PubMed Health⌕ Search

Biomedical subjects

J C Leung

Publications and source records attributed to J C Leung.

At least 19 recordsLinked to original sources
PubMed2005

Expression of the rat renal PiT-2 phosphate transporter.

BACKGROUND: NaPi-2a is the main sodium-dependent Pi (Na+-Pi) transporter in the apical membrane of the renal proximal tubule. Another group of Pi transporters, Glvr-1 (PiT-1) and Ram-1 (PiT-2), was identified. The PiT-2 cRNA induces Na+-dependent Pi uptake into Xenopus laevis oocytes. Prior studies have revealed the presence of the Pit-2 transporter in the kidney. OBJECTIVES: Further characterization of the PiT-2 transporter in the kidney and assessment of its developmental regulation. METHODS: Using primers specific for the PiT-2 mRNA and an antibody specific for the PiT-2 protein, we assessed the expression and developmental regulation of the renal PiT-2 mRNA and protein. RESULTS: RT-PCR analysis revealed that a 182 bp product was evident in the total kidney (TK), cortex (C), and medulla (M). Northern blots demonstrated a PiT-2 mRNA of approximately 4 kb (expected size) in the TK, C, and M. PiT-2 mRNA expression was similar in all kidney regions. RT-PCR and Northern blot analysis revealed that the PiT-2 cDNA was highly abundant in OK and MDCK culture cells. RT-PCR and Northern blot analysis revealed expected products at all ages studied. Densitometry demonstrated similar levels of expression of PiT-2 mRNA in the kidneys of older versus younger animals, and persistent expression in elderly rats. The PiT-2 protein was present in the TK, C, and M, and in OK and MDCK cells. PiT-2 protein abundance was similar at all ages studied. CONCLUSIONS: These studies further characterize the renal PiT-2 transporter and show that its expression is stable throughout development and ageing.

Aging↗
PubMed2004

Mutations in DYT1: extension of the phenotypic and mutational spectrum.

BACKGROUND: Most cases of early-onset primary torsion dystonia (PTD) are caused by the same three-base pair (bp) (GAG) deletion in the DYT1 gene. Exon rearrangements are a common mutation type in other genes and have not yet been tested for in DYT1. Several lines of evidence suggest a relationship of the DYT1 gene with Parkinson disease (PD). OBJECTIVE: To investigate the frequency and type of DYT1 mutations and explore the associated phenotypes in a mixed movement disorders patient cohort and in controls. METHODS: The authors screened 197 patients with dystonia (generalized: n = 5; focal/segmental: n = 126; myoclonus-dystonia: n = 34; neuroleptic-induced: n = 32), 435 with PD, and 42 with various other movement disorders, along with 812 healthy controls, for small deletions in exon 5 of DYT1 and tested for exon rearrangements by quantitative, duplex PCR in 51 GAG deletion-negative dystonia cases. RESULTS: The GAG deletion was detected in five patients: three with early-onset PTD, one with generalized jerky or clonic dystonia, and one with generalized dystonia and additional features (developmental delay, pyramidal syndrome). A novel out-of-frame four-bp deletion (934_937delAGAG) in exon 5 of the DYT1 gene was found in a putatively healthy blood donor. No exon rearrangements were identified in DYT1. CONCLUSIONS: In this mixed patient sample, the GAG deletion was rare and in two out of five cases associated with an unusual phenotype. In addition, a novel DYT1 truncating mutation of unknown clinical relevance was found in a putatively unaffected individual. DYT1 exon rearrangements, however, do not seem to be associated with PTD.

Adolescent↗
PubMed2003

Down-regulation of aquaporin 3 in bronchiectatic airways in vivo.

