Biomedical subjects

J K Huang

Publications and source records attributed to J K Huang.

At least 37 records · Page 2Linked to original sources

PubMed2001

Fendiline mobilizes intracellular Ca2+ in Chang liver cells.

1. The effects of the antianginal drug fendiline (N-[3,3-diphenylpropyl]-alpha-methyl-benzylamine) on intracellular free Ca2+ levels ([Ca2+](i)) in Chang liver cells were evaluated using fura-2 as a fluorescent Ca2+ indicator. 2. Fendiline (1-100 micromol/L) increased [Ca2+](i) in a concentration-dependent manner, with an EC50 of 25 micromol/L. 3. The [Ca2+](i) response was composed of an initial rise and a slow decay to a sustained phase. Removal of extracellular Ca2+ partly reduced the [Ca2+](i) signals. 4. Fendiline (10 micromol/L)-induced release of intracellular Ca2+ was reduced by 65% following pretreatment with 1 micromol/L thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor) to deplete Ca2+ stored in the endoplasmic reticulum. 5. After pretreatment with 10 micromol/L fendiline in Ca2+-free medium for several minutes, addition of 3 mmol/L Ca2+ induced an increase in [Ca2+](i) of a magnitude four-fold greater than control. This increase in [Ca2+](i) was not reduced by 10 micromol/L SKF96365, econazole, nifedipine or verapamil. 6. Fendiline (10 micromol/L)-induced release of intracellular Ca2+ was not altered by inhibition of phospholipase C with 2 micromol/L 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino) hexyl)-1H-pyrrole-2,5-dione (U73122). 7. The results of the present study show that fendiline induces an increase in [Ca2+](i) in Chang liver cells by releasing stored Ca2+ in an inositol 1,4,5-trisphosphate-independent manner and by causing extracellular Ca2+ influx.

Calcium↗

PubMed2001

Annual changes in the clinical features of prostatic adenocarcinoma in Taiwan.

OBJECTIVE: To determine, using a clinical and pathological database, the annual changes in the characteristics of adenocarcinoma of the prostate diagnosed in consecutive men in Taiwan. PATIENTS AND METHODS: All prostatic adenocarcinomas newly diagnosed between 1991 and 1999 in our institution were analysed. Using logistic regression for dichotomous variables, the annual trends were assessed for changes in the percentage of T1c disease, incidental carcinoma, clinically localized disease and Gleason grade 4/5 cancers. The annual trends for changes in the pathological features of disease in patients treated by radical prostatectomy were also analysed. RESULTS: The study included 694 patients; the median age at diagnosis increased significantly (P = 0.004) and there was a significant increase in clinical T1c disease (relative risk, RR, 1.142, P = 0.022). There were also significant decreases in incidental carcinomas (RR 0.789, P < 0.001), patients with a serum prostate-specific antigen (PSA) level of > 20 ng/mL (RR 0.848, P < 0.001) and with Gleason grade 4/5 tumours (RR 0.919, P = 0.005). There was no significant change in the percentage of clinically localized disease. Radical prostatectomy was undertaken in 179 men; the annual incidence of lymph node metastases decreased significantly (P = 0.035) and there was a significant 19% increase in the RR of having organ-confined disease (pT1-2N0M0) and a 19% decrease in Gleason grade 4/5 tumours. CONCLUSIONS: These results may reflect the annual trends of prostate cancer in Taiwan in the period for which the PSA assay became available. The increasing application of PSA testing was associated with a significant increase in clinical T1c disease and decrease in incidental carcinoma. There was also a significant trend towards less aggressive cancers. Despite the dramatic increase in the annual detection rate, tumours were not detected at an earlier stage. However, for patients treated with radical prostatectomy, there was a significant change to earlier stage disease and fewer de-differentiated cancers.

Adenocarcinoma↗

PubMed2001

Disulfide bond effects on protein stability: designed variants of Cucurbita maxima trypsin inhibitor-V.

