antipsychotic Agents↗
PubMed2004

Orexigenic action of peripheral ghrelin is mediated by neuropeptide Y and agouti-related protein.

Ghrelin, a stomach-derived orexigenic hormone, has stimulated great interest as a potential target for obesity control. Pharmacological evidence indicates that ghrelin's effects on food intake are mediated by neuropeptide Y (NPY) and agouti-related protein (AgRP) in the central nervous system. These include intracerebroventricular application of antibodies to neutralize NPY and AgRP, and the application of an NPY Y1 receptor antagonist, which blocks some of the orexigenic effects of ghrelin. Here we describe treatment of Agrp(-/-);Npy(-/-) and Mc3r(-/-);Mc4r(-/-) double knockout mice as well as Npy(-/-) and Agrp(-/-) single knockout mice with either ghrelin or an orally active nonpeptide ghrelin agonist. The data demonstrate that NPY and AgRP are required for the orexigenic effects of ghrelin, as well as the involvement of the melanocortin pathway in ghrelin signaling. Our results outline a functional interaction between the NPY and AgRP pathways. Although deletion of either NPY or AgRP caused only a modest or nondetectable effect, ablation of both ligands completely abolished the orexigenic action of ghrelin. Our results establish an in vivo orexigenic function for NPY and AgRP, mediating the effect of ghrelin.

Agouti-Related Protein↗
PubMed2004

Application of recipient-derived dendritic cells to induce donor-specific T-cell hyporesponsiveness.

Administration of donor-derived immature dendritic cells (DC) treated with NF-kappaB oligodeoxyribonucleotides (ODN) prevents allograft rejection. We attempted to explore the use of recipient-derived DC pulsed with donor antigens, in which the donor antigens were presented to host T cells via an indirect pathway (cross-priming). Expression of CD40, CD80, and CD86 on DC was significantly inhibited by treatment with NF-kappaB ODN, whereas MHC class I and II were minimally affected. Normal C3H DC pulsed with B10 antigens stimulated proliferative responses and donor-specific CTL activity in C3H T cells, both of which were, however, markedly inhibited when DC were treated with NF-kappaB ODN. This manipulation was associated with reduced IFN-gamma and increased IL-10 production in the supernate, suggesting a Th2 bias. More frequent apoptotic T cells were observed in cultures with NF-kappaB ODN DC. In contrast to administration of normal DC pulsed with donor antigens that accelerated rejection of B10 cardiac allografts (median survival time [MST] 7 days versus 10 days in no-DC treatment control, P < .05), a single injection of 2 x 10(6) NF-kappaB ODN DC significantly prolonged allograft survival (MST 50 days, P < .05 compared with no-DC treatment control). The anti-donor CTL activity in infiltrating T cells isolated from cardiac grafts in recipients that received NF-kappaB ODN DC was significantly suppressed. These data indicate that vaccination with immature DC, propagated from recipient BM is an attractive approach to induce T-cell hyporesponsiveness.

Animals↗
PubMed2003

Molecular cloning and characterization of a laccase gene from the basidiomycete Fome lignosus and expression in Pichia pastoris.

A cDNA encoding for a laccase was isolated from the white-rot fungus Fome lignosus by RT-PCR. It contained an open reading frame of 1,557 bp. The deduced mature protein consisted of 497 amino acids and was preceded by a signal peptide of 21 amino acids. The genomic DNA of the laccase, containing 11 introns, was cloned by PCR. The cDNA was cloned into the vectors pGAPZalphaA and pGAPZA, and expressed in the Pichia pastoris GS115. Laccase-secreting transformants were selected by their ability to oxidize the substrate 2'2-azinobis-(3-ethylbenzthiaoline-6-sufonic acid) (ABTS). The laccase activity obtained with the native signal peptide was found to be fivefold higher than that obtained with the alpha-factor secretion signal peptide. The presence of 0.4 mM copper was necessary for optimal activity of the enzyme. The highest activity value reached 9.03 U ml(-1), and the optimal secreting time was 2~3 days at 20 degrees C. The crude laccase was stable in a pH range from 6.0 to 10.0 and at temperatures lower than 30 degrees C in pH 4.5 for 24 h. The molecular mass of the enzyme was estimated to be 66.5 kDa by SDS-PAGE. The optimum pH and temperature were 2.4 and 55 degrees C. The Km and Vmax values for ABTS were 177 microM and 23.54 micromol min(-1) respectively. The extent of glycosylation of the purified enzyme was 58.6%.

Amino Acid Sequence↗
PubMed2003

Transgenic mice expressing the PS1-A246E mutation: effects on spatial learning, exploration, anxiety, and motor coordination.

