Preoperative prediction and histological stratification of intracranial solitary fibrous tumours by machine-learning models.

AIM: To explore the effectiveness and feasibility of machine-learning models based on magnetic resonance imaging (MRI) radiomics features in differentiating intracranial solitary fibrous tumour (ISFT) from angiomatous meningioma (AM) and stratifying ISFT histologically. MATERIALS AND METHODS: This study retrospectively recruited 268 patients with a histological diagnosis of ISFT (n=120) or AM (n=148), and 116 of the ISFT patients were used for stratified analysis of histological grade. The radiomics features were extracted from axial T1-weighted imaging (WI), T2WI and contrast-enhanced T1WI sequences. All patients were assigned randomly to the training group and test group in a ratio of 7:3. The models were optimised by 10-fold cross-validation in the training group, and the independent test group was used for further testing of the models. The performances of machine-learning models based on radiomics, clinical, and fusion features in predicting and stratifying ISFT were evaluated. RESULTS: ISFT and AM differed significantly in terms of age, tumour shape, enhancement pattern, and margin. There was no significant difference in the clinical characteristics between World Health Organization (WHO) grade II and WHO grade III ISFT. When used to differentiate ISFT from AM, the area under the curve (AUC) values of the machine-learning models based on radiomics, clinical, and fusion features in the test group were 0.917, 0.923 and 0.950, respectively. When used for histological stratification of ISFT, the model based on the radiomics signature achieved an AUC value of 0.786 in the test group. CONCLUSIONS: Machine-learning models can contribute in the prediction and histological stratification of ISFT non-invasively, which can help clinical differential diagnosis and treatment decisions.

[Two families with Birt-Hogg-Dubé syndrome:case report and literature review].

Objective: To improve the awareness of Birt-Hogg-Dubé syndrome. Methods: We performed a retrospective analysis with two families of Birt-Hogg-Dubé syndrome (BHD syndrome) diagnosed in Department of Respiratory and Critical Care Medicine, Shenzhen People's Hospital from 2020 to 2021. Clinical manifestations, imaging features, diagnosis and gene detection results were summarized. Relative literatures were reviewed in Wanfang Database and PubMed from 2015 to 2021 by using the search terms of "BHD syndrome" "Birt-Hogg-Dubé" "Birt-Hogg-Dubé syndrome", respectively. Results: The probands of both families were female, aged 37 and 34 years respectively. The onset manifestation was pulmonary bullae combined with pneumothorax. Chest computed tomography (CT) imaging showed multiple pulmonary cysts in both lobes, and no skin lesions or renal tumors were found in either case. History of pneumothorax was present in Family 1 while absent in Family 2. The FLCN gene of the two probands and their relatives showed the same mutation site. Totally 12 Chinese literatures and 394 English literatures were retrieved, among which 96 reported lung involvement only. A total of 10 literatures about Chinese population were screened out from the English literatures, and 115 patients, 31 males and 84 females, were included. The incidence of spontaneous pneumothorax was 66.95% (77/115), while a family history of pneumothorax was 88.31%(68/77). The onset age of spontaneous pneumothorax was between 30 and 44 years. The most common mutation site of FLCN was c.1285dup. Conclusions: BHD syndrome in Asian population may only have lung involvement. Patients with pneumothorax and pulmonary cystic lesions should be inquired of the family history. We speculate that there are many underdiagnosed cases in clinical practice.

Bone density in youth with prediabetes: results from the National Health and Nutrition Examination Survey, 2005-2006.