Attempts to increase protein stability by insertion of novel disulfide bonds have not always been successful. According to the two current models, cross-links enhance stability mainly through denatured state effects. We have investigated the effects of removal and addition of disulfide cross-links, protein flexibility in the vicinity of a cross-link, and disulfide loop size on the stability of Cucurbita maxima trypsin inhibitor-V (CMTI-V; 7 kD) by differential scanning calorimetry. CMTI-V offers the advantage of a large, flexible, and solvent-exposed loop not involved in extensive intra-molecular interactions. We have uncovered a negative correlation between retention time in hydrophobic column chromatography, a measure of protein hydrophobicity, and melting temperature (T(m)), an indicator of native state stabilization, for CMTI-V and its variants. In conjunction with the complete set of thermodynamic parameters of denaturation, this has led to the following deductions: (1) In the less stable, disulfide-removed C3S/C48S (Delta Delta G(d)(50 degrees C) = -4 kcal/mole; Delta T(m) = -22 degrees C), the native state is destabilized more than the denatured state; this also applies to the less-stable CMTI-V* (Delta Delta G(d)(50 degrees C) = -3 kcal/mole; Delta T(m) = -11 degrees C), in which the disulfide-containing loop is opened by specific hydrolysis of the Lys(44)-Asp(45) peptide bond; (2) In the less stable, disulfide-inserted E38C/W54C (Delta Delta G(d)(50 degrees C) = -1 kcal/mole; Delta T(m) = +2 degrees C), the denatured state is more stabilized than the native state; and (3) In the more stable, disulfide-engineered V42C/R52C (Delta Delta G(d)(50 degrees C) = +1 kcal/mole; Delta T(m) = +17 degrees C), the native state is more stabilized than the denatured state. These results show that a cross-link stabilizes both native and denatured states, and differential stabilization of the two states causes either loss or gain in protein stability. Removal of hydrogen bonds in the same flexible region of CMTI-V resulted in less destabilization despite larger changes in the enthalpy and entropy of denaturation. The effect of a cross-link on the denatured state of CMTI-V was estimated directly by means of a four-state thermodynamic cycle consisting of native and denatured states of CMTI-V and CMTI-V*. Overall, the results show that an enthalpy-entropy compensation accompanies disulfide bond effects and protein stabilization is profoundly modulated by altered hydrophobicity of both native and denatured states, altered flexibility near the cross-link, and residual structure in the denatured state.

Circular Dichroism↗

PubMed2001

Dual effect of the antianginal drug fendiline on bladder female transitional carcinoma cells: mobilization of intracellular CA2+ and induction of cell death.

The effect of fendiline, an antianginal drug, on cytosolic free Ca2+ levels ([Ca2+]i) in populations of bladder female transitional carcinoma (BFTC) cells was explored using fura-2 as a Ca2+ indicator. Fendiline at concentrations between 3 and 200 micromol/l increased [Ca2+]i in a concentration-dependent manner and the signal saturated at 100 micromol/l. The [Ca2+]i signal was biphasic, with an initial rise and a slow decay. Ca2+ removal inhibited the Ca2+ signal by about half in peak amplitude. Adding 3 mmol/l Ca2+ increased [Ca2+]i in cells pretreated with 100 micromol/l fendiline in Ca2+ -free medium, suggesting that fendiline induced Ca2+ influx via capacitative Ca2+ entry. In Ca2+ -free medium, pretreatment with 1 micromol/l thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor) to deplete the endoplasmic reticulum Ca2+ store inhibited most of the 100 micromol/l fendiline-induced internal Ca2+ release; and conversely, pretreatment with 100 micromol/l fendiline partly inhibited 1 micromol/l thapsigargin-induced Ca2+ release. This indicates that the major internal Ca2+ store of fendiline-induced [Ca2+]i increases is located in the endoplasmic reticulum. The Ca2+ release induced by 100 micromol/l fendiline may be partly mediated by inositol 1,4,5-trisphosphate, because the [Ca2+]i increase was inhibited by 50% by inhibiting phospholipase C with 2 micromol/l U73122. Fendiline (100 micromol/l) decreased cell viability by 12-44% after being added to cells for 2- 30 min. Together, the findings indicate that in BFTC cells, fendiline exerts a dual effect: mobilization of intracellular Ca2+ and induction of cell death.

