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C Y Hsu

Publications and source records attributed to C Y Hsu.

At least 37 records · Page 2Linked to original sources

Does treatment of non-malignant hypertension reduce the incidence of renal dysfunction? A meta-analysis of 10 randomised, controlled trials.

OBJECTIVE: It remains controversial whether non-malignant 'benign' hypertension causes renal dysfunction. The effect of lowering blood pressure on the incidence of renal dysfunction among patients with non-malignant hypertension is not clear. This meta-analysis was conducted to determine whether antihypertensive drug therapy reduces the incidence of renal dysfunction in patients with non-malignant hypertension. METHODS: Randomised, controlled trials of antihypertensive drug therapy of more than 1 year duration that reported renal dysfunction as an outcome were identified through MEDLINE search and literature review. A random effects model was used to obtain summary estimates. RESULTS: Ten trials were identified, involving 26, 521 individuals and 114 000 person-years. All excluded subjects with advanced baseline renal disease. Definition of renal dysfunction outcome varied among trials but within each trial was applied similarly to both treatment and control groups. Drug treatment consisted mostly of diuretics and adrenergic blockers. Overall, treated patients had lower blood pressure and fewer cardiovascular events. There were a total of 317 cases of renal dysfunction. Patients randomised to antihypertensive therapy (or more intensive therapy) did not have a significant reduction in their risk of developing renal dysfunction (relative risk = 0.97; 95% confidence interval (CI) 0.78-1.21; P = 0.77). CONCLUSIONS: Among patients with non-malignant hypertension enrolled in randomised trials, treated patients did not have a lower risk of renal dysfunction. The 95% CI suggests that a 25% or more true protective effect of antihypertensive drugs is unlikely.

Adult↗

Plurihormonal pituitary adenomas: immunostaining of all pituitary hormones is mandatory for correct classification.

AIMS: We studied the clinicopathological characteristics of plurihormonal pituitary adenomas. METHODS AND RESULTS: The study material included 167 plurihormonal adenomas, which consisted of 31% of the surgically removed pituitary adenomas that we collected during a 12-year period. The mean age of patients with plurihormonal adenoma was 45.7 years (range 13-75 years). There were 86 men and 81 women. All tumours were fully classified by immunohistochemical staining for seven pituitary hormones or subunits. Thirty immunohistochemical subtypes of plurihormonal adenomas were recognized. Hormonal symptoms were present in 70% of patients, while serum hormonal levels were increased in 89% of patients. Most patients had symptoms related to only one of the hormones and only 7% of patients had symptoms related to two hormones. The most common hormonal symptom was acromegaly (50%); symptoms related to hyperprolactinaemia ranked second (20%). Double immunostaining of all the possible combinations of the hormones was performed in 30 selected tumours, and they all showed mixtures of hormones in individual adenoma cells in any hormonal combinations studied. The latter finding supported the view that plurihormonal adenomas are monomorphous adenomas. CONCLUSIONS: Plurihormonal adenomas are common pituitary adenomas. Immunohistochemical staining of all pituitary hormones is mandatory for correct classification.

Adenoma↗

Magnetic resonance imaging findings in patients with delusional disorder due to diffuse cerebrovascular disease: a report of seven cases.

Delusions associated with cerebrovascular diseases have been sporadically reported. Although both psychiatrists and neurologists attempted to link delusions with anatomical locations of the brain lesion, comorbid psychiatric and neurological disorders make the interpretation of delusions difficult. The purpose of the present paper is to report the clinical features and magnetic resonance imaging (MRI) characteristics in patients with delusional disorder due to diffuse cerebrovascular diseases, and to redefine the concept of 'vascular delusion'. The clinical features and MRI findings were reviewed retrospectively in a series of seven patients with 'delusional disorder due to cerebrovascular disease' as defined in Diagnostic and Statistical Manual of Mental Disorders (DSMIV). The average age of onset is 64. No patient had a prior personal or family history of major psychiatric illness. The illness is presented as acute, subacute or stepwise course. Hypertension was present in all patients. Two had diabetes mellitus, and one had atrial fibrillation. Three had clinical evidence of previous cerebrovascular attacks, only one showed minor neurological deficits. Three had diffuse cortical slow wave in electroencephalogram. No patient had significant cognitive impairment but had multiple cortical and subcortical cerebrovascular lesions in MRI, with white-matter lesions (WML) in bilateral frontal areas. Delusional disorder due to diffuse cerebrovascular change is characterized by late-onset, stepwise course, and comorbid medical and neurological diseases. The results of vascular changes in the present study did not establish a cause-effect relationship and should be considered as multifactorial in pathogenesis. The findings suggested the hypothesis of neural circuit theory. Further studies in larger numbers of patients and newer neuroimaging techniques are needed to expand the knowledge learned from these findings.