Youth with type 2 diabetes might have suboptimal peak bone mass, but it is unknown whether similar effects are evident in youth with prediabetes. Results from this study suggest that diabetes-related effects on peak bone mass likely occur before disease onset, and involve the muscle-bone unit. INTRODUCTION: Type 2 diabetes might adversely influence bone health around the age of peak bone mass, but it is unknown whether diabetes-related effects on areal bone mineral density (aBMD) are evident in youth with prediabetes. We compared age-related trends in aBMD and associations between lean body mass (LBM) and aBMD between children and adolescents with prediabetes vs. normal glucose regulation. METHODS: Cross-sectional analysis of data from the National Health and Nutrition Examination Survey (2005-2006) in youth ages 12-20 years (49% female, 34% black) with prediabetes (n = 267) and normal glucose regulation (n = 1664). Whole body aBMD and LBM were assessed via DXA. LBM index (LBMI) and Z-scores for aBMD and LBMI were computed. RESULTS: Unadjusted between-group comparisons revealed greater mean weight and LBMI Z-scores in youth with prediabetes vs. normal glucose regulation, but similar bone Z-scores between the two groups. While accounting for differences in BMI Z-score, there was a significant interaction between prediabetes status and age with respect to whole body aBMD Z-score (P < 0.05), such that children with prediabetes tended to have increased aBMD but adolescents and young adults with prediabetes tended have lower aBMD. Furthermore, the positive association between LBMI and whole body aBMD was moderated in youth with prediabetes (P < 0.001), who had slightly lower whole body aBMD for a given LBMI (P = 0.068). Lumbar spine bone measures did not differ between the two groups. CONCLUSIONS: Type 2 diabetes-related threats to peak bone mass might occur prior to disease onset, therefore potentially impacting a considerable proportion of US youth.

Nocturia and electrocardiographic abnormalities among patients at an inner-city cardiology clinic.

AIMS: Nocturia has been increasingly recognized as a potential manifestation of cardiovascular disease. However, the relationship between nocturia and electrocardiographic (ECG) abnormalities has not been studied. This study aims to characterize the diagnostic utility of nocturia in identifying left ventricular hypertrophy (LVH), left atrial enlargement (LAE), and prolonged QTc on ECG. METHODS: Retrospective analysis of nocturnal voiding frequency and contemporaneous ECG data from consecutive patients evaluated at a university-based outpatient cardiology clinic. Three sets of three incremental binary multiple logistic regression models controlling for (1) age, (2) sex and race, and (3) body mass index, hypertension, diabetes mellitus, and diuretic utilization were performed to determine whether nocturia was predictive of LVH, LAE, and prolonged QTc. RESULTS: Included patients (n = 143, 77.6% nocturia) were predominantly African-American (89.5%), female (74.1%), and obese (61.5%), of whom 44.1%, 41.3%, and 27.3% had LVH, LAE, and prolonged QTc, respectively. Older age, African-American race, obesity, hypertension, diuretic use, LVH, and LAE were significantly associated with nocturia on univariate analysis. No significant differences were observed in the strength of associations between nocturia and LVH, LAE, or QTc prolongation based on age. Nocturia independently predicted LVH in Models I-III (odds ratios [ORs], 2.99-3.20; relative risks [RRs], 1.18 for all, p ≤ .046) and LAE in Models I-III (ORs, 4.24-4.72; RRs, 1.21 for all, p ≤ .015). No significant associations were observed between nocturia and prolonged QTc. CONCLUSIONS: Nocturia may be a risk marker for underlying structural cardiac abnormalities.

Down-regulation of MIAT suppresses osteosarcoma progression by acting as a ceRNA for miR-141-3p to regulate SIX1-mediated PI3K/AKT pathway.

OBJECTIVE: Osteosarcoma (OS) is a frequent bone malignancy. Long non-coding RNA myocardial infarction associated transcript (MIAT) has been reported to be involved in the development of human cancers, including OS. However, the mechanism underlying MIAT in OS progression remains largely unclear. PATIENTS AND METHODS: The expression levels of MIAT and sineoculis homeobox homolog 1 (SIX1) in OS tissues and cells were detected by quantitative real-time polymerase chain reaction and Western blot. Cell viability, apoptosis, migration and invasion of OS cells were determined by MTT, flow cytometry and trans-well assays, respectively. The target interaction among MIAT, miR-141-3p and SIX1 was analyzed by bioinformatics analysis and luciferase reporter assay. Phosphatidylinositide 3-kinases (PI3K)/protein kinase B (AKT) pathway was evaluated by Western blot. RESULTS: MIAT and SIX1 expression levels were enhanced in OS tissues and cells. Knockdown of MIAT or SIX1 repressed cell viability, migration and invasion but promoted apoptosis in OS cells. Moreover, overexpression of SIX1 reversed the inhibitive role of MIAT silence in OS progression. Furthermore, MIAT could increase SIX1 expression by competitively sponging miR-141-3p. Besides, inhibition of MIAT blocked PI3K/AKT pathway by decreasing SIX1 in OS cells. CONCLUSIONS: MIAT silence suppresses OS progression through inactivating PI3K/AKT signaling by sponging miR-141-3p to regulate SIX1, indicating a novel target for the treatment of OS.

