bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum Ionized versus Total Magnesium in Patients with Chronic Renal Disease
Authors: Saha H. , Harmoinen A. , Nisula M. , Pasternack A. 
Published: April 2003

<b>Background:</b> Recent technology has made it possible to assess serum ionized magnesium with user-friendly ion-selective electrodes similar to measurement of the serum calcium concentration. <b>Methods: </b>We measured the serum ionized (Mg<sup>2+</sup>) and total magnesium (tMg) concentration in 69 patients with chronic kidney disease (38 men, 31 women, age 22–85 years) and in 75 control subjects. <b>Results: </b>In control subjects the reference ranges were as follows: serum Mg<sup>2+</sup> 0.45–0.67 mmol/l, and tMg 0.67–0.96 mmol/l. In patients with chronic renal failure serum Mg<sup>2+</sup> was 0.57 ± 0.05 mmol/l and tMg 0.80 ± 0.11 mmol/l, and in transplant recipients receiving cyclosporine 0.53 ± 0.05 and 0.71 ± 0.10 mmol/l, respectively. The correlation coefficient between serum Mg<sup>2+</sup> and tMg was r = 0.73 (p < 0.001) in the patient group and r = 0.75 (p<0.001) in control subjects. Serum tMg was below the reference range in 15 of 69 measurements. However, serum Mg<sup>2+</sup> was below the reference range in only 1 of these 15 samples. Hence, 14 of 69 cases with low tMg but normal Mg<sup>2+</sup> were false-positive with respect to hypomagnesemia. <b>Conclusion: </b>We conclude that tMg may overestimate the incidence of hypomagnesemia, and the measurement of Mg<sup>2+</sup> may be of benefit when studying patients with expected hypomagnesemia.
Plasma Soluble Fas and Soluble Fas Ligand in ChronicGlomerulo nephritis
Authors: Sano Hirotake , Asano Kiyoji , Minatoguchi Shinya , Hiraoka Jitsuko , Fujisawa Koh , Nishigaki Kazuhiko , Yasuda Norio , Kumada Hirokazu , Takemura Masao , Ohashi Hiroshige , Seishima Mitsuru , Fujiwara Takako , Fujiwara Hisayoshi 
Published: April 2003

It has been reported that glomerular cells with apoptosis and positive Fas immunoreactivity are seen in proliferative glomerulonephritis (PGN). Fas induces apoptosis when it binds to Fas ligand (Fas-L) or soluble Fas-L (sFas-L). However, soluble Fas (sFas) blocks apoptosis by inhibiting binding between Fas and Fas-L or sFas-L. That is, Fas, Fas-L, and sFas-L are inducers of apoptosis, but sFas is an inhibitor of apoptosis. We studied the relationship between the plasma levels of sFas and sFas-L in 32 patients with various types of adult chronic glomerulonephritis. Patients with serum creatinine levels >1.5 mg/dl (132.6 µmol/l) were excluded. The plasma levels of sFas-L were within the normal limits in all patients. The plasma levels of sFas in the patients with minimal-change (n = 8) and membranous nephropathy (n = 7) were similar to the age- and sex-matched controls. However, the plasma sFas levels were significantly elevated in patients with mesangial PGN (n = 10) and membranoproliferative glomerulonephritis (n = 7)(3.4 ± 0.9 and 3.9 ± 1.5 ng/ml, respectively) as compared with the age- and sex-matched controls (controls: 2.1 ± 0.4 and 2.2 ± 0.6 ng/ml, respectively). In PGN, according to increase of histological grade and decrease of creatinine clearance, the number of TUNEL-positive cells in glomeruli is decreased in spite of an increase of the Fas positivity, and plasma sFas is increased. The degree of proliferative change is determined by the balance between proliferation and apoptosis and/or necrosis. Therefore, increased plasma sFas in PGN may inhibit apoptosis in glomeruli and may be one of the progressing factors in PGN. Thus, we conclude that an increase in plasma sFas levels is important to the protection of apoptosis in PGN.
Glomerular Extracellular Matrix Accumulation in Experimental Anti-GBM Ab Glomerulonephritis
Authors: Tang Winson W. , Feng Lili , Loskutoff David J. , Wilson Curtis B. 
Published: April 2003