Aged↗

Relationship between hematocrit and renal function in men and women.

BACKGROUND: Anemia is a known complication of renal insufficiency, but the relationship between level of renal function and magnitude of reduction in hematocrit is not well defined. Men have higher hematocrit and absolute glomerular filtration rate (GFR) than women; however, it is unknown whether the level of clearance associated with decreased hematocrit is the same in men and women. METHODS: We conducted a cross-sectional study of 12,055 adult ambulatory patients. General linear models were used to analyze the relationship between hematocrit and Cockcroft-Gault equation estimated creatinine clearance (C(Cr); mL/min) and Modification of Diet in Renal Disease (MDRD) formula estimated the GFR indexed to body surface area (mL/min/1.73 m(2)). RESULTS: The hematocrit decreased progressively below estimated C(Cr) 60 mL/min in men and 40 mL/min in women. Compared with subjects with C(Cr)> 80 mL/min, men with C(Cr) 60 to 50 mL/min, 50 to 40 mL/min, 40 to 30 mL/min, 30 to 20 mL/min, and < or =20 mL/min had mean hematocrits that were lower by 1.0, 2.4, 3.7, 3.5, and 10.0%, respectively; the corresponding reductions in women with C(Cr) 40 to 30 mL/min, 30 to 20 mL/min, and < or =20 mL/min were 1.7, 2.9, and 6.3% (all P < 0.05). This between-sex difference diminished when renal function measurement was indexed to body size. Compared with subjects with GFR> 80 mL/min/1.73 m(2), men with GFR 50 to 40 mL/min/1.73 m(2), 40 to 30 mL/min/1.73 m(2), 30 to 20 mL/min/1.73 m(2), and < or =20 mL/min/1.73 m(2) had mean hematocrits that were lower by 2.0, 4.4, 5.3, and 9.4%; the corresponding reductions in women with GFR 50 to 40 mL/min/1.73 m(2), 40 to 30 mL/min/1.73 m(2), 30 to 20 mL/min/1.73 m(2) and < or =20 mL/min/1.73 m(2) were 0.6, 1.6, 3.8, and 5.3% (all P < 0.05). CONCLUSIONS: A decrease in hematocrit is apparent even among patients with mild to moderate renal insufficiency. At any given level of renal function below estimated C(Cr) 60 mL/min, men have a larger decrease in hematocrit than women.

Adult↗

MR imaging of displaced meniscal tears of the knee. Importance of a "disproportional posterior horn sign".

PURPOSE: Meniscal tears associated with displaced fragments are clinically significant. We propose the "disproportional posterior horn sign" as a supportive criterion to identify a posterocentrally displaced meniscal fragment on MR imaging studies. If the meniscal posterior horn in the central portion appears larger than that in the peripheral section, it is considered positive for "disproportional posterior horn sign". MATERIAL AND METHODS: MR images obtained in 42 patients with 43 lesions, confirmed to have displaced meniscal tears, were included in this study. The MR images were retrospectively evaluated for the presence of the "disproportional posterior horn sign", as well as the other known signs. RESULTS: The "disproportional posterior horn sign" was seen in 9 (20.9%) of 43 lesions, including 1 lateral discoid meniscal tear, 5 lateral meniscal tears and 3 medial meniscal tears. Five of them also had other signs of a displaced meniscal fragment. However, the remaining 4 cases only exhibited the "disproportional posterior horn sign". For the other MR signs, the "absent bow tie sign" was detected in 40 (93%) of 43 lesions, the "flipped meniscus sign" in 27 (62.8%) of 43 lesions, the "double posterior cruciate ligament sign" in 17 (39.5%) of 43 lesions and the "notch fragment sign" in 22 (51.2%) of 43 lesions. CONCLUSION: The "disproportional posterior horn sign" is helpful in demonstrating a posterocentrally displaced meniscal fragment, especially when other characteristic signs are unremarkable or absent.