Sodium restriction improves nocturia in patients at a cardiology clinic.

This study aims to determine whether dietary sodium restriction counseling decreases nocturnal voiding frequency in cardiology patients with concomitant nocturia. Patients who had established care at a cardiology clinic from 2015 to 2018 reporting ≥1 average nocturnal void(s) underwent a comprehensive sodium intake interview by their cardiologist, who provided them with individualized strategies for dietary sodium reduction and assessed adherence at follow-up. Average nocturnal voiding frequency and dietary adherence were documented in the medical record. A nocturia database was compiled for retrospective analysis. A total of 74 patients were included. Patients considered to be adherent with dietary sodium restriction at follow-up (n = 56) demonstrated a decrease in median nocturia frequency (2.5 [2.3-3.0] vs 1.0 [1.0-2.0] voids, P < .001). Among nonadherent patients (n = 18), median nocturia frequency did not significantly change from baseline to follow-up (2.0 [1.5-3.8] vs 2.0 [1.5-4.8] voids, P = .423). Median changes were significantly different between the adherent and nonadherent groups (P < .001). Examination of second follow-up available from 37 patients showed a continued effect. In conclusion, adherence with dietary sodium counseling appears to improve nocturia. Accordingly, dietary modification may represent an important adjunct therapy to lifestyle and pharmacologic interventions for decreasing nocturia frequency. Reduction in nocturnal voiding frequency may also reflect an additional benefit of dietary sodium restriction in accordance with best practice standards for cardiovascular disease.

Time of peak nocturnal diuresis rate between men with secondary nocturnal polyuria versus nocturnal polyuria syndrome.

AIM: Compare the circadian trajectory of diuresis between nocturnal polyuria (NP) patients with versus without identifiable contributory comorbidities. METHODS: Retrospective analysis of frequency-volume charts from male patients with clinically-significant nocturia (≥2 nocturnal voids) and NP (defined by nocturnal urine production [NUP] ≥90 mL/hour or nocturnal polyuria index [NPi] ≥0.33). Patients with NP and chronic kidney disease, congestive heart failure, and/or undertreated obstructive sleep apnea (OSA) were deemed to have secondary NP. Nocturnal polyuria syndrome (NPS) was defined as NP without edema, loop diuretic use, or the aforementioned conditions. Patients with diabetes insipidus or OSA with appropriate continuous positive airway pressure utilization were excluded. The timing and volumes of nocturnal voids were used to derive "early" and "late" nocturnal diuresis rates (mL/hour of urine produced before and after the first nocturnal awakening, respectively). The likelihood of an early peak nocturnal diuresis rate (ie, early >late nocturnal diuresis rate) was compared between patients with NPS versus secondary NP using both a crude and adjusted odds ratio. RESULTS: The likelihood of an early peak nocturnal diuresis rate in patients with NPS compared with secondary NP was 2.58 (1.05-6.31) at NUP ≥ 90 mL/hour and 1.96 (0.87-4.42) at NPi ≥ 0.33 on crude analysis, and 2.44 (0.96-6.24) and 1.93 (0.83-4.48) after adjustment, respectively. CONCLUSIONS: A peak early nocturnal diuresis rate was significantly more likely in patients with NPS at NUP ≥ 90 mL/hour, with similar odds ratios at NPi ≥ 0.33 and following adjustment. Delineating nocturic patients by NP subgroup may facilitate more individualized management. PATIENT SUMMARY: Many people have to wake up to urinate because they produce too much urine at night-a condition known as "nocturnal polyuria." Nocturnal polyuria might be caused by drinking too much fluid, other behavioral factors, or conditions that make your body hold on to too much fluid, like heart disease, kidney disease, and sleep apnea. In cases of nocturnal polyuria where no clear cause can be identified, it is thought that patients may suffer from a deficiency in nighttime vasopressin, a hormone that plays a key role in how much urine you produce. In this study, we compared the pattern of nighttime urine production in patients with different causes of nocturnal polyuria, which may lead to more personalized treatment options for patients with this condition.