Anti-Arrhythmia Agents↗

PubMed2001

p53 mutation and bcl-2 expression in transitional cell carcinoma of the urinary bladder.

BACKGROUND: The purpose of our study was to examine the frequency of p53 mutation and bcl-2 expression in transitional cell carcinoma of the urinary bladder and their clinicopathologic correlates. METHODS: A total of 137 patients who underwent transurethral resection for primary transitional cell bladder carcinomas were enrolled. The paraffin-embedded tissue blocks were recut and stained by monoclonal anti-p53 (DO7) and anti-bcl-2 (124) antibodies. The bcl-2 and p53 immunoreactivity was correlated to tumor grade and pathological stage. RESULTS: p53 mutation was identified in 102 patients (78.5%). The mutation was most common in grade 3 tumors (95%) as compared to grade 2 (74%) and grade 1 (80%) tumors, but the difference was not statistically significant (p = 0.289). Stage pT2 tumors had higher incidence of p53 mutation (97%) as compared to pTa-1 tumors (71%, p = 0.0003). Only 17 tumors (13%) expressed bcl-2; the grade 3 tumors had significantly higher incidence of bcl-2 expression (p = 0.04). The bcl-2 expression was not related to pathological stage (p = 0.083). There was no interrelation between p53 mutation and bcl-2 expression (p = 0.97). Grade 3 tumors correlated well with invasive disease (p < 0.00001). When grade 2 tumors were evaluated separately, p53 mutation was positively correlated with disease invasion (p = 0.001). CONCLUSIONS: Grade 3 tumor was the most important variable associated with tumor invasion in transitional cell carcinoma of the urinary bladder. p53 mutation was positively correlated with invasive disease. Grade 2 tumors with p53 mutation had greater probability of disease invasion. Expression of bcl-2 positively correlated with tumor grade but not pathological stage.

Adult↗

PubMed2001

In vitro effect of hyperbaric oxygen on the chemolysis of infective stones.

BACKGROUND: In order to extend the feasibility of hyperbaric oxygen therapy in the urological field, the present study aimed to investigate the dissolution activity of human infective stones in UROCITRA solution under hyperbaric oxygen condition. METHODS: The dissolution activity of 7 struvite and 11 mixed struvite and carbonate apatite stones in UROCITRA solution were studied under 2.5 atmosphere (atm) hyperbaric oxygen (HBO) status in a Sigma I N-124 monoplace chamber. Another 7 struvite and 10 mixed struvite and carbonate apatite stones were also studied under normal condition. Chemolysis was performed in a drip device with a 150-ml/hour continuous flow rate. RESULTS: Under 2.5 atm HBO status, the PO2 of UROCITRA solution was 365 +/- 44 mmHg, which was significantly higher than that of tap water (113 +/- 62 mmHg) and UROCITRA solution (125 +/- 12 mmHg) under normobaric condition (p < 0.001). The decreases in the stone weight of struvite under normobaric condition were 31 +/- 8.8% after 2 h and 48 +/- 15% after 4 h of treatment. The HBO-enriched UROCITRA solution did not increase the dissolution activity as reflected by comparable decreases in the dried stone weight (31.2 +/- 14.6% and 54 +/- 19% at the 2nd and 4th post-treatment hours, respectively, p > 0.05). Similarly, there was no significant difference in the percent stone weight decrease of the mixed struvite and carbonate apatite stones under either HBO or normobaric condition. The dissolution responsiveness of struvite was significantly greater than that of the mixed struvite and carbonate apatite stones. CONCLUSIONS: The chemolysis of struvite in UROCITRA solution is significantly greater than that of the mixed struvite and carbonate apatite stones. However, the UROCITRA solution enriched with HBO does not enhance the dissolution of infective stones.