Adolescent↗

iNOS and nitrotyrosine expression after spinal cord injury.

Secondary tissue damage after spinal cord injury (SCI) may be due to inflammatory mediators. After SCI, the nuclear factor-kappaB (NF-kappaB) transcription factor can activate many pro-inflammatory genes, one of which is inducible nitric oxide synthase (iNOS). iNOS catalyzes the synthesis of nitric oxide (NO), a key inflammatory mediator, which in turn reacts with superoxide to generate peroxynitrite. Peroxynitrite is a strong oxidant that can damage cellular enzymes, membranes, and subcellular organelles through the nitration of tyrosine residues on proteins. The presence of nitrotyrosine (NT) is an indirect chemical indicator of toxic NO and peroxynitrite-induced cellular damage. Using a New York University (NYU) impactor to induce SCI in adult rats, we examined the temporal and cellular expression of iNOS and NT. We observed a progressive increase in iNOS expression in the injured cord starting at day 1 with maximal expression occurring at day 7, as determined by Western blot analysis. iNOS expression corresponded temporally to an increase in iNOS enzyme activity after SCI. In parallel with the progressive increase in iNOS activity, NT expression also increased with time after SCI. The iNOS and NT immunoreactivity was localized in neurons, astrocytes, endothelial cells and ependymal cells at the epicenter and adjacent to the region of spinal cord impact and injury. Results from the present study suggest that increased iNOS and peroxynitrite anion, as reflected by the progressive accumulation of NT in the injured impacted spinal cord, may contribute to the secondary injury process after SCI.

Animals↗

Cellular localization of tumor necrosis factor-alpha following acute spinal cord injury in adult rats.

Posttraumatic inflammatory reaction may contribute to secondary injury after traumatic spinal cord injury (SCI). Expression of tumor necrosis factor-alpha (TNF-alpha), a key inflammatory mediator, has been demonstrated in the injured cord. However, the specific cell types that are responsible for TNF-alpha expression after SCI remain to be identified. In the present study, cellular sources of TNF-alpha were examined in rats that received a spinal cord impact injury at the 9th thoracic (T9) level. Here we demonstrate that, within hours after SCI, increased TNF-alpha immunoreactivity was localized in neurons, glial cells (including astrocytes, oligodendrocytes, and microglia), and endothelial cells in areas of the spinal cord adjacent to the lesion site. Myelin breakdown was noted in oligodendrocytes that are immunopositive for TNF-alpha. In sham-operated controls, a low level of TNF-alpha immunoreactivity was detected. In antigen-absorption experiments, no TNF-alpha immunoreactivity was detected, indicating the specificity of TNF-alpha immunocytochemistry in the present study. Results suggest that various cell types, including neurons, glial cells, and vascular endothelial cells, contribute to TNF-alpha production in the injured cord.

Acute Disease↗

Induction of Tie-1 and Tie-2 receptor protein expression after cerebral ischemia-reperfusion.

