Biomedical subjects

C M Chu

Publications and source records attributed to C M Chu.

186 records · Page 11Linked to original sources

PubMedDate not supplied

Appearance and persistence of hepatitis A IgM antibody in acute clinical hepatitis A observed in an outbreak.

143 patients with acute hepatitis A observed during a common source outbreak were tested for IgM class antibody to hepatitis A virus (IgM anti-HAV) by commercially available solid phase radioimmunoassays. All patients were IgM anti-HAV positive though six of them were initially negative when tested within three days after the onset of symptoms. The levels of IgM anti-HAV peaked two to four weeks after onset, and declined gradually thereafter. The probability of IgM anti-HAV positivity was 25% at the end of the sixth month, and 3.4% at the end of the ninth month after onset. No significant sex or age difference in the persistence of IgM anti-HAV was observed. It was suggested that the timing of the assay and the level of IgM anti-HAV should be considered in the etiological diagnosis of acute hepatitis.

Adolescent↗

PubMedDate not supplied

Clinicopathological response of HBsAg-positive chronic active hepatitis to adenine arabinoside: lack of correlation with DNA polymerase response.

Fifteen patients with HBsAg-positive, severe chronic active hepatitis, nine DNA polymerase (DNAP)-positive and six negative were treated with intravenous adenine arabinoside (Ara-A) in a dose of 10 mg/kg/day for five consecutive days during each of two consecutive weeks. Of the DNAP-positive patients, two responded with histological and clinical remission as well as permanent loss of DNAP. However, histological and clinical remission were also observed in patients with unsatisfactory DNAP response and even in DNAP-negative patients. It is suggested that, in addition to its antiviral effect, Ara-A might have another mechanism, such as immunosuppression, that induced histological and clinical remission. Alternatively, the discrepancy of response might relate to the natural course of chronic type B hepatitis. Accordingly, controlled trial is mandatory for assessing the effect of Ara-A or any other agent in the treatment of chronic type B hepatitis.

Adolescent↗

PubMedDate not supplied

The aetiology of acute hepatitis in Taiwan: acute hepatitis superimposed on HBsAg carrier state as the main aetiology of acute hepatitis in areas with high HBsAg carrier rate.

The aetiology of sporadic acute hepatitis in Taiwan was studied in a consecutive series of 273 patients, 209 males and 64 females, aged from less than 1 to 73 years. Only eight patients (2.9%) had acute hepatitis A, 36 (13.2%) acute hepatitis B and 57 (20.9%) had acute non-A, non-B hepatitis (NANB). The remaining 172 patients (63.0%) were HBsAg positive but anti-HBc IgM negative and were classified as acute hepatitis in chronic HBsAg carriers. Age-specific analysis revealed that acute hepatitis types A and B accounted for 35% and 47%, respectively of acute hepatitis in patients below age 10, but their prevalence decreased dramatically with increasing age and remained quite low in patients over age 40. In contrast, acute hepatitis NANB occurred predominantly in the older patients. The prevalence of acute hepatitis NANB was 11 to 15% in patients below age 40, but increased gradually with increasing age thereafter. Of the patients over age 60, 58% had acute hepatitis NANB. Acute hepatitis in chronic HBsAg carriers accounted for 59 to 76% of acute hepatitis episodes in patients over age 10 and below age 60. Sex-specific analysis revealed that the prevalence of acute hepatitis A or B showed no significant sex difference, whereas acute hepatitis in chronic HBsAg carriers occurred predominantly in males and acute hepatitis NANB occurred predominantly in females. Of the acute hepatitis episodes in chronic HBsAg carriers about one-third was due to hepatitis Delta virus superinfection, while the remaining two-thirds were most likely acute exacerbations of the underlying hepatitis B virus infection and a few were due to non-A, non-B hepatitis superinfection.

Acute Disease↗

PubMedDate not supplied

The role of laparoscopy in the evaluation of ascites of unknown origin.