Calculi↗

PubMed2000

Novel effects of gossypol, a chemical contraceptive in man: mobilization of internal Ca(2+) and activation of external Ca(2+) entry in intact cells.

The effect of gossypol on Ca(2+) signaling in Madin Darby canine kidney (MDCK) cells was investigated by using fura-2 as a Ca(2+) probe. Gossypol evoked a rise in cytosolic free Ca(2+) levels ([Ca(2+)](i)) concentration-dependently between 2 and 20 microM. The response was decreased by external Ca(2+) removal. In Ca(2+)-free medium pretreatment with gossypol nearly abolished the [Ca(2+)](i) increase induced by carbonylcyanide m-chlorophenylhydrazone (CCCP), a mitochondrial uncoupler, and thapsigargin, an inhibitor of the endoplasmic reticulum Ca(2+) pump; but pretreatment with CCCP and thapsigargin only partly inhibited gossypol-induced Ca(2+) release. Addition of 3 mM Ca(2+) induced a [Ca(2+)](i) increase after pretreatment with 5 microM gossypol in Ca(2+)-free medium. This Ca(2+) entry was decreased by 25 microM econazole, 50 microM SKF96365 and 40 microM aristolochic acid (a phospholipase A(2) inhibitor). Pretreatment with aristolochic acid inhibited 5 microM gossypol-induced internal Ca(2+) release by 55%, but suppression of phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3, 5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione) had no effect. Gossypol (5 microM) also increased [Ca(2+)](i) in human bladder cancer cells and neutrophils. Collectively, we have found that gossypol increased [Ca(2+)](i) in MDCK cells by releasing Ca(2+) from multiple Ca(2+) stores in a manner independent of the production of inositol-1,4,5-trisphosphate, followed by Ca(2+) influx from external space.

Animals↗

PubMed2000

NPC-15199, a novel anti-inflammatory agent, mobilizes intracellular Ca2+ in bladder female transitional carcinoma (BFTC) cells.

This report demonstrates that NPC-15199 [(N-(9-fluorenylmethoxycarbonyl)L-leucine)], a novel anti-inflammatory agent, increases intracellular Ca2+ concentration ([Ca2+]i) in human bladder female transitional cancer (BFTC) cells. Using fura-2 as a Ca2+ probe, NPC-15199 (0.1-2 mM) was found to increase [Ca2+]i concentration-dependently. The response saturated at 2-5 mM NPC-15199. The [Ca2+]i increase comprised an initial rise, a slow decay, and a plateau. Ca2+ removal partly inhibited the Ca2+ signals. In Ca2+-free medium, pretreatment with 1 mM NPC-15199 abolished the [Ca2+]i increase induced by 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor); and after pretreatment with thapsigargin, NPC-15199-induced Ca2+ release was dramatically inhibited. This indicates that NPC-15199 released internal Ca2+ mostly from the endoplasmic reticulum. Adding 3 mM Ca2+ increased [Ca2+]i in cells pretreated with 1 mM NPC-15199 in Ca2+-free medium. Together, the findings suggest that in BFTC bladder cancer cells, NPC-15199 induced Ca2+ release from the endoplasmic reticulum and activating Ca2+ entry.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2000

The role of bcl-2, p53, and ki-67 index in predicting tumor recurrence for low grade superficial transitional cell bladder carcinoma.

PURPOSE: We assess the prognostic significance of bcl-2 expression, p53 mutation and ki-67 index for low grade, superficial transitional cell bladder carcinoma. MATERIALS AND METHODS: The medical records of 93 cases of primary, low grade (24 G1, 69 G2), superficial (70 pTa, 23 pT1) transitional cell carcinoma of the bladder were reviewed. Association of bcl-2, p53 and ki-67 index immunoreactivity with tumor grade and stage was examined. Prognostic significance of tumor grade, pathological stage, bcl-2 expression, p53 mutation and ki-67 index in predicting tumor recurrence was assessed. RESULTS: Of the tumors 60 (70%) had p53 mutation and 9 (10.5%) expressed bcl-2. These 2 markers did not relate to tumor grade or pathological stage. Median ki-67 index was 10.9% and positively correlated with tumor grade. Recurrence was noted in 34.9% of patients with a median followup of 26 months (range 1 to 84). The ki-67 index was the only significant prognostic indicator in univariate and multivariate analyses. This marker can further distinguish grade 2 tumors with a favorable prognosis from those with an unfavorable outcome. CONCLUSIONS: The ki-67 labeling index is an independent predictor of tumor recurrence for patients with primary superficial, low grade bladder cancers.

