Search PubMed⌕ Search

Biomedical subjects

C H Chang

Publications and source records attributed to C H Chang.

At least 667 records · Page 37Linked to original sources

[Humoral and cell-mediated immunities in patients with pulmonary tuberculosis (author's transl)].

Humoral and cell-mediated immunities were studied in 38 patients with pulmonary tuberculosis proved by sputum smears and/or cultures and chest X-rays. Nineteen healthy adults were included as control. The results showed that while the mean numbers of total white blood cell count, polymorphonuclear leukocytes, monocytes, B-lymphocytes and serum IgG concentration were significantly increased in patients, there was no difference in the mean numbers of lymphocytes, total T-lymphocytes, active T-lymphocytes, polymorphonuclear leukocytes and monocyteswith Fc and complementreceptor and serum IgA and IgM concentrations between these two groups. These data indicate that the patients with pulmonary tuberculosis are able to respond to infections with Mycobacterium tuberculosis, but subtle functional derangement of lymphocytes of patients still can not be ruled out.

Adolescent↗

Characterization and experimental use of a monospecific antiserum to factor IX.

Purified human factor IX was used to develop xenogeneic neutralizing and precipitating antibodies. The final antiserum (R2) neutralized only factor IX and was equivalent to 220 Bethesda-inhibitory units. It showed two precipitating lines, one of which disappeared after absorption with human albumin. On immunodiffusion and Laurell immunoelectrophoresis, the albumin-absorbed R2 antiserum showed one precipitin line of identity, or one rocket respectively, with normal plasma, a Red Cross factor IX preparation (rich in factors IX, II and X), the original antigen, and Hemophilia-B antigen-positive plasmas. No line or rocket developed with normal plasma absorbed with aluminum hydroxide or with antigen-negative contained only factor IX neutralizing and precipitating antibodies. Experiments with various factor IX concentrates revealed that the majority contained excess factor IX antigen compared to their coagulant activity. In addition, crossed antigen-antibody electrophoresis uncovered differences in the migration of the factor IX of Konyne preparations, when done in the presence of EDTA or calcium. This monospecific antiserum to human factor IX was subsequently used to investigate a large population of hemophilia B patients and carriers.

Animals↗

Acute renal failure in Reye's syndrome.

Three patients with initial clinical manifestations and biochemical findings suggestive of a diagnosis of Reye's syndrome had acute renal insufficiency develop and had evidence of consumptive coagulopathy, not generally considered features of the syndrome. As a group, they could not be distinguished, either on the basis of their clinical manifestations or liver pathologic findings, from the 17 patients with Reye's syndrome without renal failure seen in our institution during the same period of time. The use of osmotic diuretics in an effort to decrease cerebral edema may be life threatening in these patients with compromised renal function since hypervolemia, cardiac failure, and worsening of cerebral edema may occur.

Acute Kidney Injury↗

An enzymatic method for distinguishing deoxyuridine and deoxythymidine nucleotide pools and its application for determining ribonucleotide reductase activity.

A method is described for distinguishing deoxyuridine and deoxythymidine di- and triphosphate pools. The method utilizes a DNA polymerase assay for triphosphate determination and a coupled assay in which the disphosphate is converted to its corresponding triphosphate by nucleoside-diphosphate kinase and the triphosphate is measured by the DNA polymerase assay. By including deoxyruidine-triphosphate nucleotidohydrolase in the reaction mixture, dUTP is removed as a substrate for the polymerase. By determining differences in labelled acid-insoluble product formed in the reaction it is possible to determine dUTP, dUDP, dTDP and dTTP pools. Ribonucleotide reductase activity was determined by converting either CDP or ADP to its corresponding deoxyribonucleoside disphosphate and then using the diphosphate assay described for deoxyribonucleoside pools.

Carcinoma↗

Budd-Chiari syndrome caused by undifferentiated small round cell tumor of the liver in an adult.