The role of laparoscopy in the diagnostic evaluation of ascites of unknown origin was studied in 129 patients. Laparoscopic results were as follows: (1) Carcinomatosis peritonei in 78 (60.5%). Peritoneal biopsies in 76 of these cases revealed malignancy in 67 (adenocarcinoma 62, lymphoma 4, mesothelioma 1) and tuberculosis in 5; specimens were inadequate for diagnosis in 4. (2) Tuberculous peritonitis in 26 (20.2%). Peritoneal biopsies in 24 of these cases revealed tuberculosis in 22 and non-specific chronic peritonitis in 2. (3) Cirrhosis in 7 (5.4%). (4) No gross abnormality in 18 (14.0%). Of the latter, causes of ascites had already been identified in 13 (72.2%), including chronic renal failure in 7, systemic lupus erythematosus in 2, constrictive pericarditis in 2, chronic pancreatitis with chylous ascites in 1, and retroperitoneal lymph node metastasis with chylous ascites in 1. Thus, laparoscopic observation in combination with biopsy established the cause of ascites of unknown origin in 111 (86.0%) of 129 patients. Most of the 18 patients without gross laparoscopic abnormality had underlying disease identified as a cause of ascites; laparoscopy was indicated in these cases to exclude other processes that may also cause ascites.

Adult↗

PubMedDate not supplied

Nitric oxide production and apoptosis by GP120.

Nitric oxide (NO) is increased by gp120 in astrocytes and in monocyte-derived macrophages. Of the gp120 fragments (F1: amino acid 254-274, F2: amino acid 315-329, F3: amino acid 421-438), F1 has been shown to increase NO in astrocytes and gp120 also primes CD4+ T cells for apoptosis. Peripheral blood mononuclear cells (PBMCs) at 10(6)/ml (N = 10) were incubated at 24 and 72 hours in RPMI, 10% CO2 with low doses (100 nM) gp120 and high doses (400 nM) of the smaller fragments. Supernatants were collected and assayed for the relative contribution of gp120 and its fragments on NO production at both time points. Apoptosis was detected by in situ hybridization with and without 1 microgram/ml LPS as superantigen at 72 hours. The major contribution to apoptosis and NO production was from F1. At 24 hours F1 had a 1.9-fold increase from control, whereas F2 and F3 had 1.25- and 1.35-fold increases. At 72 hours both F1 and F2 had a 1.5-fold increase and F3 had a 1.33 increase. Thus, F1 contributed significantly to NO production at 24 hours. Both F1 and F2 had significant contributions to NO production at 72 hours. F1 had the most contribution to apoptosis both with and without lipopolysaccharide (LPS). These findings may contribute to further understanding the mechanism of HIV-induced apoptosis.

Apoptosis↗

PubMedDate not supplied

Genetic alternations of p73 are infrequent but may occur in early stage hepatocellular carcinoma.

p73, a structural homologue of the tumor suppressor gene, p53, has recently been identified and mapped to chromosome 1p36, where genomic loss of heterozygosity (LOH) often occurs in human hepatocellular carcinoma (HCC). To determine whether p73 is involved in the development of HCC and whether there is an inverse correlation between the mutations of p73 and p53, we examined 22 paired tumors/noncancerous liver tissues for allelic expression, LOH and mutation of p73 and for mutation of p53. p73 was biallelically expressed in noncancerous liver tissues and in 7 out of the 8 informative tumors. One tumor tissue expressed only a single allele. LOH of p73 was found in 2 out of the 11 (18%) informative cases. A tumor-specific five-nucleotide deletion mutation causing a reading frameshift/early truncation of p73 DNA-binding domain was found, in which case no concomitant mutation in the DNA-binding domain of p53 was identified. Nine out of the 22 cases (41%) contained tumor-specific mutations in the DNA-binding domain of p53. Two of the three cases with p73 genetic alternations had a tumor size of less than 2 centimeters. These results suggest that p73 is a biallelically expressed gene in the liver and that allelic loss and mutation of p73 is infrequent and may occur early in HCC. p73 is unlikely to be the putative tumor suppressor gene located at chromosome 1p36 in HCC.

Adult↗