Thickening of the glomerular basement membrane (GBM) results from excessive accumulation of extracellular matrix (ECM) proteins following glomerular injury. We studied the temporal relationship between the expression of growth factors, ECM accumulation, ECM degrading proteinases, and their inhibitors in a rat model of anti-GBM antibody (Ab) glomerulonephritis (GN) by the RNase protection assay and immunohistochemistry. There were two- or fourfold increases in the expression of transforming growth factor-β<sub>1</sub> (TGF-β<sub>1</sub>) and platelet-derived growth factor (PDGF) A and B chain mRNAs 4 days after anti-GBM Ab administration. These changes were temporally associated with increased accumulation of α1(III) and α2(IV) collagens, fibronectin, and heparan sulfate proteoglycan along the GBM. The increase in matrix accumulation was associated with little or no increases in the proteinases, urokinase plasminogen activator (u-PA) and transin, respectively. There was a 1.6× increase in the u-PA/28s mRNA ratio on day 4 in rats with anti-GBM Ab GN, but this was not associated with an increase in u-PA biologic activity. By comparison, the mRNAs of the proteinase inhibitors, plasminogen activator inhibitor-1 (PAI-1) and tissue inhibitor of metalloproteinase (TIMP) were 5× greater than that of control rats on day 4. PAI-1 mRNA correlate with increased biologic activity. These data demonstrate a temporal association between TGF-β<sub>1</sub> and PDGF expression and matrix accumulation within the GBM in anti-GBM Ab GN. In addition, it suggest that this matrix accumulation results from an imbalance between matrix synthesis and degradation.
Restoration of Impaired T-Cell Proliferation after Parathyroidectomy in Hemodialysis Patients
Authors: Tzanno-Martins C. , Futata E. , Jorgetti V. , Duarte A.J.S. 
Published: April 2003

<i>Background/Aims:</i> Severe secondary hyperparathyroidism is not infrequent in hemodialysis patients and recent studies suggest that parathyroid hormone (PTH) may play a role in the genesis of cell immunity abnormalities in uremia. The aim of the present study is to describe the effect of parathyroidectomy on T- and B-cell functions in hemodialysis patients. <i>Methods:</i> The study was performed on 6 patients with severe secondary hyperparathyroidism. iPTH, B, CD4<sup>+</sup>, CD8<sup>+</sup>, total number of lymphocytes, lymphoproliferative response to PHA, PWM and Candidin, and IgG, IgM, IL-2 production in vitro were determined 1 day before and 4 months after parathyroidectomy. <i>Results:</i> The lymphoproliferative response to PHA increased significantly after parathyroidectomy. We also observed a trend to an increase in production of IgG and IgM after PWM stimulation before therapy. <i>Conclusion:</i> The present study suggests that patients with extremely high levels of PTH show a complete restoration of impaired T-cell proliferation after parathyroidectomy.
Expression of Heat Shock Proteins 72/73 in Human Peritoneal Mesothelial Cells in vivo and in vitro
Authors: López-Cotarelo Cristina , Sellhaus Bernd , Baba Hideo Andreas , Manegold Edith , Luka Johanna , Handt Stefan , Mittermayer Christian , Klosterhalfen Bernd , Tietze Lothar 
Published: April 2003