Carcinoma, Transitional Cell↗

PubMed2000

NPC-14686, a novel anti-inflammatory agent, increased intracellular Ca(2+) concentrations in MDCK renal tubular cells.

The effect of NPC-14686 (Fmoc-L-homophenylalanine), a novel anti-inflammatory agent on intracellular free Ca(2+) concentrations ([Ca(2+)](i)) in Madin Darby canine kidney (MDCK) renal tubular cells, was investigated, using fura-2 as a Ca(2+) dye. At concentrations between 10 and 200 microM NPC-14686 increased [Ca(2+)](i) concentration dependently. The [Ca(2+)](i) signal comprised an initial rise and a sustained phase. Ca(2+) removal inhibited the Ca(2+) signals by 90%. In Ca(2+)-free medium, pretreatment with 100 microM NPC-14686 nearly abolished the [Ca(2+)](i) increase induced by 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor) and abolished the [Ca(2+)](i) increase induced by 2 microM carbonylcyanide m-chlorophenylhydrazone (CCCP) (a mitochondrial uncoupler). NPC-14686 (100 microM) induced a slight [Ca(2+)](i) increase after pretreatment with 2 microM CCCP and 1 microM thapsigargin. Addition of 3 mM Ca(2+) elicited a [Ca(2+)](i) increase in cells pretreated with 100 microM NPC-14686 in Ca(2+)-free medium. Inhibition of inositol-1,4,5-trisphosphate (IP(3)) production by suppressing phospholipase C with 2 microM U73122 did not alter NPC-14686-induced Ca(2+) release. Trypan blue exclusion revealed that incubation with 10 or 200 microM NPC-14686 for 1-30 min decreased cell viability by 10-20% concentration dependently. Collectively, the results demonstrate that, in MDCK tubular cells, NPC-14686 induced Ca(2+) release followed by Ca(2+) entry, with the latter playing a major role. NPC-14686 appears to release intracellular Ca(2+) in an IP(3)-uncoupled manner. NPC-14686 may be of mild cytotoxicity.

Aminobutyrates↗

PubMed2000

Clomiphene, an ovulation-inducing agent, mobilizes intracellular Ca2+ and causes extracellular Ca2+ influx in bladder female transitional carcinoma cells.

BACKGROUND/METHODS: The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca2+ levels ([Ca2+]i) in populations of BFTC human bladder cancer cells was explored by using fura-2 as a Ca2+ indicator. RESULTS: Clomiphene at concentrations between 10 and 75 microM increased [Ca2+]i in a concentration-dependent manner and the signal saturated at 50 microM. The [Ca2+]i signal was biphasic with an initial rise and a slow decay. Ca2+ removal inhibited the Ca2+ signal by about 40-50% in maximum [Ca2+]i. Adding 3 mM Ca2+ increased [Ca2+]i in cells pretreated with 50 microM clomiphene in Ca2+-free medium, suggesting that clomiphene induced capacitative Ca2+ entry. In Ca2+-free medium, pretreatment with 50 microM brefeldin A (to disrupt the Golgi complex Ca2+ store), 1 microM thapsigargin (to inhibit the endoplasmic reticulum Ca2+ pump), and CCCP (to uncouple mitochondria) inhibited 85% of clomiphene-induced intracellular Ca2+ release. Conversely, pretreatment with 50 microM clomiphene in Ca2+-free medium abolished the [Ca2+]i increase induced by brefeldin, thapsigargin or CCCP. The intracellular Ca2+ release was unaltered by inhibiting formation of inositol-1,4,5-trisphosphate (IP3) with 2 mM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122; a phospholipase C inhibitor). CONCLUSION: The [Ca2+]i increase induced by 50 microM clomiphene was not affected by 10 microM of nifedipine, verapamil or diltiazem. Collectively, the results suggest that clomiphene releases intracellular Ca2+ in an IP3-independent manner and also activates extracellular Ca2+ influx.