Tie-1 and Tie-2 are receptor tyrosine kinases (RTKs) that are exclusively expressed in endothelial cells and play important roles in endothelial cell biology. The authors have reported previously the temporal profiles of Tie-1 and Tie-2 mRNA expression after focal cerebral ischemia-reperfusion. In the current study, the localization of Tie-1/Tie-2 mRNA and proteins were further investigated in the same focal ischemia model. In situ hybridization showed that, after 60-minute ischemia and 72-hour reperfusion, both Tie-1 and Tie-2 mRNA appeared as capillary-like structures in the ischemic middle cerebral artery (MCA) cortex. Western blot analysis showed a biphasic expression of Tie-1 protein in the same region. The first peak, spanning the ischemic and early reperfusion period. was of low intensity and short-lived. The second peak was of greater intensity and spanning the period from 72 to 168 hours after reperfusion. Similarly, Tie-2 expression at the protein level also exhibited a biphasic pattern. Immunohistochemical studies, after 72 hours of reperfusion, showed that although Tie-1 and Tie-2 were detected within the ischemic cortex, they actually were expressed in different populations of endothelial cells in different regions. In agreement with the in situ hybridization study, Tie-1 immunoreactivity appeared as capillary-like structures in cortical layers 2 to 4. Similar capillary-like appearance of Tie-2 immunoreactivity was noted in the outer cortical layers. In addition, Tie-2 immunoreactivity also was observed in cortical layer 6b, where de novo large vessel formation was noted. Cellular colocalization experiments revealed that Tie-2 is expressed in proximity to its antagonist, Angpo-2, as well as basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) in cortical layer 1, where active vessel remodeling was noted. Interestingly, bFGF only partially colocalized with VEGF, suggesting differential roles for these angiogenic factors during vessel remodeling. Tie-1 protein, to a lesser degree, also colocalized with Angpo-2, bFGF, and VEGF in cortical layer 1. Magnetic resonance imaging (MRI) showed increased regional cerebral blood flow (CBF) corresponding to the expression of these angiogenesis gene products. Together, these findings suggest that the evolving expression of angiogenesis genes underlie the robust vascular remodeling after ischemia and reperfusion.

Angiopoietin-2↗

Amyloid beta peptide-induced cerebral endothelial cell death involves mitochondrial dysfunction and caspase activation.

Amyloid beta peptide (A beta), a 39 to 43 amino acid fragment of the beta-amyloid precursor protein (betaAPP), forms insoluble fibrillar accumulation in neurofibrillary tangles and vascular plaques. A beta has been implicated in neuronal and vascular degeneration in brain regions susceptible to plaque formation because of its cytotoxic effect on neurons and endothelial cells (ECs). The authors used a murine cerebral endothelial cell (CEC) line and primary cultures of bovine CECs to explore the cytotoxic mechanism of A beta. A beta 1-40 and A beta 25-35 peptides caused cell death in a dose-dependent and time-dependent manner. Exposure to either A beta 25-35 or A beta 1-40 at 10 micromol/L for 48 hours caused at least 40% cell death. Cerebral endothelial cell death was characterized by nuclear condensation, mitochondrial dysfunction, and nuclear and mitochondrial DNA damage. A beta 25-35 activated both caspase-8 and caspase-3 in murine CECs. zVAD-fmk, a broad-spectrum caspase inhibitor, prevented A beta 25-35-induced increase in caspase-3 activity and CEC death. N-acetyl-cysteine, an antioxidant, also prevented A beta-induced cell death. Together, these findings indicate that A beta-mediated CEC death is an apoptotic process that is characterized by increased oxidative stress, caspase activation, mitochondrial dysfunction, and nuclear and mitochondrial DNA damage.

Acetylcysteine↗

High-fat hypocaloric diet modifies carbohydrate utilization of obese rats during weight loss.

The effects of fat content in the hypocaloric diet on whole body glucose oxidation and adipocyte glucose transport were investigated in two animal-feeding experiments. Diet-induced obese rats were food restricted to 75% of their previous energy intakes with either a high (45% by calorie) or a low (12% by calorie) corn oil diet for 9 wk (experiment 1) or 10 days (experiment 2). The losses of body weight (P < 0.05) and adipose depot weight (P < 0.05) were less in the 45% compared with the 12% fat group. During the dynamic phase of weight loss (day 10 of food restriction), plasma glucose and insulin concentrations were higher (P < 0.05) in the 45% than those in the 12% fat group. Whole body carbohydrate oxidation rate in response to an oral load of glucose was increased (P < 0.001) by food restriction in both dietary groups; however, carbohydrate oxidation rates were lower (P < 0.01) in the 45% than in the 12% fat-fed rats during the weight loss period. Adipocyte glucose transport was greater (P < 0.02) in the 45% than in the 12% fat group in an intra-abdominal adipose depot but not in subcutaneous fat. These data suggest that dietary fat content modifies whole body glucose oxidation and intra-abdominal adipocyte glucose uptake during weight loss.

