Lipoprotein(a) concentrations in chronic renal failure and following renal transplantation.
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Biomedical subjects
Publications and source records attributed to C W Yang.
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Air was used to distend the gastrointestinal tract and act as a contrast medium to effectively delineate the other abdominal organs/masses and to outline intraluminal or mural lesions. We used a nasogastric tube to introduce air into the stomach. Metoclopramide was administered to propel air throughout the gastrointestinal tract. Bowel peristalsis was then controlled by scopolamine butylbromide. Most of the alimentary tract could be distended by air. The normal bowel walls were barely visible between intraluminal signal-void air and extraluminal high-signal fat. Intraluminal tumor, wall thickening, and adjacent structures could be clearly delineated.
Alterations in the balance between synthesis and degradation of extracellular matrix may result in glomerulosclerosis. The interaction between metalloproteinases and their inhibitors presumably modulates the rate of glomerular matrix degradation. We examined the gene expression of tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 in human glomeruli and TIMP-2 protein in tissue sections. Kidney tissue was obtained from adults undergoing nephrectomy for renal tumor (n = 9) or biopsy for nephrosis and renal failure (n = 1). Glomeruli were microdissected and subjected to reverse transcription. TIMP cDNAs were quantitated by competitive polymerase chain reaction assays. Five nephrectomy specimens had normal glomeruli and four had diffuse glomerulosclerosis. TIMP-1 and TIMP-2 cDNA levels, detected in glomeruli from all patients, were increased fourfold and threefold, respectively, in patients with glomerulosclerosis. The elevated TIMP cDNA levels could not be attributed to an increased number of glomerular cells. TIMP-2 protein was detected within normal and sclerotic glomeruli. In conclusion, both TIMP genes were expressed in normal glomeruli, and their level of expression was increased in glomerulosclerosis associated with renal carcinoma, suggesting that expression of these inhibitors may correlate with the development of sclerosis.
Experimental evidence has suggested that insulin-like growth factor-I (IGF-I) may contribute to diabetic complications. Previously, we and others have shown that normal glomerular mesangial cells have receptors for, synthesize, and exhibit a mitogenic response to IGF-I. We investigated the IGF-I response in cells derived from a genetic model of diabetes, the nonobese diabetic (NOD) mouse. Mesangial cell lines were derived from diabetic (D-NOD) and nondiabetic adult mice. D-NOD cells released more IGF-I into the supernatant and had a decreased binding of IGF-I to surface receptors. Analysis according to Scatchard revealed a decreased number of receptor sites on D-NOD cells, although the structure of the IGF-I receptor visualized by cross-linking was identical for both cell types. Preincubation of D-NOD cells with an antibody to IGF-I resulted in an increase in the number of receptor sites. This suggested that autocrine IGF-I was responsible for the decrease in D-NOD receptor number and that diabetes had resulted in a stable phenotypic change.
This study focuses on the beneficial effect of HLA matching on long-term graft survival rates in CsA-treated living primary kidney transplants at Catholic Medical Center, 1984 to 1993. 1. An impressive 26% difference in kidney graft survival was observed at 5 years between recipients who received 0 and 2 HLA-DR mismatches (79% vs 53%). 2. Five-year kidney graft survival rates in the 0, 1, 2, and 3-HLA-B+DR mismatches were 87%, 76%, 77%, and 74%, respectively, which was significantly different from 54% survival rates in the 4-HLA-B+DR mismatch group. 3. The 5-year kidney graft survivals in the 0, 1, 2, HLA-DR-mismatched living-nonrelated donor group were 84%, 76%, and 39%, respectively, which were significant differences. 4. The 5-year kidney graft survivals in the 0, 1, 2, HLA-DR-mismatched living-related donor group were 75%, 79%, and 72%, respectively, which were not significant. 5. The effect of HLA-A, B, A+B, A+DR, and A+B+DR mismatches showed little difference among the groups with different mismatch numbers. In conclusion, better matching for the HLA-DR, B+DR antigens significantly improved kidney graft survivals in our CsA-treated primary living-donor transplant recipients.
We reviewed the sonograms of 16 cases with scrotal trauma and documented the spectrum of abnormalities that may be present in sonography after a scrotal injury. The sonographic findings included scrotal hematoceles, post-traumatic epididymitis, epididymal hematoma, testicular hematoma and/or infarction, testicular rupture, testicular swelling and hyperemia. Ultrasound is able to distinguish intratesticular and extratesticular lesions. The integrity of the testis could be evaluated as well. It should be the imaging modality of choice for the evaluation of scrotal trauma.
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BACKGROUND: Mice transgenic for bovine growth hormone (bGH) gene have increased body weight and severe glomerulosclerosis leading to death in uremia. EXPERIMENTAL DESIGN: The aim of this study was to determine if body growth and glomerulosclerosis were mediated by different bGH regions. Amino acid substitutions in the bGH alpha-helix III were generated, and lines of transgenic mice that expressed these products were developed. Female transgenic mice carrying the native bGH gene (bGH mice), a mutated bGH gene that encodes a destabilized alpha-helix III (bGH-L121P, E126G; bGH-m11 mice), or a mutated bGH gene that encodes a perfect amphiphilic alpha-helix III (bGH-E117L, G119R, A122D; bGH-m8 mice) were examined at 2-3 months and 6-9 months of age. Body, kidney, and heart weights were measured. Urinary glucose, albumin, creatinine, and serum glucose were measured in all mice. Serum levels of insulin-like growth factor I (IGF-I) were measured in the 2-3 month group. Whole blood hemoglobin A1 was measured in some mice of the 6-9 month group. Kidney sections were examined by light and immunofluorescence microscopy. Glomerular volume was measured and related to body weight by allometry. RESULTS: The bGH-m11 mice developed glomerulosclerosis indistinguishable from that seen in bGH transgenic mice, even though they had normal body size. Glomerular growth exceeded body growth by allometry in both bGH and bGH-m11 strains. bGH-m8 mice had glomeruli of appropriate size and normal histologic appearance; however, they were dwarfs. IGF-I was increased in bGH mice; they also had an increased albumin/creatinine ratio at 6-9 months. None of the mice were hyperglycemic. CONCLUSIONS: These data indicated that development of glomerulosclerosis and body growth promotion were mediated by different regions of the growth hormone molecule. The glomerular response to bGH was unique and consisted of increased size and glomerulosclerosis.