Calcium↗

PubMed2000

Prediction of biochemical relapse for stage pT3 prostate cancer following radical prostatectomy.

BACKGROUND: Approximately 30% to 50% of clinically localized prostate cancers are found to be locally advanced after radical prostatectomy. Without adjuvant therapy, more than 30% of stage pT3 patients will have biochemical failure in a median follow-up of three years. Whether adjuvant therapy should be given remains controversial. Identification of prognostic indicators may be helpful to select patients at risk of biochemical failure for postoperative adjuvant therapy. METHODS: The medical records of 22 pT3 prostate cancer patients were analyzed retrospectively. Postoperative management included surveillance (7 patients), adjuvant hormone therapy (7) and radiotherapy (8). Patients were monitored every three months using serum prostate-specific antigen (PSA). Biochemical failure was defined as an elevation in PSA of more than 0.2 ng/ml. The clinical outcome was correlated with tumor grading, pathologic staging, preoperative PSA level, and p53 and bcl-2 status. RESULTS: Five patients (23%) experienced biochemical relapse within a median follow-up time of 52 months (range, 10-71 months). A Gleason score of 8 or more (p = 0.001) and seminal vesicle involvement (p = 0.014) were significant prognostic indicators in the univariate analysis. Patients with low preoperative PSA levels (< 20 ng/ml) had a significantly higher failure rate (p = 0.031). However, most of these patients (56%) had tumors with Gleason scores of 8 or more. Neither p53 gene mutation nor bcl-2 overexpression predicted PSA failure. Postoperative adjuvant therapy did not appear to reduce the risk of disease recurrence. In multivariate analysis, the Gleason score was the only significant factor predicting biochemical failure (p = 0.017). CONCLUSIONS: Patients with poorly differentiated tumors and/or seminal vesicle invasiveness are at higher risk of biochemical failure after radical prostatectomy. Our limited experience did not support the routine application of adjuvant therapy for this subgroup of patients. A larger sample size with a longer follow-up period is necessary to reach a definitive conclusion.

Aged↗

PubMed2000

Fatty acids enhanced tubermycin production by Pseudomonas strain 2HS.

A new microbial isolate, Pseudomonas 2HS, produced trace amounts of a greenish-yellow pigment when grown aerobically in a 1% yeast extract medium at 30 degrees C and shaken at 250 rpm for 5 days. In contrast, cells produced more greenish-yellow pigment (2.16 mg/15 ml culture) when grown in the presence of 0.5% 12-hydroxyoctadecanoic acid (w/v). The greenish-yellow pigment was identified as phenazine-1-carboxylic acid (tubermycin B), and the Pseudomonas 2HS was identified as P. aeruginosa 2HS. This is the first report that 12-hydroxyoctadecanoic, ricinoleic and other fatty acids can enhance the production of phenazine-1-carboxylic acid by a Pseudomonas species.

Animals↗

PubMed2000

Effects of bombesin on gut mucosal immunity in rats after thermal injury.