Adipocytes↗

Reduction and restoration of mitochondrial dna content after focal cerebral ischemia/reperfusion.

BACKGROUND AND PURPOSE: Oxidative damage of mitochondrial DNA (mtDNA) in the ischemic brain is expected after ischemia/reperfusion injury. A recent study demonstrated limited patterns of mtDNA deletion in the brain after ischemia/reperfusion. We studied the ischemia/reperfusion-induced global changes of mtDNA integrity and its restoration in a rat model of transient focal ischemia in vivo. METHODS: Changes in mtDNA content in the ischemic brain were assessed with the use of a rat stroke model featuring transient severe ischemia confined to the cerebral cortex of the right middle cerebral artery territory for 30 or 90 minutes. A new long polymerase chain reaction method, using mouse DNA as an internal standard, was applied to measure the relative content of intact rat mtDNA. Southern hybridization following alkaline gel electrophoresis was conducted in a parallel study to confirm long polymerase chain reaction results. RESULTS: A reduction in mtDNA content was found after ischemia for 30 and 90 minutes. The mtDNA was restored to near nonischemic levels 24 hours after 30- but not 90-minute ischemia. CONCLUSIONS: These results confirm that ischemia/reperfusion causes mtDNA damages. Restoration of the mtDNA content to nonischemic levels after 30-minute ischemia raises the possibility that mtDNA repair or repletion occurs after brief ischemia.

Animals↗

Laser-matrix-fluoride effects on enamel demineralization.

Laser and fluoride have been shown to inhibit enamel demineralization. However, the role of organic matrix and their interactions remains unclear. This study investigated the interaction among CO2 laser irradiation, fluoride, and the organic matrix on the demineralization of human enamel. Twenty-four molars were selected and cut into halves. One half of each tooth was depleted of its lipid and protein. The other half served as a matched control. Each tooth half had two window areas, treated with a 2.0% NaF gel. All left windows then received a laser treatment. Next, the tooth halves were subjected to a four-day pH-cycling procedure that created caries-like lesions. Tooth sections were cut from the windows, and microradiographs were used for quantification of the demineralization. The combined fluoride-laser treatment led to 98.3% and 95.1% reductions in mineral loss for enamel with and without organic matrix, respectively, when compared with sound enamel.

Analysis of Variance↗

Bacteriology of chronic sinusitis after amoxicillin-clavulanate potassium therapy.

The bacteriology of chronic sinusitis was studied after amoxicillin-clavulanate potassium therapy. Patients with chronic sinusitis were randomly divided into 2 groups. In the study group, 90 patients were given a 2-week course of amoxicillin-clavulanate potassium before functional endoscopic sinus surgery. In the control group, 113 patients did not take any antibiotics within 2 weeks before the surgery. Swab specimens were taken from the maxillary and ethmoid sinuses during surgery and sent for aerobic and anaerobic culture. In the study group, the culture rates of maxillary and ethmoid sinuses were 45.6% and 28.9%, respectively. In the control group, the culture rates of maxillary and ethmoid sinuses were 53.1% and 34.5%, respectively. The culture rates between the control group and the study group were not significantly different, either for the maxillary sinus or the ethmoid sinus. This showed that treatment with amoxicillin-clavulanate potassium did not change the bacteriology of chronic sinusitis.

Adolescent↗

Cardiovascular effects of the R- and S-enantiomers of ibutilide in conscious beagle dogs.