Leukocyte accumulation during peritonitis leads to an injurious microenvironment which is involved in the host defense reaction but is also thought to cause peritoneal damage. We tested the hypothesis that mesothelial cells (MC) respond to the injurious microenvironment during peritonitis by an increased expression of heat shock proteins (HSP 72/73), a basic way by which cells are protected against injury. Comparison of resting MC and activated MC during peritonitis in vivo by means of immunohistochemistry revealed an increased expression of HSP 72/73. As assessed by Western immunoblotting, incubation of MC in vitro with tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) caused a time-dependent induction of HSP 72/73 expression, which was maximal 6 h after stimulation. We suggest that the increased HSP 72/ 73 expression of MC during peritonitis is in part induced by TNF-α and IL-1β and may exert a cell-protective function, lessening MC damage during peritonitis.
Melatonin, a Pineal Hormone with Antioxidant Property, Protects against Gentamicin-Induced Nephrotoxicity in Rats
Authors: Shifow A.A. , Kumar K.V. , Naidu M.U.R. , Ratnakar K.S. 
Published: April 2003

The present study investigated the effects of melatonin, an antioxidant, on gentamicin-induced nephrotoxicity in rats. Melatonin (5 mg/kg p.o.) was used 3 days before and 8 days simultaneously with gentamicin (80 mg/kg i.p.) Saline-treated animals served as controls. Determinations of urinary creatinine, N-acetyl-β-<i>D</i>-glucosaminidase, glucose, protein, blood urea, serum creatinine, plasma and kidney tissue malondialdehyde (MDA), and antioxidant enzyme levels in kidney tissue were done after 8 days of gentamicin treatment. The kidneys were also examined for morphological changes using histological techniques. Gentamicin caused nephrotoxicity as evidenced by marked elevation in blood urea and serum creatinine. Mean blood urea and serum creatinine levels were 289 ± 50, and 2.5 ± 0.5 mg/dl, respectively, in rats treated with gentamicin. Melatonin significantly protected the rats from gentamicin-induced nephrotoxicity; blood urea and serum creatinine levels were 23 ± 2.7 and 0.88 ± 0.19 mg/dl, respectively. The creatinine clearance was decreased with gentamicin treatment (0.048 ± 0.007 ml/min) as compared with controls (0.41 ± 0.08 ml/h/kg). In rats treated with melatonin plus gentamicin, the creatinine clearance was similar to controls (0.41 ± 0.08 ml/h/kg). The product of lipid peroxidation (MDA) was markedly increased in plasma (2.10 ± 0.15 nmol) and kidney tissue (8.87 ± 3.2 nmol/mg protein) with gentamicin treatment. Melatonin prevented the gentamicin-induced rise in plasma MDA (1.03 ± 0.27 nmol) and kidney tissue MDA (2.57 ± 0.87 nmol/mg protein). An increased excretion of urinary N-acetyl-β-<i>D</i>-glucosaminidase, glucose, and protein by gentamicin was also prevented by melatonin. Kidneys from gentamicin-treated rats showed tubular epithelial loss with intense granular degeneration involving more than 50% of renal cortex, while there were findings comparable to controls in melatonin plus gentamicin treated rats. The present study indicates that melatonin significantly protects against gentamicin-induced renal toxicity in Wistar rats.
Haemodialysis and Cerebral Oedema
Authors: Walters R.J.L. , Fox N.C. , Crum W.R. , Taube D. , Thomas D.J. 
Published: April 2003

<i>Background:</i> Haemodialysis may cause neurological symptoms ranging from inconvenient feelings of disequilibrium to life-threatening neurological complications. There are animal data to suggest cerebral swelling may accompany haemodialysis and contribute symptomatically to dialysis disequilibrium. However, MR images acquired following haemodialysis often fail to demonstrate evidence of cerebral oedema. We wished to quantify any potential cerebral volume change which is caused by haemodialysis treatment. <i>Method:</i> Five renal patients and 5 control subjects had a two volumetric T1-weighted MRI scans on the same day. The patients were imaged immediately before and after haemodialysis. None were taking steroids. Precise positional matching (registration) was used to quantify cerebral volume change. <i>Results:</i> Patients had an increase in cerebral volume following dialysis which averaged 32.8 ml (SE 7.4 ml, 3% brain volume). The change in the controls was 1.4 ml (SE 0.6 ml), p < 0.001. No patient had significant neurological symptoms. <i>Conclusion:</i> Cerebral oedema developed in the patients following dialysis. There is a good biological model for these observations. Modifications to dialysis may help. Common problems which increase cerebral volume, e.g. acute stroke, require careful appraisal in these patients. These observations need consideration when quantifying atrophy in dialysis patients.
Cyclosporine-Associated Thrombotic Microangiopathy during Daclizumab Induction: A Suggested Therapeutic Approach
Authors: Trimarchi H. , Freixas E. , Rabinovich O. , Schropp J. , Pereyra H. , Bullorsky E. 
Published: April 2003