Bronchiectasis is characterized pathologically by permanent abnormal bronchial dilation, and clinically by chronic sputum production. Aquaporin 3 (AQP3), a recently described water channel that is also found in large airway cell membrane, could play a role in the pathogenesis and particularly that of bronchorrhea in bronchiectasis. However, little is known of its in vivo distribution and physiological role in human airways. We have, therefore, performed this quantitative immunohistochemistry study on endobronchial biopsies to evaluate the expression and clinical relevance of AQP3 in patients with idiopathic bronchiectasis (n = 25, 15 F, 64.3 +/- 11.5 years) and control subjects (n = 14, 5 F, 57.5 +/- 12.0 years). Quantitative image analysis was performed to evaluate the expression of AQP3 in the bronchial epithelial cells. Our results show that AQP3 was predominantly expressed in the basal cells of the epithelial layer in both groups. Expression of AQP3 was significantly reduced in the basal, but not columnar, epithelial cells in bronchiectasis compared with control airways (p = 0.02, 0.35). Only bronchiectatic patients with regular sputum production, but not their counterparts, had significant downregulation of epithelial AQP3 expression compared with control airways (p = 0.004, 0.24). Our findings suggest that AQP3 could have an important role in the pathogenesis of increased mucus production in bronchiectasis.

Aquaporin 3↗
PubMed2001

Novel mutation in the TOR1A (DYT1) gene in atypical early onset dystonia and polymorphisms in dystonia and early onset parkinsonism.

Dystonia is a movement disorder involving sustained muscle contractions and abnormal posturing with a strong hereditary predisposition and without a distinct neuropathology. In this study the TOR1A (DYT1) gene was screened for mutations in cases of early onset dystonia and early onset parkinsonism (EOP), which frequently presents with dystonic symptoms. In a screen of 40 patients, we identified three variations, none of which occurred in EOP patients. Two infrequent intronic single base pair (bp) changes of unknown consequences were found in a dystonia patient and the mother of an EOP patient. An 18-bp deletion (Phe323_Tyr328del) in the TOR1A gene was found in a patient with early onset dystonia and myoclonic features. This deletion would remove 6 amino acids close to the carboxy terminus, including a putative phosphorylation site of torsinA. This 18-bp deletion is the first additional mutation, beyond the GAG-deletion (Glu302/303del), to be found in the TOR1A gene, and is associated with a distinct type of early onset dystonia.

Adolescent↗
PubMed2001

Charge-dependent binding of polymeric IgA1 to human mesangial cells in IgA nephropathy.

BACKGROUND: IgA nephropathy (IgAN) is characterized by raised serum IgA1 and predominant mesangial IgA1 deposits of polymeric nature. The mechanism of polymeric IgA1 (pIgA1) deposition in the kidney mesangium is poorly understood in IgAN. It has been suggested that increased sialic acid content and anionic charge of the pIgA1 molecules may be operational in the IgA1 deposition in human mesangial cells (HMCs). The present study examined the binding of pIgA1 with different surface charges to HMCs. The binding characteristics of IgA1 to HMCs in the presence of polycation (poly-L-lysine) or polyanion (heparin) were also investigated. METHODS: IgA1 was purified in sera from patients with IgAN and from healthy controls by jacalin affinity chromatography. IgA1 was further separated into pIgA1 and monomeric IgA1 (mIgA1) by fast protein liquid chromatography (FPLC). pIgA1 or mIgA1 with different net charges on their surface were resolved by ion exchange chromatography (IEC) with a Mono Q column. The binding characteristics of pIgA1 and mIgA1 to HMCs in the presence or absence of polycation or polyanion were examined by flow cytometry. RESULTS: In patients with IgAN, the absolute amount of mIgA1 and pIgA1 is significantly higher than that of healthy controls (P < 0. 001). There was significant increase in binding of pIgA1 from patients with IgAN to HMC and cell lysate. pIgA1 that interacted strongly with the ion exchanger also bound more to HMCs when compared with IgA1 interacted weakly with the ion exchanger (P < 0. 001). The anionic charged pIgA1 from patients was significantly higher than that of healthy controls (P < 0.001). Preincubation with poly-L-lysine increased the binding of pIgA1 to HMCs. The binding of pIgA1 to HMCs was decreased by preincubation with heparin. CONCLUSIONS: The binding of IgA to HMCs is charge dependent. Polymeric IgA with the highest net negative charge binds more to HMCs. Preincubation with polyanion decreased the binding of polymeric IgA to HMCs. These results suggest an important role for anionic charge in IgA1 deposition onto the kidney mesangial cells.

