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Chih-Jen Cheng

Publications and source records attributed to Chih-Jen Cheng.

13 recordsLinked to original sources
PubMed2007

Joint optimization of word alignment and epenthesis generation for Chinese to Taiwanese sign synthesis.

This work proposes a novel approach to translate Chinese to Taiwanese sign language and to synthesize sign videos. An aligned bilingual corpus of Chinese and Taiwanese Sign Language (TSL) with linguistic and signing information is also presented for sign language translation. A two-pass alignment in syntax level and phrase level is developed to obtain the optimal alignment between Chinese sentences and Taiwanese sign sequences. For sign video synthesis, a scoring function is presented to develop motion transition-balanced sign videos with rich combinations of intersign transitions. Finally, the maximum a posteriori (MAP) algorithm is employed for sign video synthesis based on joint optimization of two-pass word alignment and intersign epenthesis generation. Several experiments are conducted in an educational environment to evaluate the performance on the comprehension of sign expression. The proposed approach outperforms the IBM Model 2 in sign language translation. Moreover, deaf students perceived sign videos generated by the proposed method to be satisfactory.

Algorithms↗
PubMed2006

Syndrome of inappropriate antidiuretic hormone secretion in a patient with cryptococcal meningoencephalitis: a hidden mediastinal small cell carcinoma.

We report a 59-year-old man with cryptococcal meningoencephalitis who presented with typical features of syndrome of inappropriate antidiuretic hormone secretion (SIADH). There was no evidence of lung disease or drugs causing SIADH. Studies for endocrine functions and tumor markers were normal. The patient's hyponatremia was refractory to treatment (Na 120-125 mmol/L) after resolution of the cryptococcal infection. Three months after completion of antifungal treatment, a radiograph of the chest disclosed widening of the mediastinum. Computed tomography revealed a mediastinal mass. A tentative diagnosis of extrapulmonary cryptococcoma or a tumor was made. Positron emission tomography using F-fluorodeoxy glucose demonstrated an intense uptake mass in the mediastinum without lesions elsewhere in the body. A biopsy of the mass clearly showed small cell carcinoma (SCC) with positive immunoreactivity for arginine vasopressin and atrial natriuretic peptide. The hyponatremia completely resolved and tumor size dramatically decreased after chemotherapy. To the best of our knowledge, this is the first case of mediastinal SCC associated with SIADH. Patients with otherwise unexplained SIADH should be meticulously scrutinized for a possible malignancy.

Carcinoma, Small Cell↗
PubMed2006

Pylephlebitis associated with acute infected choledocholithiasis.

Pylephlebitis, also called septic thrombophlebitis of the portal vein, is a life-threatening complication of intra-abdominal infection. Although rare, it remains a less recognized entity with a high rate of mortality. We present a 66-year-old man with acute infected choledocholithiasis complicated with Bacteroides fragilis bacteremia. The contrast-enhanced computed tomography scan of the abdomen showed nearly total thrombotic occlusion of the left portal vein. The comprehensive studies for hypercoagulation disorders all yielded negative results. After endoscopic extraction of bile duct stones and broad-spectrum antibiotic therapy, the patient recuperated with complete recanalization of the occluded portal vein. To our knowledge, pylephlebitis associated with acute infected choledocholithiasis has never been reported. This report details the clinical features, radiographic findings, pathogenesis, and treatment of this distinctly unusual manifestation. Early identification of pylephlebitis and underlying intra-abdominal infection can be achieved by exquisite imaging studies with raised awareness in the clinical setting. Eradication of infectious foci and judicious administration of antimicrobials are essential to reduce the catastrophic morbidity and mortality of pylephlebitis.

Abdominal Cavity↗
PubMed2006

Early diagnosis of thyrotoxic periodic paralysis: spot urine calcium to phosphate ratio.

OBJECTIVES: To identify a clinically reliable index of thyrotoxic periodic paralysis (TPP), a life-threatening emergency with unique and effective therapies. DESIGN: Diagnostic study. SETTING: University teaching hospital. PATIENTS: Fifty-three consecutive patients with hypokalemic paralysis during a 3-yr period and 30 thyrotoxic patients without paralysis as the thyrotoxic control group. INTERVENTIONS: For patients with hypokalemic paralysis, blood and second-void spot urine samples were obtained and measured by routine laboratory prior to therapy. For the thyrotoxic control group, blood and spot urine were collected when they visited outpatient clinics. MEASUREMENTS AND MAIN RESULTS: Twenty-nine patients fulfilled the criteria for TPP. Compared with the thyrotoxic control group, the TPP group had significant decreases in plasma potassium (K) and phosphate concentrations associated with very low urine K and phosphate excretion. Compared with the non-TPP group, the TPP group had significantly lower plasma creatinine and phosphate levels, a significantly higher urine calcium to creatinine ratio (0.25 +/- 0.12 vs. 0.08 +/- 0.07 mg/mg, p < .001), and a significantly lower urine phosphate to creatinine ratio (0.08 +/- 0.05 vs. 0.31 +/- 0.23 mg/mg, p < .001). The urine calcium to phosphate ratio had greater discriminatory power between TPP and non-TPP hypokalemic paralysis (4.1 +/- 2.3 vs. 0.5 +/- 0.6 mg/mg, p < .001). Using a urine calcium to phosphate ratio cutoff value of 1.7 mg/mg, sensitivity and specificity for TPP were 100% and 96%, respectively. CONCLUSIONS: Hypercalciuria and hypophosphaturia are characteristic features of TPP.