A woman on daclizumab developed thrombotic microangiopathy secondary to cyclosporine after a living-unrelated kidney transplant. Despite cyclosporine discontinuation, hemolysis persisted. The second dose of daclizumab was postponed 24 h, and after a maximum of two sessions of plasmapheresis (to avoid further modifications in daclizumab schedule) with plasma exchange, daclizumab was administered. Plasma infusions were prescribed until D-dimer and fibrinogen-degradation products normalized; thereafter, FK-506 was started without recurrence of the hemolytic picture and renal function restored. This observation suggests that in patients on daclizumab who develop thrombotic microangiopathy secondary to immunosuppressants, if discontinuation of the offending drug is unsuccessful, plasmapheresis with plasma exchange can be performed when the lowest levels of daclizumab exist, followed by daclizumab infusion. Plasma prescription must be continued thereafter until D-dimer and figrinogen-degradation products normalize. However, if hemolysis persists when daclizumab levels are high, plasma infusions are useful and plasmapheresis avoided. FK-506 administration did not result in recurrence of hemolysis during daclizumab induction.
Pregnancy Outcome in Nephrotic Syndrome with Mixed Connective Tissue Disease
Authors: Horita Yoshio , Tsunoda Sei , Inenaga Takashi , Kawano Yuhei , Ishibashi-Ueda Hatsue , Chiba Yoshihide , Takishita Shuichi 
Published: April 2003

We describe two pregnancies of a young woman with mixed connective tissue disease. In June 1983, she was diagnosed as having Raynaud’s phenomenon, arthralgia, and proteinuria. She then developed nephrotic syndrome. Methylprednisolone was initially prescribed at a large dose of 1 g/day which was slowly tapered to 5 mg/day. The proteinuria disappeared. During both pregnancies (the first beginning in December 1988 and the second in May 1992), the patient was placed on a prednisolone maintenance dose (5 mg/day). Both neonates were born healthy at term with no complications. Continuing prednisolone may be useful in pregnant women, and aggressive treatment to prevent mixed connective tissue disease exacerbation may be appropriate during pregnancy.
Delayed Cerebral Atrophy following Moderate Hypoxia-Ischemia in the Immature Rat
Authors: Geddes Rastafa , Vannucci Robert C. , Vannucci Susan J. 
Published: April 2003

Hypoxia-ischemia (H/I) damages cells in the immature brain and interferes with subsequent brain development; the extent of the damage has been related to the severity, or duration, of the initial insult. This study examined the effects of both severe and moderate duration of H/I on the evolution of damage through 8 weeks of recovery. Seven-day-old rat pups were subjected to either 75 min or 2 h of 8% oxygen following a unilateral carotid artery ligation. Evaluation of brain damage included morphometric analysis of hemispheric diameter at 2, 4, and 8 weeks of recovery, and hematoxylin and eosin for evaluation of pathology at 8 weeks. Two hours of H/I produced severe infarction in the ipsilateral hemisphere in the majority of the survivors, apparent by 2 weeks of recovery with no change at 4 or 8 weeks. In marked contrast, 75 min of H/I produced no significant damage during the initial 2 weeks of recovery but resulted in progressive cerebral atrophy with delayed infarction such that the extent of damage at 8 weeks was not different from the 2-hour group. Thus, even a mild-moderate ischemic insult to the perinatal brain establishes a vulnerable region which ultimately dies without intervention.
Neurodegeneration in the Thalamus following Neonatal Hypoxia-Ischemia Is Programmed Cell Death
Authors: Northington Frances J. , Ferriero Donna M. , Martin Lee J. 
Published: April 2003