The functional consequence of the PS1-A246E mutation was assessed in transgenic mice on a background lacking the endogenous PS1 gene. These mice have elevated concentrations of A-beta protein (Abeta(42)) in the absence of plaque formation. By comparison to a mixed background strain (50% B6, 25% SJl, 25% 129Sv) controlled for age and gender, PS1-A246E transgenic mice displayed disinhibitory tendencies, as indicated by increased entries and duration in the open arms of the elevated plus-maze. Despite normal spontaneous alternation rates in a T-maze, latencies before responding were higher in PS1-A246E transgenic mice than controls. Moreover, the PS1-A246E transgenic mice fell more often from two stationary beams, but not from the coat-hanger and the rotorod. By contrast, ambulation in an automated photocell chamber and in an open-field was not affected. Nor was acquisition of place learning in the Morris water maze task. These results indicate that elevated Abeta(42) levels were insufficient for causing spatial defects but caused disinhibition, psychomotor slowing, and loss of motor skills in this model of familial Alzheimer's disease.

Alzheimer Disease↗
PubMed2003

Efficient and long-term intracardiac gene transfer in delta-sarcoglycan-deficiency hamster by adeno-associated virus-2 vectors.

Intracardiac gene transfer and gene therapy have been investigated with different vector systems. Here we used adeno-associated virus (AAV) vectors to deliver either a reporter gene or a therapeutic gene into the heart of golden Syrian hamsters. The method of gene delivery was direct infusion of the AAV2 vectors into the coronary artery ex vivo in a heterotopically transplanted heart. When an AAV2 vector carrying the Lac-Z gene driven by CMV promoter was delivered into the heart of healthy hamsters, effective gene transfer was achieved in up to 90% of the cardiomyocytes. Lac-Z gene expression persisted for more than 1 year without immune rejection or promoter shutoff. Furthermore, when an AAV2 vector carrying human delta-sarcoglycan gene was similarly delivered into the heart of Bio14.6 Syrian hamster, a congestive heart failure and limb girdle muscular dystrophy animal model, widespread therapeutic gene transfer was achieved in a majority of the cardiomyocytes. Efficient expression of the human delta-sarcoglycan gene in the dystrophic hamster hearts restored the entire sarcoglycan complex that was missing due to the primary deficiency of delta-sarcoglycan. Transgene expression persisted for 4 months (the duration of the study) without immune rejection or promoter shutoff. These results indicate that AAV is a promising vector system for cardiac gene therapy.

Animals↗
PubMed2001

Costimulation blockade promotes the apoptotic death of graft-infiltrating T cells and prolongs survival of hepatic allografts from FLT3L-treated donors.

BACKGROUND: Mouse liver grafts are accepted across major histocompatibility complex (MHC) barriers and induce donor-specific tolerance without immunosuppressive therapy. By contrast, hepatic allografts from donors treated with the hematopoietic growth factor fms-like tyrosine kinase 3 ligand (FL), which dramatically increases hepatic interstitial dendritic cells (DC), are rejected acutely (median survival time 5 days). This switch from tolerance to rejection is associated with a marked reduction in apoptotic activity of graft-infiltrating T cells. We hypothesized that T-cell costimulation, provided by markedly enhanced numbers of donor antigen presenting cells (APCs), might inhibit apoptosis, promote expansion of T helper 1 cells and play a key role in acute liver rejection. METHODS: C3H (H2k) recipients of orthotopic liver grafts from FL-treated B10 (H2b) donors were given cytotoxic T-lymphocyte antigen 4: immunoglobulin (CTLA4Ig), a chimeric fusion protein that blocks the B7-CD28 costimulatory pathway, or control human immunoglobulin (200 microg) on the day of transplantation (day 0). Livers and spleens were removed on day 4. Cryostat sections were stained for interleukin (IL)-12 or by terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL). Expression of mRNA encoding interferon (IFN)-gamma and IL-10 was determined by RNase protection assay. Suspensions of graft-infiltrating cells (GICs) and spleen cells were analyzed for apoptotic (TUNEL+) T-cell subsets by flow cytometry. CTL activity of GICs and circulating alloantibody levels were determined by cytotoxicity assays. RESULTS: Survival of liver grafts from FL donors was markedly prolonged by CTLA4Ig administration. This effect was associated with reductions in IFN-gamma and IL-10 gene transcripts within the GIC population, and with decreases in donor-specific CTL and NK cell activities and circulating anti-donor alloantibody levels. At the same time, there were marked increases in TUNEL+ CD4+ and especially CD8+ cells, both within the grafts and in the spleens of CTLA4Ig-treated mice. CONCLUSIONS: Signaling via the B7-CD28 pathway appears to play a key role in the switch from tolerance to rejection that is precipitated by markedly enhanced numbers of donor DCs. Inhibition of acute liver allograft rejection by CTLA4Ig, linked to restoration of apoptotic activity of graft-infiltrating T cells, further suggests that deletion of these cells may be critical for promotion of long-term allograft survival.

