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Y F Lin

Publications and source records attributed to Y F Lin.

At least 37 records · Page 2Linked to original sources
PubMed2001

Acute correction of metabolic acidosis increases serum procollagen type I carboxyterminal propeptide in patients with chronic renal failure.

BACKGROUND AND PURPOSE: Previous in vitro study has shown that an acidic medium increases osteoclastic and inhibits osteoblastic activity. The present study sought to determine the role of alkali therapy in osteoblast function in patients with chronic renal failure by assessing the serum concentration of procollagen type I carboxyterminal propeptide (PICP), a marker of bone formation, before and after bicarbonate infusion. PATIENTS AND METHODS: Eighteen patients with chronic renal failure (creatinine clearance 12 +/- 6.6 mL/min) associated with mild to moderate metabolic acidosis were enrolled in this study. None had undergone dialysis. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was clamped at the preinfusion level by calcium gluconate infusion throughout the procedure. RESULTS: After bicarbonate infusion, there were significant increases in plasma pH (7.31 +/- 0.04 to 7.40 +/- 0.03, p < 0.001), bicarbonate concentration (18.46 +/- 2.49 to 23.66 +/- 2.72, p < 0.001), serum total calcium concentration (2.01 +/- 0.24 to 2.12 +/- 0.24 mmol/L, p < 0.001), and PICP concentration (137.3 +/- 56.25 to 159.6 +/- 57.30 micrograms/L, p < 0.05), whereas serum parathyroid hormone concentrations assessed by radioimmunoassay decreased significantly (153.7 +/- 88.6 to 111.5 +/- 78.7, p < 0.001). Serum ionized calcium concentrations showed no significant difference before and after bicarbonate infusion. CONCLUSION: These results suggest that acute correction of metabolic acidosis improves osteoblast function and appear to underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.

Acidosis↗
PubMed2000

The polar T1 interface is linked to conformational changes that open the voltage-gated potassium channel.

Kv voltage-gated potassium channels share a cytoplasmic assembly domain, T1. Recent mutagenesis of two T1 C-terminal loop residues implicates T1 in channel gating. However, structural alterations of these mutants leave open the question concerning direct involvement of T1 in gating. We find in mammalian Kv1.2 that gating depends critically on residues at complementary T1 surfaces in an unusually polar interface. An isosteric mutation in this interface causes surprisingly little structural alteration while stabilizing the closed channel and increasing the stability of T1 tetramers. Replacing T1 with a tetrameric coiled-coil destabilizes the closed channel. Together, these data suggest that structural changes involving the buried polar T1 surfaces play a key role in the conformational changes leading to channel opening.

Amino Acid Substitution↗
PubMed2000

Regulation of ATP-sensitive potassium channel function by protein kinase A-mediated phosphorylation in transfected HEK293 cells.

ATP-sensitive potassium (K(ATP)) channels regulate insulin secretion, vascular tone, heart rate and neuronal excitability by responding to transmitters as well as the internal metabolic state. K(ATP) channels are composed of four pore-forming alpha-subunits (Kir6.2) and four regulatory beta-subunits, the sulfonylurea receptor (SUR1, SUR2A or SUR2B). Whereas protein kinase A (PKA) phosphorylation of serine 372 of Kir6.2 has been shown biochemically by others, we found that the phosphorylation of T224 rather than S372 of Kir6.2 underlies the catalytic subunits of PKA (c-PKA)- and the D1 dopamine receptor-mediated stimulation of K(ATP) channels expressed in HEK293 cells. Specific changes in the kinetic properties of channels treated with c-PKA, as revealed by single-channel analysis, were mimicked by aspartate substitution of T224. The T224D mutation also reduced the sensitivity to ATP inhibition. Alteration of channel gating and a decrease in the apparent affinity for ATP inhibition thus underlie the positive regulation of K(ATP) channels by PKA phosphorylation of T224 in Kir6.2, which may represent a general mechanism for K(ATP) channel regulation in different tissues.