Adult↗
PubMed2006

An unrecognized cause of recurrent hypercalcemia: immobilization.

We report a 66-year-old Chinese man with chronic renal insufficiency (creatinine 1.7 mg/dL) and gout suffering from slurred speech and right hemiplegia for 3 days. Acute cerebral infarction was confirmed by computed tomography. Conscious disturbance occurred on the tenth hospital day without significant changes on imaging study when compared with a previous scan. Hypercalcemia (total calcium 14.1 mg/dL) and acute exacerbation of chronic renal failure (serum creatinine 2.5 mg/dL) were noticed. Hypercalciuria (FECa 3.2%), and low serum levels of intact parathyroid hormone and 1,25(OH)2D3 suggested nonparathyroidal hypercalcemia. An extensive workup failed to identify any etiology of hypercalcemia. Hypercalcemia and renal failure were temporarily ameliorated after aggressive volume expansion and loop diuretic treatment but recurred 2 weeks later. Immobilization hypercalcemia was considered after the exclusion of other discernible causes and was successfully treated with rehabilitative exercises and bisphosphonates without further recurrence during a 2-year follow-up. Clinical alertness to immobilization as a possible cause of hypercalcemia may avoid unnecessary and invasive examinations, life-threatening complications and annoying recurrences.

Aged↗
PubMed2005

Phenotype and genotype analysis in Chinese patients with Gitelman's syndrome.

Inactivation mutations of the luminal thiazide-sensitive NaCl cotransporter (NCC) in the distal convoluted tubules or the basolateral chloride channel (CLCNKB) in the distal nephron are the most common genetic mutations in Gitelman's syndrome (GS) or Bartter's syndrome (BS). We conducted clinical and molecular studies in Chinese patients with GS or BS. Twenty patients with chronic hypokalemia (15 males and five females, age 25 +/- 7 yr) from 15 unrelated Chinese families were investigated. All had renal K+ wasting, metabolic alkalosis, and normotension. The urinary calcium excretion rate was used to distinguish between BS or GS on clinical grounds. Clinical symptoms and biochemical studies were recorded. Molecular analysis included PCR single-strand confirmational polymorphism, direct sequencing of both the NCC and CLCNKB genes, and restriction fragment length polymorphism. Sixteen patients had a clinical diagnosis of GS with hypocalciuria and four BS without hypocalciuria. Four of these 20 patients did not have hypomagnesemia. The males had severe hypokalemia [1.9 +/- 0.4 mEq/liter (mmol/liter)] with paralytic episodes, whereas females had moderate hypokalemia [2.6 +/- 0.2 mEq/liter (mmol/liter)] and less severe symptoms. There were no mutations detected in CLCNKB. Twelve NCC mutations, including six novel mutations and nine recurrent ones, were identified. Allele frequency of the detected NCC mutations was 3% in 100 healthy subjects. Some GS patients with NCC mutations may have normocalciuria and/or normomagnesemia. Gender differences may account for phenotype variability. Screening of these identified NCC mutations remains the gold standard for the diagnosis of GS.

Adolescent↗
PubMed2005

An unusual cause of hypokalemic paralysis: aristolochic acid nephropathy with Fanconi syndrome.

Aristolochic acid nephropathy (AAN) with Fanconi syndrome presenting as hypokalemic paralysis is extraordinarily rare and may be unrecognized. We describe a 41-year-old man who presented with the inability to ambulate upon awakening in the morning. Physical examination revealed symmetric paralysis of bilateral lower limbs. Laboratory studies showed profound hypokalemia with renal potassium (K) wasting, hyperchloremic metabolic acidosis, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, and glycosuria, consistent with Fanconi syndrome. Mild renal insufficiency was also observed. A meticulous search for underlying causes of Fanconi syndrome was unrevealing. However, a significant amount of aristolochic acid (AA) was detected in the consumed Chinese herb mixture (AA-I, 7 microg/g) for the treatment of his leg edema for the past 2 months. His hypokalemia, renal insufficiency, and Fanconi syndrome completely resolved 2 months after the withdrawal of Chinese herb mixture and the supplementation of potassium citrate and active vitamin D3. AAN with Fanconi syndrome should be considered as a cause of hypokalemia in any patient administered undefined Chinese herbs.

Adult↗
PubMed2005

Unusual cause of hypokalemic paralysis in aged men: Sjögren syndrome.