To support its class III antiarrhythmic candidacy, we examined the acute cardiovascular effects of ibutilide and its R- and S-enantiomers in conscious beagle dogs. Eight dogs were given stepped i.v. doses (0.01, 0.1, and 1.0 mg/kg) of these agents while monitoring changes in mean arterial pressure (MAP), heart rate (HR), and lead II ECG QTc length (index of class III activity). None of the treatments affected MAP and only R-ibutilide slightly increased HR. The R-isomer was also slightly more potent in prolonging QTc at the lowest dose, but its mean peak QTc change (+44 msec) overlapped those achieved with racemic (+37 msec) and S-ibutilide (+41 msec). Plasma drug analyses showed that total drug levels (sum of enantiomers) were similar with each agent, averaging 1, 12, and 170 ng/ml at 30 min after the low, middle, and high doses, respectively. Nearly equal enantiomer proportions were seen after racemic ibutilide, and no chiral inversion was seen after enantiomer administration. All treatments were well tolerated without enhanced ventricular ectopy. These data demonstrate that in conscious dogs, racemic, R-, and S-ibutilide similarly prolong QTc independent of appreciable cardiovascular changes, differential pharmacokinetics, or dysrhythmias, thereby helping to establish racemic ibutilide as the optimal developmental candidate.

Animals↗

Inducible nitric oxide synthase neutralizes carbamoylating potential of 1,3-bis(2-chloroethyl)-1-nitrosourea in c6 glioma cells.

Expression of iNOS in glioma and other tumors has been extensively documented but the effects of NO derived from iNOS on tumor-killing mechanisms of chemotherapy drugs remain to be fully defined. We note that increased NO synthesis by cytokine exposure or iNOS overexpression neutralized the cytotoxicity of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), but not cisplatin, in rat C6 glioma cells. Suppression of BCNU cytotoxicity associated with iNOS overexpression could be abolished by pharmacological inhibition of NOS or coexpression of an antisense RNA against iNOS. Both BCNU and CCNU are chloroethylnitrosoureas that kill tumor cells via carbamoylating and alkylating actions. Further studies using compounds that each carry these different activities indicate that iNOS neutralized carbamoylating, but not alkylating, action of chloroethylnitrosoureas. Temozolomide, a novel chemotherapy drug recently available for treating brain tumors, carries only alkylating, but not carbamoylating, action. Overexpression of iNOS in C6 cells failed to neutralize temozolomide cytotoxicity. Results from the present study demonstrate the ability of iNOS-derived NO to confer chemoresistance against the carbamoylating potential of chloroethylnitrosoureas in vitro. Further investigation is needed to test whether iNOS expression, frequently noted in malignant brain tumors, also enhances chemoresistance against chloroethylnitrosoureas in vivo.

Animals↗

Endoscopic sinus surgery for the treatment of chronic sinusitis in geriatric patients.

Although endoscopic sinus surgery is a well-documented procedure for the treatment of chronic sinusitis in children and adults, no study has been conducted to specifically investigate its application in a geriatric population. We undertook to fill this void by analyzing the records of 1,112 patients who had undergone endoscopic sinus surgery for chronic sinusitis in our department between April 1988 and March 1998. We categorized these patients by age. There were 171 patients (15.4%) in the geriatric group (age: > or = 65 yr), 837 patients (75.3%) in the adult group (age: 17 to 64), and 104 patients (9.4%) in the pediatric group (age: < or = 16 yr). We found that the geriatric group experienced a disproportionately larger share of operative complications, but most of them were minor. Outcomes were similar in all three groups. We conclude that endoscopic sinus surgery is a safe and effective treatment for older patients with chronic sinusitis.

Adolescent↗

Diagnosis and treatment of lipomas of the internal auditory canal.

A Chinese woman came to the otolaryngology department with a complaint of a longstanding progressive left hearing loss and intractable tinnitus. A finding of asymmetry on sensorineural hearing loss and auditory brainstem response testing provided evidence of a retrocochlear lesion on the left side. Computed tomography and magnetic resonance imaging detected a tumor in the left internal auditory canal (IAC). In addition to these radiologic features, our suspicion of the possibility of an IAC lipoma was raised by the observation of multiple lipomas over the patient's trunk and limbs. The patient underwent a complete tumor resection via the translabyrinthine approach, Pathology confirmed the diagnosis of an IAC lipoma. Although we were not able to preserve the hearing in her left ear, the patient was satisfied that we had relieved her constant tinnitus. In this article, we review the particulars of this case and discuss the clinical, radiologic, and pathologic features of IAC lipomas.

Adult↗