BACKGROUND AND PURPOSE: Severe burns induce a disruption in gastrointestinal mucosal integrity and facilitate bacterial translocation (BT). Bombesin (BBS), a tetradecapeptide analogous to mammalian gastrin-releasing peptide, can induce the release of all gut hormones except secretin. This study examined the effects of BBS on mucosal immunity in rats after thermal injury. METHODS: Forty-two Sprague-Dawley rats were divided into one sham control group and six burn groups. Burn groups were subjected to 35% total body surface area burn injury. One to 6 days after the injury, six animals (one from each group) were killed every 24 hours. Biliary secretory immunoglobulin A (SIgA), jejunal mucosal height, intestinal permeability, and BT to the mesenteric lymph nodes (MLNs), liver, and spleen were examined. In a second experiment, three groups of rats (6 in each) received either sham treatment and saline injection, or thermal injury and saline injection, or thermal injury and BBS injection. Twenty-four hours after burns or sham treatment, six animals (1 from each group) were killed. The biliary SIgA, jejunal mucosal height, and BT to the MLNs, liver, and spleen were examined. RESULTS: The biliary SIgA decreased to one-seventh of normal levels 1 day after burn injury, and increased thereafter. The jejunal mucosal height decreased significantly to two-thirds of the normal value 1 day after burn injury. The intestinal mucosal permeability increased significantly to three times the normal level 2 days after the burn injury, and decreased thereafter. BBA significantly reduced the BT incidence and significantly increased the biliary SIgA and jejunal mucosal height 1 day after burn injury. CONCLUSIONS: The results of this study show that, in rats, the intestinal permeability increased, the gut mucosal barrier failed, and the gut immunity deteriorated in the first few days after burn injury. BBS therapy helped to restore the postburn gut mucosal barrier in rats, by increasing biliary SIgA levels and the jejunal mucosal height.

Animals↗

PubMed2000

Evaluation of optic disc changes in severe myopia.

PURPOSE: To evaluate the changes in the optic nerve head in highly myopic subjects by means of confocal laser scanning opthalmoscope. METHODS: Using laser scanning and a three-dimensional image analysis system, we studied 114 young (21.4 +/- 1.4 years), highly myopic subjects with refractive errors greater than -8.0 D and a control group of 29 subjects (18.9 +/- 1.2 years) with myopia of -3.0 D or less. Measurements included cycloplegic refraction, corneal curvature, biometric axial length, and morphometric values of the optic disc obtained with a laser scanning disc analyzer. RESULTS: The optic disc area in highly myopic eyes was similar to that in mildly myopic eyes. However, regression analysis revealed that the optic disc area increased with axial length in subjects with severe myopia. The cup/disc ratio, the disc depth, the neuroretinal rim area, and the tilting of the disc were not significantly different between the severe and mild myopia groups. CONCLUSIONS: These findings may be useful in further investigations of myopic progression and of the mechanisms responsible for the development of myopic complications.

Adolescent↗

PubMed1999

AA-861-induced Ca(2+) mobilization in Madin Darby canine kidney cells.

The effect of 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1, 4-benzoquinone (AA-861), a 5-lipoxygenase inhibitor, on Ca(2+) mobilization in Madin Darby canine kidney (MDCK) cells has been examined by fluorimetry using fura-2 as a Ca(2+) indicator. AA-861 at 10-200 microM increased [Ca(2+)](i) concentration dependently. The signal comprised an initial rise and a sustained phase. Ca(2+) removal inhibited the Ca(2+) signals by reducing both the initial rise and the sustained phase. In Ca(2+)-free medium, pretreatment with 50 microM AA-861 abolished the Ca(2+) release induced by thapsigargin (1 microM), an endoplasmic reticulum Ca(2+) pump inhibitor, and carbonylcyanide m-chlorophenylhydrazone (CCCP; 2 microM), a mitochondrial uncoupler. Pretreatment with CCCP, thapsigargin and gly-phe-beta-naphthylamide to deplete the Ca(2+) stores in mitochondria, the endoplasmic reticulum, and lysosomes, respectively, only partly inhibited AA-861-induced Ca(2+) release. This suggests AA-861 released Ca(2+) from multiple internal pools. Addition of 3 mM Ca(2+) induced a [Ca(2+)](i) rise after pretreatment with 50 microM AA-861 in Ca(2+)-free medium. AA-861 (50 microM)-induced internal Ca(2+) release was not altered by inhibition of phospholipase C with U73122 (2 microM) but was inhibited by 40% by inhibition of phospholipase A(2) with aristolochic acid (40 microM). Collectively, we found that AA-861 increased [Ca(2+)](i) in MDCK cells by releasing Ca(2+) from multiple internal stores in a manner independent of the formation of inositol-1,4,5-trisphosphate, followed by Ca(2+) entry from external medium.