Differential Nocturnal Diuresis Rates Among Patients with and Without Nocturnal Polyuria Syndrome.

BACKGROUND: The mechanism of nocturnal polyuria (NP), a leading cause of nocturia, is poorly understood. OBJECTIVE: To characterize NP in terms of diuresis rate changes before and after the first nocturnal awakening. DESIGN, SETTING, AND PARTICIPANTS: A frequency-volume chart (FVC) database of 773 entries from 440 veterans treated at a Veterans Affairs urology clinic was analyzed. The first FVCs completed by male patients aged ≥18 years with two or more nocturnal voids were included. Patients were excluded if they were taking diuretics or had sleep apnea, heart failure, edema, kidney disease, or diabetes insipidus. The 130 included individuals were divided into two cohorts: patients with NP and patients below this threshold. Analyses were performed using two different cutoffs for NP: nocturnal urine production (NUP) >90ml/h and nocturnal polyuria index (NPi) >0.33. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: We compared "early nocturnal diuresis rate" (ENDR; first nocturnal voided volume/length of first uninterrupted sleep period), "late nocturnal diuresis rate" (LNDR; remaining nocturnal urine volume/remaining hours of sleep), and diurnal diuresis rate (daytime urine volume/hours awake) in patients with the nocturnal polyuria syndrome (NPS). RESULTS AND LIMITATIONS: Within groups, there were significant differences between ENDR and LNDR for NPS patients at NUP >90ml/h (152 vs 120ml/h, p=0.02) and NPi >0.33 (120 vs 91ml/h, p=0.02) but not for those without NPS at NUP ≤90ml/h (60 vs 59ml/h, p=0.29) or NPi ≤0.33 (75 vs 75ml/h, p=0.25). Limitations include retrospective design, single institution participation, and small sample size. CONCLUSIONS: There exists a significant drop-off in nocturnal diuresis rate after the time of first awakening that is unique to patients with NPS. The large volume of urine produced in the early hours of sleep may provide the specific substrate for short-acting antidiuretics approved for use in patients with nocturia owing to NPS. PATIENT SUMMARY: We analyzed adult males diagnosed with nocturnal polyuria syndrome to determine how their rate of urine production changed throughout the night. Our finding that these individuals produce urine at the highest rate in the early hours of sleep suggests that they may benefit from pharmaceuticals specifically designed to reduce urine production during this period.

MiR-652-3p promotes bladder cancer migration and invasion by targeting KCNN3.

OBJECTIVE: Increasing evidence indicated that microRNAs (miRNAs) are crucial regulators for cancer development. Bladder cancer (BCa) is a major threat to human health. The aim of this study was to analyze the roles of miR-652-3p in BCa, and to explore the associated mechanisms. MATERIALS AND METHODS: MiR-652-3p expression in BCa cell lines was explored using Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) method. MiR-652-3p expression level in BCa tissues was explored at StarBase. Cell Counting Kit-8 (CCK-8) assay, wound-healing assay, and transwell invasion assay were conducted to investigate the biological roles of miR-652-3p. The underlying mechanisms of miR-652-3p in NSCLC were investigated using luciferase activity reporter assay and rescue experiments. RESULTS: We showed that miR-652-3p expression level was upregulated in both BCa tissues and cell lines. The knockdown of miR-652-3p significantly inhibited BCa cell proliferation, migration, and invasion in vitro. Moreover, we showed that potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3 (KCNN3) was a functional target for miR-652-3p. Besides, the expression of KCNN3 in BCa tissues was negatively correlated with miR-652-3p. CONCLUSIONS: Collectively, these results showed that miR-652-3p could promote BCa cell proliferation, migration, and invasion via directly regulating KCNN3, which may provide a novel therapeutic target for BCa treatment.