Abatacept↗
PubMed2001

Loss of presenilin 1 is associated with enhanced beta-catenin signaling and skin tumorigenesis.

Presenilin 1 (PS1) is required for the proteolytic processing of Notch and the beta-amyloid precursor protein (APP), molecules that play pivotal roles in cell-fate determination during development and Alzheimer's disease pathogenesis, respectively. In addition, PS1 interacts with beta-catenin and promotes its turnover through independent mechanisms. Consistent with this activity, we report here that PS1 is important in controlling epidermal cell proliferation in vivo. PS1 knockout mice that are rescued through neuronal expression of human PS1 transgene develop spontaneous skin cancers. PS1-null keratinocytes exhibit higher cytosolic beta-catenin and beta-catenin/lymphoid enhancer factor-1/T cell factor (beta-catenin/LEF)-mediated signaling. This effect can be reversed by reintroducing wild-type PS1, but not a PS1 mutant active in Notch processing but defective in beta-catenin binding. Nuclear beta-catenin protein can be detected in tumors. Elevated beta-catenin/LEF signaling is correlated with activation of its downstream target cyclin D1 and accelerated entry from G(1) into S phase of the cell cycle. This report demonstrates a function of PS1 in adult tissues, and our analysis suggests that deregulation of beta-catenin pathway contributes to the skin tumor phenotype.

Animals↗
PubMed2001

Liver-derived DEC205+B220+CD19- dendritic cells regulate T cell responses.

Leukocytes resident in the liver may play a role in immune responses. We describe a cell population propagated from mouse liver nonparenchymal cells in IL-3 and anti-CD40 mAb that exhibits a distinct surface immunophenotype and function in directing differentiation of naive allogeneic T cells. After culture, such cells are DEC-205(bright)B220+CD11c-CD19-, and negative for T (CD3, CD4, CD8alpha), NK (NK 1.1) cell markers, and myeloid Ags (CD11b, CD13, CD14). These liver-derived DEC205+B220+ CD19- cells have a morphology and migratory capacity similar to dendritic cells. Interestingly, they possess Ig gene rearrangements, but lack Ig molecule expression on the cell surface. They induce low thymidine uptake of allogeneic T cells in MLR due to extensive apoptosis of activated T cells. T cell proliferation is restored by addition of the common caspase inhibitor peptide, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk). T cells stimulated by liver-derived DEC205+B220+D19- cells release both IL-10 and IFN-gamma, small amounts of TGF-beta, and no IL-2 or IL-4, a cytokine profile resembling T regulatory type 1 cells. Expression of IL-10 and IFN-gamma, but not bioactive IL-12 in liver DEC205+B220+CD19- cells was demonstrated by RNase protection assay. In vivo administration of liver DEC205+B220+CD19- cells significantly prolonged the survival of vascularized cardiac allografts in an alloantigen-specific manner.

Animals↗
PubMed2001

Il-12 antagonism enhances apoptotic death of T cells within hepatic allografts from Flt3 ligand-treated donors and promotes graft acceptance.

Mouse livers are accepted across MHC barriers and induce donor-specific tolerance without immunosuppressive therapy. By contrast, livers from donors treated with Flt3 ligand, which dramatically increases hepatic interstitial dendritic cells, are rejected acutely (median survival time 5 days). This switch from tolerance to rejection is associated with a marked reduction in apoptotic activity of graft-infiltrating cells. We hypothesized that IL-12 production by enhanced numbers of donor APC might inhibit apoptosis, promote expansion of Th1 cells, and play a key role in liver rejection. Therefore, C3H (H2(k)) recipients of liver grafts from Flt3 ligand-treated B10 donors were given neutralizing anti-IL-12 mAb (200 or 500 microg) on days 0 and 2 after transplant. Graft survival was markedly prolonged at the higher mAb dose, with 50% of grafts surviving >100 days. This effect was associated with reductions in IFN-gamma gene transcripts within the graft-infiltrating cell population and with reductions in circulating IFN-gamma and IL-10 levels, donor-specific CTL and NK cell activities, and circulating alloantibody levels. At the same time, there were marked increases in apoptotic (TUNEL(+)) CD4(+) and especially CD8(+) cells, both within the grafts and in spleens of anti-IL-12 mAb-treated mice. In vitro, exogenous IL-12 inhibited apoptotic death induced in naive allogeneic T cells by liver nonparenchymal cells. These findings suggest that suppression of rejection by IL-12 antagonism, linked to restoration of apoptotic activity within the peripheral alloreactive T cell population, is important for liver allograft survival and tolerance induction.