Animals↗

PubMed1999

Tea consumption: fluid intake and bladder cancer risk in Southern Taiwan.

OBJECTIVES: To determine whether tea consumption and intake of other beverages increases bladder cancer risk. METHODS: A case-control study was conducted in Kaohsiung, Taiwan between August 1996 and June 1997. Index patients studied were consecutive patients with histologically confirmed, newly diagnosed bladder cancer in two major hospitals. For each patient, 4 controls were selected from patients with non-neoplastic and nonurologic diseases undergoing surgical operations in the same hospital and individually matched by sex, age, and date of admission. Using a structured questionnaire, a trained interviewer interviewed 40 patients and 160 controls. Conditional logistic regression analysis adjusting for ethnicity, family history, and smoking status and matching variables were used to estimate the odds ratio (OR) and 95% confidence interval (CI). RESULTS: Tea consumption overall was associated with increased bladder cancer risk (OR 3.29, 95% CI 1.34 to 8.05). Compared with non-tea drinkers, the odds ratios of bladder cancer for oolong tea drinkers was 3.00 (95% CI 1.20 to 7.47); for non-oolong tea drinkers (black and/or other green tea), it was 14.86 (95% CI 2.13 to 103.83). The risk was greater among those who began to drink tea before age 40 (OR 9.50, 95% CI 2.39 to 37.75) and those who had been drinking tea for more than 30 years (OR 17.75, 95% CI 3.00 to 105.17). Coffee, tap water, and alcohol consumption were associated with a slightly increased risk, and both soy juice and rice juice consumption were associated with reduced risk; none of these odds ratio estimates were statistically significant, however. CONCLUSIONS: Our results suggest that tea consumption is associated with an increased risk of bladder cancer.

Aged↗

PubMed1999

The efficacy of potassium citrate based medical prophylaxis for preventing upper urinary tract calculi: a midterm followup study.

PURPOSE: We examined the efficacy of potassium citrate based medical prophylaxis for preventing upper urinary calculous recurrence, and compared it with the stone recurrence rate in patients who only received intermittent or no medical prophylaxis. MATERIALS AND METHODS: We retrospectively reviewed the records of 493 patients with upper urinary calculi, of whom 237 men and 76 women with a mean age of 56.1 and 51.4 years, respectively, were enrolled in the study. Of the 313 participants 64 (group 1, 20.4%) received regular medical prophylaxis for 24 to 42 months (mean 27.8), 80 (group 2, 25.6%) received intermittent medical prophylaxis for 1.5 to 19 months (mean 7.9) and 169 (group 3, 54%) did not receive any medical prophylaxis. RESULTS: At midterm followup of 24 to 60 months 107 patients (34.2%) had stone recurrence. In group 1 the stone recurrence rate was 7.8%, which was significantly less (p <0.001) than in groups 2 (30%) and 3 (46.2%). Similarly new calculous events in patients with a history of multiple stone recurrence were less frequent in group 1 than in groups 2 and 3 (9.7, 47.4 and 52.2%, respectively, p <0.001). Multiple stone recurrence history, hypercalciuria, hyperuricosuria and calcium oxalate dihydrate calculi were independent risk factors for stone recurrence. CONCLUSIONS: Regular medical prophylaxis may effectively prevent stone recurrence regardless of previous treatment modalities, stone composition, metabolic abnormalities and stone-free status. Cost effectiveness, patient compliance and gastrointestinal upset may limit patient acceptability and clinical use of medical prophylaxis. However, patients with a history of multiple stone recurrence, calcium oxalate dihydrate stones, hypercalciuria and hyperuricosuria benefit from regular medical prophylaxis.

Adult↗