An undifferentiated small round cell tumor of the liver in a 60 year old black male is described. Although the light microscopic findings in this tumor were strongly suggestive of embryonal rhabdomyosarcoma, the ultrastructural study disclosed no myofibrils or other specific characteristics. Thus, we classify this tumor as an embryonic tumor or primitive mesenchymal tumor of the liver.

Budd-Chiari Syndrome↗

Malacoplakia of the vagina.

Malacoplakia of the vagina was incidentally discovered in a 47-year-old white woman with a history of chronic active hepatitis and steroid hormone therapy. The relation between malacoplakia, liver disease, and steroid therapy is discussed.

Chronic Disease↗

Biochemical and morphological correlates of acute experimental myocardial ischemia in the dog. IV. Energy mechanisms during very early ischemia.

Tissue energy metabolism was examined in posterior (ischemic) and anterior ("control") regions of canine ventricles after 5 and 10 minutes of left circumflex coronary artery occlusion. When compared to identical regions of normal hearts, the following changes were found: (1) decreases in glycogen and phosphorylase activity in the anterior and posterior regions, (2) depressed state 3 rates of oxygen consumption of isolated mitochondria in both anterior and posterior regions, (3) shifts in optimum substrate concentrations for palmityl-CoA (+ carnitine) oxidation by mitochondria in the anterior and posterior regions, and (4) decreases in the apparent zero order and first order rates of mitochondrial palmitylcarnitine production. These changes correlated with a marked decrease in developed tension in the posterior regions. Depression in tension development in the posterior regions of the heart still was present after 30--60 minutes of reperfusion following a 10-minute period of occlusion. Glycogen content in the reperfused areas was significantly decreased after 60 minutes of reperfusion when compared to normal areas and to control hearts perfused for 70 minutes. After reperfusion, mitochondrial function appeared to return toward "normal." However, the slow restoration of contraction of the ischemic area suggests that cellular mechanisms operative in vivo to restore pump function still might be abnormal.

Acyl Coenzyme A↗

Substrate specificity of human ribonucleotide reductase from Molt-4F cells.

Nucleoside triphosphates were examined as the activator for various nucleoside diphosphate reductions catalyzed by a highly purified ribonucleotide reductase obtained from Molt-4F cultured human cells. It was found that cytidine 5'-diphosphate and uridine diphosphate reductions are activated by adenosine 5'-triphosphate with apparent Ka's of 0.63 +/- 0.03 (S.E.) and 1.25 +/- 0.10 mM, respectively. Guanosine 5' diphosphate reduction is activated by deoxythymidine 5'-triphosphate with an apparent Ka of 1.25 +/- 0.11 microM, and adenosine 5'-diphosphate reduction is activated by guanosine 5'-triphosphate or deoxyguanosine 5'-triphosphate with an apparent Ka of 1.1 +/- 0.09 or 1.1 +/- 0.08 mM, respectively. In the presence of saturating amounts of their best activating nucleoside triphosphates, the Km's of various nucleotide diphosphates for this purified enzyme were studied. Double reciprocal plots of velocity against substrate concentration were found to be linear for all four substrates in the concentration range tested and yielded apparent Km's of 7 +/- 0.3 microM for cytidine 5'-diphosphate, 80 +/- 6.5 microM for adenosine 5'-diphosphate, 33 +/- 3.1 microM for guanosine 5'-diphosphate, 50 +/- 2.0 microM for uridine 5'-diphosphate. The reduction of one ribonucleoside diphosphate could be inhibited by other ribonucleoside diphosphates in a noncompetitive manner.

Adenosine Diphosphate↗

Childhood sarcoidosis with fatal cor pulmonale.

A 14 year-old white girl who developed fatal cor pulmonale from severe pulmonary sarcoidosis had a previous clinical diagnosis of cystic fibrosis. Chest radiographs demonstrated marked pulmonary fibrosis without the changes of severe bronchiectasis that would be anticipated with cystic fibrosis.

Adolescent↗