Comparison of nocturia etiology in black and white male patients.

INTRODUCTION: Much of what is known about the etiology of nocturia (i.e., nocturnal polyuria [NP], small bladder capacity [SBC], etc.) at the population level stems from the Krimpen study, which enrolled aging males from a homogenous municipality in the Netherlands. Given the higher prevalence of benign prostatic hyperplasia and overactive bladder in black versus white males in population research, we aim to test the hypothesis that black males seeking treatment for lower urinary tract symptoms (LUTS) are more likely to have nocturia owing to SBC. MATERIALS AND METHODS: We retrospectively analyzed 24 hour frequency-volume charts (FVCs) completed by males seeking treatment for LUTS at a Veterans Affairs urology clinic from 2008-2016. Patients were included if they were ≥ 18 years, identified as either Caucasian or African American, and had a complete baseline FVC showing ≥ 1 nocturnal void. Patients were stratified by race and classified as having nocturia owing to SBC (defined by a maximum voided volume < 200 mL or a nocturnal bladder capacity index > 1.3); NP (defined by a nocturnal polyuria index > 0.33); 'mixed' (SBC + NP); or 'other' (neither SBC nor NP). RESULTS: Between white and black patients, 28 (24%) versus 28 (26%) had NP, 32 (27%) versus 33 (30%) had SBC, and 35 (30%) versus 30 (28%) had mixed nocturia. Overall, there was no difference in distribution of underlying etiology by race (p = 0.51). CONCLUSIONS: Our results demonstrate no difference in the etiology of nocturia between black and white males. Accordingly, race should not play a role in the evaluation of patients seeking treatment for nocturia.

Overnight Urge Perception in Nocturia Is Independent of Depression, PTSD, or Anxiety in a Male Veterans Administration Population.

STUDY OBJECTIVES: The goal of this study was to compare the urge perception associated with nocturnal voiding at the time of voiding in individuals with and without depression, posttraumatic stress disorder (PTSD), or anxiety diagnoses to test the hypothesis that patients with such diagnoses are more likely to experience insomnia-driven convenience voiding during the sleep period. METHODS: A database of voiding diaries with urge perception grades (UPGs) from 429 adult males seeking treatment for nocturia at a Veterans Affairs-based urology clinic was analyzed. The UPG categorizes perception for urinating from 0 (out of convenience) to 4 (desperate urge). Diaries completed by males age 18 years and older showing ≥ 2 nocturnal voids were included. Those included (n = 178) were divided into two cohorts based on the presence (n = 62) or absence (n = 116) of one or more previously established mental health diagnoses (depression, PTSD, or anxiety). The chi-square test was used to determine significance between groups. RESULTS: Patients with a mental health diagnosis were more likely to report convenience voiding compared to those without depression, PTSD, or anxiety (14.5% versus 0.8%, P < .01). However, most voids in both groups were associated with the perception of urinary urgency. There were no differences in urinary volumes or hourly rates of urine production between the groups. CONCLUSIONS: A relatively small subset of urology patients experience nocturnal voiding because they are awake for reasons other than the urge to void. Mental health factors had a substantial, albeit minimal, effect. Most nocturia reflects urgency to urinate rather than voiding by convenience.

SETD2-mediated crosstalk between H3K36me3 and H3K79me2 in MLL-rearranged leukemia.

Previously, we identified SETD2 loss-of-function mutations in 22% of MLL-rearranged (MLLr) acute leukemia patients, implicating a mechanism for cooperativity between SETD2 mutations and MLL fusions. However, the detailed mechanism of how SETD2-H3K36me3 downregulation accelerates MLLr leukemia remains unclear. Here, we show that in MLLr leukemia, both H3K79me2 and H3K36me3 are aberrantly elevated and co-enriched in a group of genes. SETD2 inactivation leads to a global reduction of H3K36me3 and a further elevation of H3K79me2, but does not change the expression of known MLL fusion target genes. Instead, this pattern of histone changes is associated with transcriptional deregulation of a novel set of genes; downregulating tumor suppressors (for example, ASXL1) and upregulating oncogenes (for example, ERG). Taken together, our findings reveal a global crosstalk between the oncogenic DOT1L-H3K79me2 axis and the tumor suppressive SETD2-H3K36me3 axis in gene regulation, provide molecular insights into how SETD2 mutations accelerate MLLr leukemogenesis through differential regulation of additional tumor suppressors and oncogenes.

miR-199a impairs autophagy and induces cardiac hypertrophy through mTOR activation.