Adenosine Triphosphate↗
PubMed2000

The role of lung scintigraphy in the diagnosis of nephrotic syndrome with pulmonary embolism.

PURPOSE: Patients with nephrotic syndrome (NS) have an increased tendency to develop thrombosis and even to progress to pulmonary embolism (PE). This study was performed to determine the incidence of PE in NS with severe hypoalbuminemia and to investigate the possible role of ventilation-perfusion (V/Q) lung scans to evaluate these patients. METHODS: Eighty-nine patients with NS (serum albumin concentration < 2 g/dl) and risk factors for PE were studied. In all patients, the probability that PE would develop was assessed based on the results of V/Q lung scans (Xe-133 for ventilation and Tc-99m MAA for perfusion imaging). The lung scans were judged using the modified Prospective Investigation of Pulmonary Embolism Diagnosis criteria. In 25 (28%) patients whose lung scans showed an intermediate or low probability, but for whom there was a strong clinical indication of PE, pulmonary angiography was performed. The patients' clinical symptoms and signs on initial examination were observed. Additional examinations included electrocardiograms, chest radiography, and hematochemical tests such as albumin, blood urea nitrogen, creatinine, cholesterol, triglycerides, fibrinogen, antithrombin III, prothrombin time, and activated partial thromboplastin time. RESULTS: Based on the findings of lung scans, 19 (21%) of the patients were categorized as having a high probability of PE. However, pulmonary angiography found that 10 (11%) other patients had PE despite having lung scan findings categorized as intermediate or low probability of PE. Except for plasma fibrinogen and antithrombin III levels, neither the clinical symptoms and signs, electrocardiogram findings, chest radiograph results, nor values of hematochemical testing were consistent with the occurrence of PE in these 29 patients. CONCLUSION: The results of this study suggest that PE is not a rare complication in patients with NS, and is usually clinically silent. In this series, the occurrence of PE did not appear to be always correlated with the clinical or hematochemical severity of NS, except for the association with elevated levels of fibrinogen and antithrombin III. When treating the clinical symptoms of patients with NS, physicians should be alert to the possible complication of PE. Serial V/Q lung scans may provide valuable clues in the evaluation of these patients.

Angiography↗
PubMed2000

Acute lymphoblastic leukemia in one of two siblings with Alstrom syndrome.

Alstrom syndrome is a rare autosomal recessive disease; less than 60 cases have been reported. No Chinese patient with this disease has been reported previously in the literature. Here, we describe an 11-year-old Chinese boy with this condition. His elder sister also had Alstrom syndrome, and his father had non-insulin-dependent diabetes mellitus. Both siblings had degenerative retinopathy, obesity, mental retardation, perceptive hearing loss, short stature, non-insulin-dependent diabetes mellitus, nephropathy, hyperlipidemia, acanthosis nigricans, and hepatic dysfunction. The boy also developed acute lymphoblastic leukemia, which was confirmed by cytochemistry and immunophenotyping findings. He received chemotherapy and radiotherapy for the malignancy. The present case suggests that acute lymphoblastic leukemia may be coincident with or may be a previously undescribed systemic manifestation of Alstrom syndrome.

Adolescent↗
PubMed1998

Differences in the cellular zinc content and 5'-nucleotidase activity of normal and acrodermatitis enteropathica (AE) fibroblasts.