Adult↗
PubMed2001

In vitro studies of aquaporins 1 and 3 expression in cultured human proximal tubular cells: upregulation by transferrin but not albumin.

Dysregulated renal water handling is a cardinal feature of nephrotic syndrome that has been shown in animal models of experimental nephrosis to mediate renal aquaporin (AQP) expression. However, data on the effect of proteinuria on the proximal tubule, which is heavily vested with AQP1 and therefore may participate in water homeostasis, are limited. To investigate this, we exposed primary human proximal tubular epithelial cells (PTECs) to two key proteinuric components shown to perturb tubule function: human serum albumin and transferrin. Using reverse-transcriptase polymerase chain reaction and immunocytochemical techniques, PTECs in the quiescent state were found to express AQP3 in addition to AQP1 gene and protein, which was also validated in a human proximal tubule cell line, HK-2. Immunohistochemical staining localized AQP1 synthesis to the apical and basolateral membranes and AQP3 synthesis to the basolateral membrane of proximal tubule epithelium. Transferrin in doses reaching nephrotic range upregulated PTEC transcription and translation of both AQP1 and AQP3 in a time- and dose-dependent manner. After 24 hours of stimulation, transferrin led to a 2.4- and 2.2-fold increase in AQP1 and APQ3 messenger RNA expression, whereas protein synthesis surged by 40.7% +/- 2.48% and 24.2% +/- 0.9% compared with control, respectively. These effects were not observed with albumin challenge and were not caused by osmolality fluctuation with transferrin treatment. In summary, our novel finding of AQP3 in PTECs indicates a role for AQP3 in proximal tubule water reabsorption. The pathophysiological significance of heightened AQP1 and AQP3 expression in PTECs on protein challenge as occurs in the nephrotic state requires further investigation.

Albumins↗
PubMed2000

Changes of cytokine profiles during peritonitis in patients on continuous ambulatory peritoneal dialysis.

Continuous ambulatory peritoneal dialysis (CAPD) has emerged as an important dialysis treatment modality worldwide. One of the major complications is bacterial peritonitis, which may result in subsequent technique failure because of loss of peritoneal clearance or peritoneal fibrosis. Bacterial peritonitis leads to the release of proinflammatory cytokines from resident and infiltrating cells in the peritoneal cavity. We studied 35 patients undergoing CAPD with acute bacterial peritonitis. All patients treated with antibiotics for 2 weeks after the clinical diagnosis of peritonitis had a good recovery. Peritoneal dialysate effluent (PDE) was collected on days 1, 3, 5, 10, 21, and 42 after the start of treatment. Cell populations were monitored by flow cytometry. PDE levels of interleukin-1beta (IL-1), IL-6, transforming growth factor-beta (TGF-beta), and basic fibroblast growth factor (FGF) were measured by enzyme-linked immunosorbent assay. Gene transcription of TGF-beta in macrophages from PDE was measured by quantitative polymerase chain reaction. Bacterial peritonitis was associated with a sharp increase in total cell and neutrophil counts (400-fold) in PDE up to 3 weeks after peritonitis despite clinical remission (P < 0.0001). There was an increased absolute number of macrophages during the first 3 weeks despite the reduced percentage of macrophages among total cells in PDE compared with noninfective PDE. There was a progressive increase in the percentage of mesothelial cells or dead cells in the total cell population in PDE over the entire 6-week period. PDE levels of IL-1, IL-6, TGF-beta, and FGF increased markedly on day 1 before their levels decreased gradually. PDE levels of these cytokines or growth factors were significantly greater than those in noninfective PDE (n = 76) throughout the study period (P < 0.01). Similarly, TGF-beta complementary DNA (cDNA) molecules per macrophage were significantly greater than those of macrophages in noninfective PDE throughout this period (P < 0.01). There was no significant correlation between PDE levels of TGF-beta and TGF-beta cDNA molecules per macrophage, suggesting that peritoneal macrophages are not the only source of TGF-beta in PDE. We conclude there is an active release of proinflammatory cytokines and sclerogenic growth factors through at least 6 weeks despite apparent clinical remission of peritonitis. The peritoneal cytokine networks after peritonitis may potentially affect the physiological properties of the peritoneal membrane.