Hypokalemic paralysis is a less recognized but reversible disorder in elderly patients. This report describes two elderly Chinese males (age 74 and 78 years) who had progressive muscle weakness and eventually paralysis. Physical examination showed symmetrical flaccid paralysis of extremities. Both had the major biochemical abnormality of profound hypokalemia (1.4 and 1.8 mmol/L) accompanied by high urine K+ excretion and hyperchloremic metabolic acidosis. A positive urine anion gap and alkaline urine pointed to the diagnosis of distal renal tubular acidosis. Large doses of potassium chloride supplementation were required to restore muscle strength. Pertinent investigations, including elevated titers of antinuclear antibody and rheumatoid factor, positive anti-Ro antibody, low serum C3 and C4 levels, and delayed saliva excretion on salivary scintigraphy suggested Sjögren syndrome. Despite the lack of sicca syndrome at the initial presentation, both had development of typical sicca syndrome and positive Schirmer test at the 5-month and 1-year follow-up, respectively. Potassium citrate supplement and prednisolone therapy completely corrected the hypokalemia and metabolic acidosis. Extraglandular involvement with distal renal tubular acidosis preceding the typical sicca syndrome may induce hypokalemic paralysis and unveil Sjögren syndrome in elderly males.

Aged↗
PubMed2004

A hidden cause of hypokalemic paralysis in a patient with prostate cancer.

Hypokalemic paralysis is a medical emergency due to the risks of cardiac arrhythmia, respiratory failure, and rhabdomyolysis. Besides supplementing patients with KCl to hasten recovery, the astute physician must search for the underlying cause to avoid missing a treatable and curable disorder. We report on an elderly Korean man who presented with marked limb paralysis, myalgias, and mild hypertension. He had prostate cancer treated with orchiectomy and hormone therapy 2 years previously. The major biochemical abnormalities were hypokalemia (K+: 1.7 mmol/l) associated with high renal K+ wasting and metabolic alkalosis (HCO3-: 42.6 mmol/l). Low plasma renin activity, low aldosterone concentration, and normal cortisol concentration pointed to a state of pseudohyperaldosteronism. While reviewing his drug history, the patient revealed he had been consuming eight packs (100 ml/pack) of a Korean herbal tonic daily to treat his prostate cancer for the past 2 months. A significant amount of glycyrrhizic acid (0.23 mg/ml), an active ingredient of licorice, was detected in the tonic. Discontinuation of the herbal tonic along with KCl supplementation achieved recovery in 2 weeks. As many complementary/alternative medicines for cancer contain licorice, this must be kept in mind as a cause of hypokalemia in cancer patients.

Aged↗
PubMedDate not supplied

Acute hyperkalemic paralysis in a uremic patient.

Hyperkalemia is a less-recognized life-threatening cause of paralysis. We describe a 38-year-old uremic man on regular hemodialysis (HD) without interruption who suffered from muscle weakness progressing to ascending symmetric paralysis, and inability to masticate. Physical examination revealed flaccid paralysis with areflexia of the four limbs. Computed tomography of the brain and cervical spine did not demonstrate any organic lesions. Laboratory investigations revealed serum K+ 8.1 mmol/L, urea nitrogen 32 mmol/L, creatinine 919 micromol/L. Of note, electrocardiography (ECG) did not show typical features of hyperkalemia. Emergent HD with low K+ dialysate (1.0 mmol/L) rapidly normalized serum K+ (4.7 mmol/L) and reversed all neuromuscular symptoms within one hour. Upon reviewing his food and medication history, he admitted drinking 750 ml of raw coconut juice per day (K+ concentration 44.3 mmol/L) to quench his thirst for three consecutive days. Hyperkalemia should be born in mind in the differential diagnosis of acute paralysis despite no ECG changes. Hidden sources of K+ intake, such as coconut juice, should not be overlooked, especially in patients with impaired renal function.

Adult↗
PubMedDate not supplied

Recurrent hyponatremia in a patient with chronic kidney disease.

Hyponatremia, albeit common in chronic renal insufficiency, necessitates a detailed search of the underlying hidden causes. We report on a 67-year-old woman with chronic kidney disease (creatinine 230 micromol/L) and hypertension who suffered from general fatigue, dizziness, nausea, vomiting and abdominal fullness off and on for 6 months. Hyponatremia (plasma Na(+) 106-125 mmol/L) on 4 occasions during the past 6 months was noticed. Her extracellular volume status was apparently normal. Plasma Na(+) concentration 110 mmol/L was the most striking laboratory abnormality with mild metabolic acidosis (HCO(3)- 19.8 mmol/L). Her urine Na(+) concentration and osmolality were inappropriately high. Her hyponatremia was refractory to normal saline, hypertonic NaHCO(3) and 0.1-microg 9 alfa-fludrocortisone. Despite normal plasma cortisol and thyroid hormone concentrations, a provocation test with cosyntropin (250 microg) showed a blunted cortisol (<579 nmol/L) but intact aldosterone response. Magnetic resonance imaging of her brain displayed a normal pituitary gland and hypothalamus. A history of intermittent intravenous steroid therapy to treat her allergic rhinitis for 3 years was uncovered. Steroid supplements induced water diuresis and corrected hyponatremia to 135 mmol/L in 5 days. With nonspecific clinical symptoms, glucocorticoid insufficiency must be kept in mind as a cause of hyponatremia even in patients with impaired renal function and normal plasma cortisol concentration.

Aged↗