Basal autophagy is tightly regulated by transcriptional and epigenetic factors to maintain cellular homeostasis. Dysregulation of cardiac autophagy is associated with heart diseases, including cardiac hypertrophy, but the mechanism governing cardiac autophagy is rarely identified. To analyze the in vivo function of miR-199a in cardiac autophagy and cardiac hypertrophy, we generated cardiac-specific miR-199a transgenic mice and showed that overexpression of miR-199a was sufficient to inhibit cardiomyocyte autophagy and induce cardiac hypertrophy in vivo. miR-199a impaired cardiomyocyte autophagy in a cell-autonomous manner by targeting glycogen synthase kinase 3ß (GSK3ß)/mammalian target of rapamycin (mTOR) complex signaling. Overexpression of autophagy related gene 5 (Atg5) attenuated the hypertrophic effects of miR-199a overexpression on cardiomyocytes, and activation of autophagy using rapamycin was sufficient to restore cardiac autophagy and decrease cardiac hypertrophy in miR-199a transgenic mice. These results reveal a novel role of miR-199a as a key regulator of cardiac autophagy, suggesting that targeting miRNAs controlling autophagy as a potential therapeutic strategy for cardiac disease.

Contribution of calpain to myoglobin efflux from cardiomyocytes during ischaemia and after reperfusion in anaesthetized rats.

AIM: Calpain activation has a putative role in ischaemia-reperfusion injury of cardiomyocytes. This study clarified the in vivo contribution of calpain to disruption of cardiomyocyte sarcolemma during ischaemia and after reperfusion in anaesthetized rats. METHODS: Using a microdialysis technique in the hearts of anaesthetized rats, we investigated the effects of the calpain inhibitors on myocardial interstitial myoglobin level in the ischaemic region during coronary occlusion and after reperfusion. The calpain inhibitors were administered locally via a dialysis probe. Two durations of coronary occlusion were tested. RESULTS: Thirty-minute coronary occlusion: dialysate myoglobin concentration increased markedly from 385 ± 46 ng mL(-1) at baseline to 3701 ± 527 ng mL(-1) at 20-30 min of occlusion. After reperfusion, dialysate myoglobin concentration further increased, reaching a peak (12 296 ± 1564 ng mL(-1) ) at 10-20 min post-reperfusion and then declined gradually. The calpain inhibitors, MDL-28170 and SNJ-1945 did not change dialysate myoglobin concentration during occlusion but attenuated the increase after reperfusion to 6826 ± 1227 and 8130 ± 938 ng mL(-1) at 10-20 min post-reperfusion (P < 0.05), respectively. Ninety-minute coronary occlusion: dialysate myoglobin concentration increased from 516 ± 33 ng mL(-1) at baseline to 5463 ± 387 ng mL(-1) at 80-90 min after occlusion. After reperfusion, there was no significant increase in dialysate myoglobin concentration. MDL-28170 did not affect dialysate myoglobin concentration during occlusion or after reperfusion. CONCLUSION: Calpain contributes to sarcolemmal disruption immediately after reperfusion following 30-min coronary occlusion, but has little effects during ischaemia and after reperfusion in 90-min coronary occlusion.

Contribution of serotonin uptake and degradation to myocardial interstitial serotonin levels during ischaemia-reperfusion in rabbits.