Bacterial Infections↗
PubMed2000

Magnetic resonance imaging in primary bone tumors.

MRI plays a major role in the evaluation and treatment planning of bone tumors. It should be used following plain films and before biopsy. The MR appearance of most tumors is nonspecific; however, the entire extent of the tumor and its relationship to adjacent structures can be determined at MRI providing a road map for the surgeon. The role of dynamic enhancement is evolving and has not yet been determined.

Bone Neoplasms↗
PubMed1999

Increased sialylation of polymeric immunoglobulin A1: mechanism of selective glomerular deposition in immunoglobulin A nephropathy?

Immunoglobulin A nephropathy (IgAN) is characterized by raised serum IgA and predominant mesangial IgA deposits of polymeric nature. The abnormal glycosylation of the carbohydrate moieties in the hinge region of the IgA molecule has recently attracted much attention. In this study we investigated the galactosylation and sialylation of monomeric and polymeric IgA1 isolated from patients with IgAN. Total IgA1 in serum samples from patients with IgAN or from healthy controls was isolated with a jacalin-agarose column as jacalin-bound protein (JBP). Monomeric and polymeric IgA1 were distinctly separated by fast protein liquid chromatography. Lectin binding assays were designed to examine the sialylation and the expression of terminal galactose and N-acetyl galactosamine of the O-linked carbohydrate in the hinge region of the IgA molecule. Reduced terminal galactosylation was demonstrated in serum IgA and monomeric IgA1 isolated from patients with IgAN as compared with results in healthy control subjects. However, a reduction in terminal galactosylation was not found in polymeric IgA1 isolated from patients with IgAN. Instead, increased sialylation of IgA1 (alpha2-3 linked to galactose) was demonstrated in polymeric IgA1. This abnormality of IgA1 could bear considerable implication on the pathogenesis of IgAN, because the masking effect of sialic acid may hinder the clearance of polymeric IgA1 by the asialoglycoprotein receptor (ASGP-R) of the liver cells. An increase in the sialylated content would also render the polymeric IgA from patients with IgAN more anionic. These immunochemical properties may contribute to the selective glomerular deposition of polymeric IgA1 in IgAN.

Adult↗
PubMed1999

Increased production of hyaluronan by peritoneal cells and its significance in patients on CAPD.

Hyaluronan (HA) is a polysaccharide that forms a critical component of extracellular matrices. HA is present in high concentrations in tissues undergoing remodeling and morphogenesis, and it appears to have an important role in the early stages of wound healing. Here, we studied the level of HA in the peritoneal dialysate effluent (PDE) from 116 stable continuous ambulatory peritoneal dialysis (CAPD) patients. Longitudinal studies over a period of 6 weeks were performed in seven of these patients who developed peritonitis. The median HA level in PDE from these patients was 154.6 microg/L (range, 29.7 to 820.2 microg/L). Dialysate level of HA increased with age of the patients, but no such correlation was shown between HA level in PDE and duration of CAPD treatment or previous episodes of peritonitis. Patients with high or average peritoneal membrane transport of small solutes had a higher HA level in the PDE than those with a low peritoneal membrane transport (P = 0.046). A significant correlation was observed between PDE level of HA and interleukin-1beta (IL-1beta) or IL-6. The plasma level of HA in these patients was significantly greater than that of healthy controls (P < 0.0001), yet the plasma concentration of HA was only 85% that of the PDE concentration. In CAPD patients with peritonitis, there was a sharp increase in the PDE levels of HA, IL-1beta, and IL-6. These values decreased progressively with resolution of peritonitis. The changes in the PDE levels of HA closely followed those of IL-1beta or IL-6. In vitro [3H]-glucosamine incorporation studies suggest that the main bulk of HA is derived from synthesis by the peritoneal mesothelial cells, whereas the amount synthesized by macrophages is trivial. We conclude that elevated levels of HA found in the PDE of stable CAPD patients originate from increased synthesis by peritoneal mesothelial cells. This event may serve as a marker of regeneration and remodeling of the peritoneal lining.