The acrodermatitis enteropathica (AE) mutation affects zinc (Zn) metabolism in human fibroblasts. We hypothesize that the mutation affects the cell Zn content, which subsequently affects the activity of various zinc-dependent enzymes, such as 5'-nucleotidase. Therefore, normal and AE fibroblasts were grown in normal medium containing physiological levels of Zn (16 micromol/L) for approximately 24 h. The medium was replaced by normal medium (16 micromol/L Zn), Zn-depleted medium (1.5 micromol/L Zn), or Zn-supplemented medium (200 micromol/L Zn) for another 24 h. Regardless of the Zn concentration of the growth medium, the AE fibroblasts contained significantly less Zn than normal fibroblasts grown in comparable medium. Nevertheless, growth of the fibroblasts in 200 micromol/L Zn medium significantly increased the cell Zn content fourfold of both normal and AE fibroblasts. The activity of 5'-nucleotidase in the AE fibroblasts grown in 16 micromol/L Zn or 1.5 micromol/L Zn medium was also significantly lower than in normal fibroblasts. Changing the growth medium from 16 micromol/L Zn to 1.5 micromol/L Zn medium did not affect the activity of the enzyme in either genotype. Cells grown in 200 micromol/L Zn medium exhibited threefold greater 5'-nucleotidase activity in AE fibroblasts, but had no affect on enzyme activity in normal cells. In summary, altering the cell Zn content of normal fibroblasts did not result in a significant change in their 5'-nucleotidase activity. However, AE fibroblasts grown in 200 micromol/L Zn medium exhibited recovery of their 5'-nucleotidase activity to normal levels. These results support the hypothesis that the AE mutation affects the cellular Zn content. The lower cell Zn content subsequently affects the activity of 5'-nucleotidase.

5'-Nucleotidase↗
PubMed1998

Administration of dexamethasone induces proteinuria of glomerular origin in mice.

The administration of glucocorticoids has been reported to exacerbate proteinuria in a few patients with glomerulonephritis. This effect has not been well recognized, and the pathogenetic mechanism responsible for this phenomenon remains to be clarified. In this study, we observed that a high daily oral dose (0.5 mg/kg body weight) of dexamethasone was capable of inducing overt proteinuria in mice, beginning on day 5 and persisting for a 19-day duration. One fourth of mice also intermittently presented with slight hematuria beginning on day 12. Renal lesions in the dexamethasone-treated mice, which were killed on day 23, were characterized by mild mesangial expansion, segmental or global hyalinosis/sclerosis in deep cortical glomeruli, and focal tubular changes. No glomerular inflammatory cell infiltration or proliferative lesion was noted in any of the mice. Ultrastructural features of glomeruli included mesangial widening characterized by either an increase of mesangial matrix, dilated mesangial channels filled with slightly electron-dense material or mesangial lysis-like appearance showing intracytoplasmic microcysts filled with electron-lucent material, and evidence to support injury of endothelial cells, erythrocytes, and podocytes. An immunofluorescence study revealed enhanced glomerular deposition of IgG, IgA, IgM, and fibrinogen (P < 0.001, compared with normal control mice), but no glomerular C3 deposition was identified in any of the dexamethasone-treated mice. Charge analysis showed no impairment in anionic property of glomerular tufts in the dexamethasone-treated mice. In addition, the dexamethasone-induced proteinuria was greatly attenuated by treatment with a low molecular weight heparin, although it was not reduced by an angiotensin-converting enzyme inhibitor. Data from these experiments suggest that a large dose of glucocorticoids is potentially nephrotoxic. Alteration of a size-dependent permeability may predominantly contribute to the dexamethasone-induced proteinuria. However, the effect of glomerular hyperfiltration may be only partially involved in the pathogenesis of this dexamethasone-induced glomerulopathy in mice.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Involvement of immunopathogenic mechanisms in a spontaneously occurring glomerulopathy in mice.

Mice have been found to be susceptible to spontaneous renal localization of immune deposits. However, the significance of these immune deposits is still debated. We investigated the immunopathogenesis of a naturally occurring glomerulopathy associated with progressive proteinuria and glomerulosclerosis in 75 BALB/c mice. The mice were divided into five groups of 15 and killed at the age of 1, 3, 6, 12, or 18 months for laboratory and renal pathologic studies. These mice showed persistently increasing serum levels of immune complexes, a marked increase of glomerular immune deposits which were capable of fixing C3, and interstitial infiltration of lymphocytes and plasma cells, followed by the occurrence of proteinuria, mesangiopathy, and glomerulosclerosis. Our findings suggest that an immune system mediated process occurred in the kidneys of the mice tested.