AIM: Although deleterious effects of serotonin (5-HT) have been demonstrated during myocardial ischaemia-reperfusion, little information is available on myocardial interstitial 5-HT kinetics. This study evaluated the contribution of 5-HT reuptake and degradation to myocardial interstitial 5-HT levels during ischaemia-reperfusion. METHODS: Using microdialysis technique in anaesthetized rabbits, we monitored myocardial interstitial 5-HT levels in the ischaemic region during ischaemia (30 min) followed by reperfusion (60 min) and investigated the effects of local infusion of fluoxetine, a 5-HT uptake inhibitor, and/or pargyline, a monoamine oxidase inhibitor. RESULTS: In vehicle control, dialysate 5-HT concentration increased gradually from 16 ± 3 at baseline to 85 ± 18 nM during 20-30 min of ischaemia. Dialysate 5-HT concentration further increased to 236 ± 47 nM at 0-10 min of reperfusion and then began to decline. Averaged 5-HT concentration was 61 ± 11 during ischaemia and 113 ± 13 nM during reperfusion. Fluoxetine elevated dialysate 5-HT level at baseline and at 10-30 min of reperfusion; it increased averaged dialysate 5-HT concentration by approx. 304% during reperfusion compared to control. Pargyline elevated averaged dialysate 5-HT concentration during ischaemia by approx. 243% and that during reperfusion by approx. 250% compared to control. The changes in dialysate 5-HT concentration by fluoxetine + pargyline were similar to those of fluoxetine alone. CONCLUSION: The 5-HT reuptake function plays an important role in the clearance of myocardial interstitial 5-HT during reperfusion. When 5-HT reuptake function is intact, degradation of 5-HT by monoamine oxidase contributes to reduce myocardial interstitial 5-HT level throughout ischaemia-reperfusion.

Palladium film decoupler for amperometric detection in electrophoresis chips.

Demonstrated in this article is that a palladium metal film can be applied to decouple the electric circuitry of electrochemical detection from that of the electrophoretic separation in an electrophoresis chip. The Pd solid-state field decoupler, as well as the working electrodes, is thermally evaporated onto the plastic chip and oriented vertically across the separation channel. After the sample zones flow over the Pd decoupler, their electrochemical response is measured at working electrodes in the downstream pathway. Because the electrodes are on the separation channel, the electrode channel alignment is no longer a problem. For a separation channel of roughly 200 microm in width and 75 microm in depth in 10 mM phosphate (pH 5.1), the noise level at the working electrode is < 15 pA at an electric field of 570 V/cm.

L-Altruronic acid formed by epimerization of D-galacturonic acid methyl esters during saponification of citrus pectin.

While searching for oligosaccharides containing rhamnose residues in the endopolygalacturonase (EPG) digest of saponified citrus pectin, we found several oligomers containing, in addition to galacturonic acid, a sugar previously unreported in pectin. The 1- and 2-D 1H NMR spectra of the oligosaccharides were consistent with the sugar being a uronic acid with its 2- and 3-hydroxyls being axial and 4-hydroxyl being equatorial. MALDI-TOF mass spectrometry indicated that the oligomers consisted solely of uronic acids. Reduction of the uronic acids in the oligosaccharides converted them to galactose and altrose. The altrose was found to be the L enantiomer by comparison of its trimethylsilyl (-)-2-butyl glycosides to those of authentic D-altrose and a racemic mixture. The sugar was not found in oligosaccharides prepared from EPG digestion of citrus pectin deesterified with pectin methylesterase rather than saponification. Thus, it appears that during saponification, a small proportion of the methylesterified galacturonic acid residues in pectins is epimerized at C-5 leading to formation of L-altruronic acid residues.

Determination of urine catecholamines by capillary electrophoresis with dual-electrode amperometric detection.

Demonstrated in this study is that without pretreatment and preconcentration nanomolar-level catecholamines in human urine samples can be quantitatively determined with ease by utilizing capillary electrophoresis coupled with amperometric detection. The detector employs a parallel-opposed dual-electrode scheme assembled with an on-capillary electrode and a disk electrode and takes advantage of the redox cycling of analytes between the two working electrodes to improve the limit of detection. The matrix effect of urine samples significantly decreases the detection sensitivity from that obtained in standard solutions. Therefore, calibration curves derived from standard solutions cannot be used in quantitative determination of catecholamines. Methods of standard addition and internal standard have been studied. The results suggest that isoproterenol is a good internal standard to facilitate the measurements of dopamine, epinephrine, and norepinephrine in human urine samples.