Adult↗
PubMed1999

Gene expression and synthesis of natriuretic peptides by cultured human glomerular cells.

BACKGROUND: Atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide belong to a family of hormones that have natriuretic and vasodepressor activity and may play a pathophysiologic role in hypertension, heart failure and renal failure. Whereas immunoreactive human forms of these three natriuretic peptides are found in renal tubules, it is not clear whether they are derived from the systemic circulation or from local production. OBJECTIVE: To examine the gene expression of natriuretic peptides in cultured human glomerular cells. MATERIALS AND METHODS: We sought to determine the presence of messenger RNA encoding for these natriuretic peptides using polymerase chain reaction following reverse transcription. The polymerase chain reaction products were confirmed by direct sequencing. Atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide in cell-culture supernatants were measured by radioimmunoassays (with detection limits of 2.1, 2.1 and 0.21 pmol/l, respectively). RESULTS: Atrial natriuretic peptide messenger RNA was not found in mesangial or glomerular epithelial cells (despite stimulation with tumor necrosis factor-alpha) except when the cells were cultured with a high concentration of fetal bovine serum (> 10%). Similarly, this peptide was not detected in supernatant unless the cells were cultured with fetal bovine serum at concentrations of > 10%. Brain natriuretic peptide messenger RNA was readily detected in cultured mesangial and glomerular epithelial cells with a lower concentration in the former. Brain natriuretic peptide was not found in the supernatant of resting mesangial cells but became detectable when incubated with tumor necrosis factor-alpha or fetal bovine serum. C-type natriuretic peptide messenger RNA was detected in mesangial and glomerular epithelial cells with a higher concentration in the latter. C-type natriuretic peptide was detected in the supernatant of resting glomerular epithelial cells and levels rose when incubated with increasing concentrations of tumor necrosis factor-alpha or fetal bovine serum. However, C-type natriuretic peptide was not detected in the supernatant of resting mesangial cells and remained undetectable following incubation with tumor necrosis factor-alpha or fetal bovine serum. CONCLUSION: Our results suggest differences in the synthesis of natriuretic peptides between glomerular mesangial and epithelial cells.

Atrial Natriuretic Factor↗
PubMed1999

Thickening of the diaphragm: a new computed tomography sign of diaphragm injury.

Computed tomography examination is becoming a standard method of evaluating injury in blunt trauma. This report describes a previously unreported computed tomography sign of diaphragmatic injury. A retrospective review of imaging findings was performed on eight patients with surgically proven traumatic diaphragmatic rupture. Thickening of the diaphragm was present on computed tomography in six of eight patients with surgically proven diaphragm rupture. Two patients demonstrated previously established computed tomography signs of diaphragm rupture and two patients had no findings to suggest diaphragm injury. Diaphragm thickening is associated with diaphragm rupture and may be a useful diagnostic sign in the evaluation of patients with blunt trauma.

Adult↗
PubMed1999

Growth factors in continuous ambulatory peritoneal dialysis effluent. Their relation with peritoneal transport of small solutes.