We studied neuronal cell body, axonal, and terminal degeneration in brains from 7-day-old rat pups recovered for 0, 1.5, 3, 6, 24, 48, 72 h, and 6 days following hypoxia-ischemia and identified proteins involved in the delayed neurodegeneration in the thalamus. We found that injury is biphasic with initial necrosis in the ipsilateral forebrain by 3 h following hypoxia-ischemia, in contrast to more delayed and apoptotic-like injury in the ventral-basal thalamus, brainstem, and other remote non-forebrain regions. Prior to the appearance of large numbers of apoptotic profiles in the ventral-basal thalamus, expression of Fas death receptor protein, activated forms of caspase 8 and caspase 3, and pro-apoptotic Bcl-2 proteins are increased. This manuscript combines our data on hypoxic-ischemic injury in the developing brain and presents evidence for at least two forms of neurodegeneration, namely, acute necrosis in the forebrain and delayed neurodegeneration in the thalamus, which is death-receptor-mediated programmed cell death.
High-Rising Terminals and Fall-Rise Tunes in Australian English
Authors: Fletcher Janet , Harringtonb Jonathan 
Published: April 2003

AbstractIt is usually claimed that statement high rises in Australian English are more or less phonetically identical to yes/no question rises. In this paper, statement high rises and question rises were examined in a corpus of controlled spontaneous speech (i.e. map task dialogues) to see if this is the case. It appears that speakers in this study used different kinds of rises for declaratives and questions. The majority of statement high rises were realized with a low pitch accent onset, whereas almost all question rises were produced with high pitch accent onsets. High-range fall-rises also appeared to be used by some speakers in the same way as statement high rises. Implications of these findings for the current ToBI analysis of Australian English are considered.
Response to Shiga Toxin-1, with and without Lipopolysaccharide, in a Primate Model of Hemolytic Uremic Syndrome
Authors: Siegler Richard L. , Pysher Theodore J. , Lou Randall , Tesh Vernon L. , Taylor Jr. Fletcher B. 
Published: April 2003

Shiga toxin (Stx) and lipopolysaccharide (LPS) both participate in the pathogenesis of post-diarrheal hemolytic uremic syndrome (HUS), yet little is known about the factors that modulate the host response to these toxins. We have previously shown that the baboon develops HUS if 100 ng/kg of purified Stx-1 is administered rapidly as a single bolus, but not if it is given as four 25-ng/kg doses every 12 h. We therefore used this baboon model to study the response to small intravenous doses of Stx-1, with and without the co-administration of LPS. The co-administration of two 1-mg/kg doses of LPS (given at 0 and 24 h) and four 25-ng/kg doses of Stx-1 (given at 0, 12, 24, and 36 h) resulted in HUS, but the administration of either toxin separately did not. The development of HUS was associated with a rise in urinary, but not plasma concentrations of TNF, and a rise in both urinary and plasma concentrations of IL-6 and IL-8. We speculate that LPS is not required for disease expression in the human, but that it can augment the response to otherwise subtoxic amounts of Stx and this augmentation may be mediated by LPS-induced cytokine release.
Vitamin D Receptor Gene Polymorphism and Bone Mineral Density in Hypercalciuric Calcium-Stone-Forming Patients
Authors: Heilberg Ita Pfeferman , Teixeira Sergio Henrique , Martini Ligia Araujo , Boim Mirian Aparecida 
Published: April 2003