Mice transgenic for bovine growth hormone (bGH) develop an increase in body weight and glomerular lesions characterized by a disproportionate increment in glomerular volume and progressive mesangial sclerosis. The relationship between glomerular size and body growth in bGH mice was further investigated by examining mice transgenic for a mutated GH gene (bGH-m11) which failed to enhance body growth. The glomeruli in bGH-m11 mice exhibited an increase in size and glomerulosclerosis comparable to those found in bGH mice. The levels of alpha 1 type IV collagen mRNA, as measured by the competitive polymerase chain reaction in isolated microdissected glomeruli, were markedly elevated in mice transgenic for both bGH and bGH-m11 genes. These data suggest that body growth on one hand, and glomerular hypertrophy and sclerosis on the other hand, are mediated by different portions of GH or different second messenger signaling systems.
Ventricular neoplasms can be grouped together as a single disease entity because of the behavior of some of the tumors and similarities between the access of therapy and procedure of operation. In our series, the incidence of various ventricular neoplasms (shown in decreasing order) were metastasis, astrocytoma, ependymoma, meningioma, choroid plexus papillomas and oligodendroglioma. The intraventricular tumors included some metastasis involved by hematogenous spread, meningioms, and choroid plexus papilloma while paraventricular tumors included some of the systemic myeloproliferative disorders with ventricular seeding along with tumors with glial origins. Most of the patients with symptoms of intraventricular tumors also had symptoms related to increased intracranial pressure while those with paraventricular neoplasm presented symptoms related to focal signs or symptoms. CT scan with enhancement could provide a very good image modality except in some involvements in the posterior cranial fossa.
We previously reported that one of the main components of the sclerotic material in human glomerular diseases was type IV collagen. In this study we examined the contribution of increased synthesis to this process at the gene expression level. Sufficient material has not been available to study type IV collagen synthesis by normal or sclerotic glomeruli in humans. We took advantage of the availability of nephrectomy specimens from patients with renal carcinoma, and of the observation that approximately 50% of these patients develop varying degrees of glomerulosclerosis. We microdissected glomeruli from 10 patients and analyzed them using in situ reverse transcription coupled with polymerase chain reaction (PCR) analyses (in situ RT-PCR). alpha 2IV collagen mRNA, after reverse transcription into cDNA, was detected in all patients and appeared to be increased in those with glomerulosclerosis (n = 5). A competitive PCR assay was developed to quantitate this change. There was an average 3.7-fold increase in glomerular type IV collagen cDNA in patients with significant sclerosis. This change was not due to an increased number of glomerular cells. Thus, glomerulosclerosis in humans is associated with an elevation of glomerular type IV collagen gene expression, suggesting that increased synthesis of type IV collagen may represent one component of this process.
The neurogenic myopathy of spinal muscular atrophy (SMA) is degeneration of anterior horn cells of the spinal cord and associated muscle weakness. In three patients with the severe type, according to Dubowitz's classification, magnetic resonance imaging (MRI) of the lower extremity showed severe atrophy of the entire muscle bundles of the thigh and the calf. Nine intermediate type patients had ragged atrophy of muscle bundles of the thigh and the calf with selective preservation of adductor longus muscle. Five patients with the mild type had fatty infiltration of muscle bundles and increased intermuscular fat planes. MRI was insufficient for the evaluation of cervical cord abnormalities. MRI of the lower extremity was a reliable complementary modality for the diagnosis and follow-up of SMA patients.
Goodpasture's syndrome is a disease characterized by diffuse pulmonary hemorrhage and glomerulonephritis with circulating anti-glomerular basement membrane antibody (anti-GBM antibody). Although it is reported in the western world, it is rarely diagnosed in Taiwan. We report a 26-year-old male admitted due to pulmonary hemorrhage and rapid progressive glomerulonephritis. Renal biopsy showed diffuse glomerular proliferation and 90% crescent formation, and immunofluorescence stain showed diffuse linear staining of IgG, C3, IgA, IgM along glomerular basement membranes and tubular basement membranes. He was treated with immunosuppressive agents. Pulmonary hemorrhage improved rapidly, but his renal function was severely impaired and he remained dialysis dependent.
Malaria had a wide distribution and high prevalence throughout the Three Gorges region of the Yangtze River. After antimalarial program, its incidence rate was reduced to 2.2% in 1985, but sporadic cases still occurred in 34.7% of the townships and local outbreaks were not uncommon. Therefore, potential factors of malaria outbreak are still present. It is predicted that maximum risk of malaria outbreak will take place, during construction and after the completion of the reservoir, the breeding sites of Anopheles would be extended to irrigation network, low-lying of flooded land, and malaria prevalence might be increased.
The immunofluorescence study revealed that both our established human hepatoma cell lines, HA22T/VGH and HA47T/VGH, were absent of cytokeratin. This observation was further confirmed by a western blot study. However, they as well as the other human hepatoma cells, Hep G2, Hep 3B, and SK-Hep-1 expressed vimentin.
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