Recent studies reveal conflicting results on the change of solute transfer with time on continuous ambulatory peritoneal dialysis (CAPD) and recurrent peritonitis. Herein, we performed a cross-sectional study of 76 patients on CAPD to examine their peritoneal permeability by measuring the dialysate to serum ratio of creatinine (D/P) and the mass transfer area coefficients of creatinine (MTACCr) or glucose (MTACGlu). Transforming growth factor-beta1 (TGF-beta1), platelet-derived growth factor (PDGF), and epidermal growth factor (EGF) were measured in the dialysate by ELISA. TGF-beta1 mRNA in peritoneal macrophages were determined by a quantitative polymerase chain reaction. We failed to observe any correlation between the duration on dialysis and the peritoneal permeability in those patients with no previous peritonitis. Frequency of peritonitis episode did not affect the MTACCr, MTACGlu, or D/P. The MTACCr correlated well with MTACGlu (r = 0.78, p = 0. 001) and with D/P (r = 0.98, p < 0.0001). No inverse correlation was demonstrated between dialysate PDGF or EGF and the peritoneal permeability. A positive correlation was demonstrated between the dialysate TGF-beta1 and MTACCr, MTACGlu or D/P (r = 0.64, 0.54, and 0.64 respectively, p < 0.001). The dialysate TGF-beta1 levels in patients with low D/P (</=0.5) were only half of that in patients with normal or high D/P (p = 0.0002). The dialysate levels of TGF-beta1 did not correlate with PDGF or EGF. These findings raise the possibility that, other than diffusion across the peritoneal membrane from circulation, there could also be an intrinsic production of TGF-beta1 by peritoneal cells in these CAPD patients. Our findings raise the speculation that TGF-beta1 in dialysate from stable CAPD patients may exert an inhibitory action to fibroblast. Such action of TGF-beta1 could reduce the risk of peritoneal sclerosis and hence, maintains a satisfactory peritoneal permeability to small solutes.

Biological Transport↗
PubMed1998

Gene transcription and synthesis of adrenomedullin by cultured human renal cells.

Adrenomedullin (ADM) is a novel 52 amino acid peptide with a potent vasodilator effect. Gene expression of ADM is found in human kidney but the exact cell source in the kidney is uncertain. Its plasma level is raised in association with changes in sympathetic nervous activity and body fluid volume in hypertension and chronic renal failure. Herein, we examined the presence of mRNA encoding for ADM in cultured human glomerular cells. Adrenomedullin in cell culture supernatant was measured by a radio-immunoassay (with a detection level of 3.2 pmol/l). Adrenomedullin mRNA was found in cultured mesangial and glomerular epithelial cells as well as in vascular endothelial cells. Supernatant levels of ADM for cultured mesangial and glomerular epithelial cells were 21.2 and < 3.2 pmol/l respectively. Contrary to vascular smooth muscle cells, the gene expression for ADM in mesangial cells was up-regulated when incubated with increasing concentration of TNF-alpha or fetal bovine serum (FBS) but this effect was not observed with very high concentration. Parallel results were observed in adrenomedullin levels in supernatant from mesangial cell cultures. Forskolin, captopril, or TGF-beta had no effect on the transcription or synthesis of ADM in mesangial cells. The gene expression for ADM in glomerular epithelial cells was down-regulated when incubated with increasing concentration of TNF-alpha, forskolin or FBS. The ADM levels in all supernatant from resting glomerular epithelial cell cultures were < 3.2 pmol/l. Recent murine data show that ADM stimulates the release of cAMP but suppresses mitogenesis in cultured mesangial cells. Our results suggest ADM is synthesized by mesangial cells in an autocrine fashion and the peptide may potentially be involved in intra-renal blood pressure control.

Adrenomedullin↗
PubMed1998

Increased ascitic level of hyaluronan in liver cirrhosis.

Hyaluronan (HA) is a polysaccharide that forms a critical component of extracellular matrixes. It is present in high concentrations in tissues undergoing remodeling and morphogenesis. Serum HA is elevated in patients with chronic liver disease, and this has been considered to be caused by impaired degradation by the liver endothelial cells. We studied the level of HA in the ascitic fluid and plasma from 27 patients with cirrhotic ascites. These values were compared with peritoneal dialysate effluent (PDE) and plasma from 33 patients with uremia who were undergoing continuous ambulatory peritoneal dialysis (CAPD). The median HA levels in ascitic fluid and plasma from our 26 patients with cirrhosis were significantly higher than corresponding PDE and plasma values from the 33 CAPD patients (p < 0.0001). The median peritoneal/plasma ratios of creatinine, albumin, and immunoglobulin G in either cirrhotic or CAPD patients were less than unity. In contrast, the median peritoneal/plasma ratios of HA in both groups of patients exceeded one with a higher peritoneal/plasma ratio of HA in patients with cirrhosis (p = 0.0035). A significant correlation was observed between the ascitic level of HA and interleukin-1beta, interleukin-6, or transforming growth factor-beta. Our in vitro cell culture studies revealed that HA is synthesized by both mesothelial cells and macrophages. We observed an additive effect in the synthesis of HA by mesothelial cells when the macrophage-conditioned medium was added to the RPMI culture medium. We conclude that a high level of HA is found in ascites from patients with cirrhosis. Our results strongly suggest that simultaneous increased synthesis of HA by the peritoneal cells and a reduction of degradation by liver endothelial cells occur in these patients with cirrhosis with ascites. This event of increased HA synthesis may be contributory to remodeling and regeneration of the peritoneal lining.