Reduced bone mineral density (BMD) and an increased risk of vertebral fracture have been reported in calcium-stone-forming (CSF) patients presenting with idiopathic hypercalciuria. We investigated the association between <i>Bsm</i>I vitamin D receptor (VDR) polymorphism and BMD in 68 hypercalciuric CSF patients (35 males and 33 premenopausal females, mean age ± SD = 39 ± 10 years). BMD was measured at lumbar spine (L<sub>2</sub>–L<sub>4</sub>) and femur neck sites using dual energy X-ray absorptiometry. A 72-hour dietary record and a 24-hour urine sample were obtained from each patient to determine calcium intake and excretion. The allelic frequency found for the sample as a whole was 16% <i>BB</i>, 44% <i>Bb</i> and 40% <i>bb</i>. Mean BMD values did not significantly differ among <i>BB</i>, <i>Bb</i> and <i>bb</i> patients at L<sub>2</sub>–L<sub>4</sub> (1.162 ± 0.10, 1.133 ± 0.11 and 1.194 ± 0.19 g/cm<sup>2</sup>, mean ± SD, respectively) or at neck sites (0.920 ± 0.11, 0.931 ± 0.15 and 0.982 ± 0.15 g/cm<sup>2</sup>, respectively). Calcium intake and excretion were also not significantly different among the three genotypes. Patients were then divided into two groups, normal BMD, T-score ≧–1 (n = 34) and low BMD, T-score <–1 (n = 34), to further evaluate the allele influence on previous bone loss. Despite a trend for a higher mean BMD at spine or neck sites for patients with one or two <i>b</i> alleles when compared to <i>BB</i> patients, the difference did not reach statistical significance. The distribution of <i>BB</i>, <i>Bb</i> and <i>bb</i> genotypes in the low-bone-mass group (15, 47 and 38%, respectively) was similar to that in the normal-bone-mass group (18, 41 and 14%, respectively). These data suggest that <i>Bsm</i>I VDR polymorphism does not play an important role in the bone loss seen in hypercalciuric CSF patients.
The Effect of Renal Transplantation on Pulmonary Function
Authors: Kalender Betül , Erk Müzeyyen , Pekpak Meltem (Ayaz) , Apaydın Süheyla , Ataman Rezzan , Serdengeçti Kamil , Sarıyar Muzaffer , Erek Ekrem 
Published: April 2003

In patients with chronic renal failure, mechanical and hemodynamic changes could occur in the lungs without obvious pulmonary symptoms and findings and their effects could pave the way to pulmonary functional disorders. In this study, pulmonary functional disorders and especially alveolocapillary defects, which are frequently seen in uremia, were determined in renal transplanted patients. Pulmonary functions and diffusion capacity were assessed in uremic patients (n = 20) and in successfully transplanted patients (n = 20) without any lung disease or pulmonary edema symptoms and findings. Patients were selected randomly among outpatients who were followed up in a Nephrology and Transplantation Unit. Forced vital capacity (FVC), forced expiratory volume in 1 s (FEV<sub>1</sub>), and peak expiratory flow (PEF<sub>25–75</sub>) were measured. Single breath carbon monoxide diffusion test and diffusion lung capacity adjusted for hemoglobin concentration (DLAdj) were done. The means of the spirometric values such as FVC, FEV<sub>1</sub> and FEV<sub>1</sub>/FVC were normal in the nondialyzed uremic group, but the PEF<sub>25–75</sub> value (68.7%) and diffusion capacity (DLAdj 72.7%) were found to be slightly low. There were 2 patients with normal values and 18 patients with some functional abnormalities in this nondialyzed uremic group. The means of all spirometric parameters and diffusion capacities were found to be normal in the transplanted group. There were 7 patients with normal function and 13 patients with some functional abnormalities in this transplanted group. When the nondialyzed uremic group and the transplanted group were compared statistically, significant differences were found between their spirometric values (except for FVC) and their diffusion capacities. Even though the uremic patients did not show any symptoms, their pulmonary function tests, especially diffusion capacity, were found to be disturbed. Although the transplanted patients as a group had normal mean spirometric values and diffusion capacity there were nevertheless many individual transplanted patients with defective diffusion capacity and abnormal spirometric values.