Animals↗
PubMed1998

Experimental focal segmental glomerulosclerosis in mice.

Although a lot of animal models of proteinuria have been established, proposals for the mechanisms of proteinuria are still controversial. In this work, during an 18-day trial, mice injected with a single dose of adriamycin (AD) rapidly showed combined glomerular albuminuria and immunoglobulinuria, progressively elevated levels of nitrite/nitrate in urine, hypercholesterolemia, abnormal renal function, segmentally or globally glomerular hyalinosis/sclerosis associated with tubular atrophy, enhanced glomerular deposition of immunoglobulins and fibrinogen, augmented expression of matrix components in the whole glomerular tuft, and loss of glomerular negative charge property. These laboratory and pathological features are comparatively similar to those of human focal segmental glomerulosclerosis in the advanced state. Juxtamedullary glomeruli appear to be more susceptible to the AD-related nephrotoxicity than those in the superficial renal cortex. A change in size-dependent glomerular permselectivity may precede a charge-dependent defect in glomeruli in this mouse model of proteinuria. Data in this study confirm the hypothesis of glomerular hyperfiltration involved in the pathogenesis of this chronic glomerulopathy associated with proteinuria in mice. In addition, nitric oxide may play a crucial role in the progression of the chronic glomerulopathy model.

Animals↗
PubMed1998

Clinical manifestations and prognostic features of acute methamphetamine intoxication.

The prevalence of amphetamine abuse and the frequency of emergency department visits for amphetamine intoxication have increased dramatically worldwide. In this study, we retrospectively investigated the relationship between the prognostic features and clinical manifestations among patients admitted to the emergency department of a university hospital for acute methamphetamine intoxication during a 6-year period. Data collected included gender, age, route of abuse, time between drug exposure and arrival at the emergency department, estimated dose, signs and symptoms, laboratory values, and complications. Emergency therapy and cooling procedures were also recorded. After excluding 26 patients with multiple-drug intoxication, 18 patients (male-to-female ratio, 11:7) were include in the analysis. The mean age was 25.6 years. Thirteen patients survived and five died. Patients who died often presented with coma (80% vs 0%, p = 0.002), shock (60% vs 8%, p = 0.044), convulsions (100% vs 23%, p = 0.007), oliguria (80% vs 0%, p = 0.002), and high body temperature (41.4 +/- 0.5 degrees C vs 39.4 +/- 2.1 degrees C, p = 0.005). Furthermore, patients who died had significantly higher concentrations of blood urea nitrogen (8.7 +/- 2.1 vs 5.6 +/- 2.0 mmol/L, p = 0.01) and serum creatinine (212 +/- 71 vs 115 +/- 27 mumol/L, p = 0.033), and lower values of arterial pH (7.12 +/- 0.12 vs 7.34 +/- 0.10, p = 0.03), than those who survived. In the fatality group, the most common complication was rhabdomyolysis with acute renal failure (5 of 5); multiple organ failure resembling that from heatstroke was the leading cause of death from acute methamphetamine intoxication. In conclusion, the adverse prognostic features in patients with acute methamphetamine intoxication include coma, shock, convulsion, oliguria, and high core temperature. Acidosis, volume depletion, and ischemic renal damage were potential risk factors for development of acute renal failure in these patients.

Acute Disease↗
PubMed1998

[Effectiveness of videotape education for mothers of prematurity].

To investigate the effectiveness of an educational videotape on preterm mothers' knowledge, confidence, perceived stress, and social support, mothers who had given birth prematurely were recruited to participate in this study. Sixty-two mothers were randomly assigned to a control or experimental group. During hospitalization, mothers assigned to the experimental group received additional educational videotape which was designed by researchers for this particular study, regarding the knowledge and skills of caring for premature infants. While mothers in the control group received routine educational care. Both groups of mothers filled out the questionnaire including knowledge of prematurity, maternal confidence, perceived stress and perceived social support at three time periods (before discharge, one week after discharge, and one month after discharge). The findings indicated that mothers who received a videotape education reported having higher knowledge and confidence of caring for their preterm babies than mothers who were in the control group. Moreover, mothers in the experimental group perceived lower stress than the control group mothers when their babies were one month old. The scores of perception of stress, parity, and receiving a videotape education are the best predictors to maternal confidence a week after discharge. Further, the mothers' perception of stress, parity, and the perception of social support can predict and explain 47.1% of the variance of the maternal confidence. These results can apply to clinical practice for nursing mothers who have given preterm births. A convenient videotape education can improve mothers' knowledge and confidence of caring for their premature babies at home.