Adult↗
PubMed1998

Compartmentalization of pro-inflammatory cytokines in tuberculous pleurisy.

Increased levels of interleukin-6 (IL-6) and IL-8 are found in various immunologically mediated inflammatory disorders. Concentrations of IL-6, IL-8 and the soluble form of the IL-6 receptor (sIL-6R) were determined in serum and effusion fluid of 25 patients with tuberculous pleurisy utilizing enzyme linked immunosorbent assays (EIA). Serum IL-6 levels were only slightly increased in patients with tuberculous pleurisy in comparison to controls (11.1 +/- 2.1 vs 7.3 +/- 1.0 pg ml-1). IL-8 could not be detected in the serum of tuberculosis patients, but it was detected in the serum of healthy controls (8.0 +/- 1.5 pg ml-1). In comparison to serum, IL-6 and IL-8 were found in high concentrations in pleural effusions (IL-6: 932 +/- 70 vs 11.1 +/- 2.1 pg ml-1, P < 0.0001; IL-8: 450 +/- 85 vs 0 +/- 0 pg ml-1). In contrast, sIL-6R concentrations were much higher in serum compared to pleural effusion levels [30,477 +/- 1905 vs 9881 +/- 1177 pg ml-1, P < 0.0001 (mean +/- SEM)]. The authors conclude that elevated levels of IL-6 and IL-8 in pleural effusions are compartmentalized at the site of active disease. The low levels of sIL-6R in the presence of high levels of IL-6 in pleural effusions, and the high levels of sIL-6R in the presence of low levels of IL-6 in serum suggest that the expression or shedding of sIL-6R may be downregulated in the presence of excessive amounts of IL-6.

Adult↗
PubMed1998

Gene expression of the renin-angiotensin system in human kidney.

BACKGROUND: Immunocytochemical studies have revealed that all components of the renin-angiotensin system are widely distributed in human tissues yet the information on the gene expression of the renin-angiotensin system in various types of cell remains scarce. OBJECTIVE: We explored the presence of a local renin-angiotensin system in human kidney. METHODS: We sought to determine the presence of messenger RNA (mRNA) encoding for renin, angiotensinogen, and angiotensin converting enzyme (ACE) in cultured human glomerular cells and human umbilical vein endothelial cells using a two-step polymerase chain reaction. The gene expression of the renin-angiotensin system in normal human kidney and in diseased kidney was studied by in-situ hybridization using synthetic oligonucleotides. RESULTS: By using a two-step polymerase chain reaction, renin, angiotensinogen, and ACE mRNA were found in cultured mesangial and epithelial cells but only ACE mRNA was present in human umbilical vein endothelial cells. Renin mRNA was detected in juxtaglomerular granular cells and also in glomerular and tubular epithelia in normal kidney by in-situ hybridization. A similar tubular, but not mesangial, distribution was found with angiotensinogen and ACE mRNA. In contrast, stronger signals for renin, angiotensinogen and ACE mRNA were detected in mesangial and epithelial cells of kidney tissues from hypertensive patients and from patients with renal pathology characterized by mesangial proliferation (immunoglobulin A nephropathy, diabetes mellitus, or lupus nephritis). CONCLUSIONS: That gene expression of the renin-angiotensin system occurs in resident glomerular cells supports the hypothesis that there is a local renin-angiotensin system in human kidney. Our findings support the previous speculation that the renin-angiotensin system could be a local factor involved in the progression of chronic renal failure and consequent development of hypertension.

Angiotensinogen↗