Adjuvants, Immunologic↗
PubMed2001

The potent antitumor effects of combined p16 gene and GM-CSF gene therapy through efficient induction of antitumor immunity.

PURPOSE: Tumor suppressor gene therapy and cytokine gene therapy have limited antitumor effects when used alone. Thus, in the present study, we investigated the antitumor potentials of the combined transfer of the p16 tumor suppressor gene and the murine granulocyte-macrophage colony-stimulating factor (GM-CSF) gene. METHODS: The adenovirus-harboring p16 gene (Adp16) and adenovirus-harboring GM-CSF (AdGMCSF) gene were utilized for the treatment of established tumors in vivo. The mice were inoculated s.c. with Renca renal carcinoma cells and 3 days later received an intratumoral injection of Adp16 in combination with AdGMCSF. RESULTS: The results demonstrated that tumor-bearing mice treated with Adp16 and Ad-GMCSF showed more potent inhibition of tumor growth and a prolonged survival period than mice treated with Adp16. AdGMCSF, adenovirus-expressing beta-galactosidase or PBS (P<0.01). Treatments of the mice with Adp16 alone or AdGMCSF alone also showed obvious antitumor effects as compared with those mice treated with PBS (P<0.05). After combined p16 and AdGMCSF gene therapy, the expression of H2Kd and Fas molecules on freshly isolated tumor cells increased markedly, and more CD(4)+ T cells and CD(8)+ T cells infiltrated in the tumor sites. The cytotoxicity of natural killer cells and specific cytotoxic T lymphocytes increased more significantly after the combined therapy. CONCLUSIONS: Our results demonstrated that combination p16 gene and GM-CSF gene therapy could inhibit the growth of established tumors in mice more significantly through efficient induction of antitumor immunity.

Adenoviridae↗
PubMed2001

Effective treatment of small murine hepatocellular carcinoma by dendritic cells.

Hepatocellular carcinoma (HCC) is a common malignancy with a poor prognosis. This investigation examined whether dendritic cell-based immunotherapy can treat murine HCC effectively. Bone marrow-derived dendritic cells were propagated from C57BL/10J mice in GM-CSF (4 ng/mL) and interleukin (IL)-4 (1,000 micro/mL). The dendritic cells were pulsed with a Hepa1-6 lysate overnight and employed to treat murine HCC. For in vivo study, HCC was created by inoculation of hepa1-6, 5 x 10(5) cells, in the flank of C57BL/10J mice. HCC were categorized into small (3 x 3-mm) and large (5 x 5-mm) tumors. These HCC were treated by dendritic cells intravenously, twice at weekly intervals. The results revealed that lymphocytes could be gathered around small HCC after administration of Hepa1-6 lysate-pulsed dendritic cells. Seven of 12 (58.3%) small HCC could be eradicated completely by dendritic cell-based immunotherapy, and 33.3% of the small tumors responded to immunotherapy partially which were held in a stable condition for 34.0 +/- 7.4 days before the tumors regrew. For large HCC, lymphocytes did not gather around the tumors, and the tumors cannot be eradicated effectively by dendritic cells. However, dendritic cell-based immunotherapy could slow down the growth rate of large tumors (116.2 +/- 91.4 mm(3) vs. 234.0 +/- 149.1 mm(3) of the control on day 7, P =.043; and 280.3 +/- 224.7 mm(3) vs. 870.0 +/- 418.9 mm(3) of the control on day 17, P <.001). Conclusively, dendritic cells pulsed with a Hepa1-6 lysate can be employed to treat small HCC in vivo effectively. However, the efficacy of dendritic cell-based immunotherapy decreases while tumors grow.

Animals↗
PubMed2001

Pneumatic lithotripsy versus laser lithotripsy in the endoscopic treatment of ureteral calculi.

PURPOSE: To compare the efficacy, safety, and features of pneumatic lithotripsy (PL) with those of laser lithotripsy (LL) and present our clinical experience in the endoscopic management of ureteral calculi. PATIENTS AND METHODS: From August 1994 to February 2000, 285 consecutive patients underwent endoscopic lithotripsy with either the Swiss Lithoclast pneumatic lithotripter (145 patients) or the Ho:YAG laser lithotripter (140 patients) for the treatment of ureteral calculi. RESULTS: In one single session, the overall successful stone fragmentation rate of LL was higher than that of PL (95.7% v 69.7%; P < 0.01). The average time to stone-free status was shorter for LL than for PL (18 days v 31 days; P < 0.01). No major complications were observed in LL, while five ureteral perforations were encountered in PL. CONCLUSIONS: Laser lithotripsy has advantages over PL in high efficiency of stone fragmentation and a low complication rate. Laser lithotripsy is a powerful, effective, and safe treatment modality for ureteral calculi.

Adolescent↗