Adult↗
PubMed1997

Energy metabolism in exertional heat stroke with acute renal failure.

BACKGROUND: Heat stroke is the clinical syndrome produced when the body overheats. It can develop in the army and in healthy civilian populations who physically exert themselves in a hot and humid environment during the summer, and may result in a significant number of heat-related deaths. Since strenuous exercise is one of the major exacerbating and precipitating factors, the incidence of exertional heat stroke (ExHS) is high among military personnel undergoing military training. Furthermore, acute renal failure (ARF) may occur in 25% of patients with ExHS and it can cause metabolic alterations that affect amino acid, carbohydrate, and lipid metabolism. Adequate nutritional support is essential for the treatment of ARF. The most important determinant of nutrient requirement in ARF is the degree of hypercatabolism caused by disease associated with renal function impairment. Indirect calorimetry (IDCM) is the method by which metabolic rate is estimated from measurements of oxygen consumption and carbon dioxide production. It can also provide information about the type and rate of substrate utilization in vivo (protein, carbohydrate, and fat). METHOD: The present clinical study is a comprehensive analysis of metabolic changes which includes energy expenditure (EE) and substrate utilization in 10 patients with ExHS with ARF and 10 patients with exertional heat exhaustion (ExHE) by the use of IDCM. RESULTS: Serum urea nitrogen, creatinine, peak creatine phosphokinase levels and heart rate were significantly increased in ExHS patients during ARF stage. Serum albumin levels were significantly decreased in ExHS patients with ARF. Resting energy expenditure (REE) was increased in patients with ExHS induced ARF and was not correlated with body temperature (r = 0.421). The average increase in EE during ARF stage was about 24%. The respiratory quotient in patients with ExHS induced ARF was lower than that in normal subjects and also in patients with ExHE. Urea nitrogen appearance rate increased in patients with ExHS induced ARF and in patients with ExHE without ARF. The percentage of total REE derived from fat in ExHS induced ARF and ExHE increased, while in patients with ExHS induced ARF and ExHE, the percentages of total REE derived from carbohydrate and protein were lower than those in control subjects. CONCLUSIONS: The present results suggest that patients with exertional heat injury (both ExHS and ExHE) have hypermetabolism during the acute stage. Furthermore, patients with exertional heat-induced rhabdomyolysis and ARF have a moderately higher hypermetabolism than those without ARF during the acute stage. We believe that this mainly reflects a more pronounced reduction of the vital cell mass (muscle) in relation to body weight, and/or a compromised substrate oxidation in ExHS with ARF. Whether or not this subgroup of patients will require a higher energy/caloric support merits further investigation.

Acute Kidney Injury↗
PubMed1996

Fatal Aeromonas hydrophila bacteremia in a hemodialysis patient treated with deferoxamine.

A 49-year-old woman undergoing long-term hemodialysis and treated with deferoxamine (DFO) 1.5 g twice weekly for aluminum bone disease developed fever and bilateral calf pain caused by myonecrosis with gas gangrene. She had a rapidly fatal outcome. The cultures of blood and aspirates from both calf muscles demonstrated Aeromonas hydrophila. No obvious entry point could be traced. The in vitro growth of the patient's strain was found to be stimulated by the deferoxamine-iron complex in an iron-deprived medium. It is suggested that high-dose DFO therapy in this patient was responsible for promoting a bacterial infection by this microorganism.

Aeromonas hydrophila↗