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Biomedical subjects

Z J Li

Publications and source records attributed to Z J Li.

At least 73 records · Page 4Linked to original sources

Iron deficiency and hearing loss. Experimental study in growing rats.

Cochlear changes were studied in 141 growing rats raised on a basic iron-deficient diet for 7-100 days; 130 rats served as normal or chronic anemia controls. Electrophysiological findings showed that the incidence of an auditory threshold elevation of more than 15 dB was 31.85% in the iron-deficient rats, but it was unchanged in all the control animals. The main cochlear histopathological changes induced by iron deficiency were strial atrophy and reduction of spiral ganglion cells. It is concluded that the observed anomalies may be attributed solely to iron deficiency of the cochlear tissue.

Animals↗

Prenatal diagnosis of partial trisomy 22 derived from a maternal t(11; 22) (q23; q11).

A fetus with partial trisomy 22 was detected by amniocentesis in a pregnant woman with balanced translocation, 46, XX, t(11; 22) (q23; q11). The aborted fetus had multiple congenital anomalies consisting of microcephaly, cleft lip and palate. The extra acrocentric chromosome was identified as der (22), t(11; 22) (q23; q11). The aborted fetus is compared with other trisomic cases described in literatures, and perinatal diagnosis of this case was discussed.

Adult↗

Mechanism of the therapeutic effect of anisodamine in disseminated intravascular coagulation: study of platelet adhesion and aggregation, malondialdehyde, thromboxane B2, 6-keto-prostaglandin F1 alpha, and microcirculation.

Acute disseminated intravascular coagulation (DIC) is a life-threatening condition that may be encountered in many situations, especially in cases of shock with uncontrollable hemorrhage. Anisodamine, an alkaloid extracted from a Chinese herb, is well known for its dramatic therapeutic effect on DIC. Sixty male rabbits were used to establish an acute DIC model. A total of 240 blood samples were taken for laboratory assays of changes in blood coagulation factors, platelet count, platelet adhesion, platelet aggregation, malondialdehyde (MDA), thromboxane B2 (TXB2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). Changes of the microcirculatory status and the rate of the blood flow in the conjunctival capillaries of 60 rabbits were observed with WXS-II microcirculation microscope. Pathological sections of the lungs and kidneys were studied. Our investigation showed the presence of microthrombi in the microvasculature. After treatment with anisodamine, the prothrombin time stayed in the normal range, fibrinogen consumption was lessened, adenosine-diphosphate-induced platelet aggregation was inhibited, thromboxane B2 and malondialdehyde concentrations were significantly lower than in the control group, and the elevated quantity of 6-keto-PGF1 alpha was spared. We concluded that the anti-platelet-aggregating, microcirculation-facilitating, thromboxane-B2-inhibiting, malondialdehyde-inhibiting, and 6-keto-PGF1 alpha-sparing effects of anisodamine are the important mechanisms of its dramatic therapeutic effect on DIC.

6-Ketoprostaglandin F1 alpha↗

[Prostaglandin E (PGE) and gastric carcinoma].

Since 1984, an experimental and clinical study on the relation between PGE and gastric carcinoma has been performed by determining PGE content in the bioptic gastric mucosa and plasma. It is found the PGE content in the gastric mucosa and plasma is increased in all patients with gastric cancer, especially with signet ring cell carcinoma. It is higher in the regional lymph node metastasis than in the early cancer, extensive metastases and normal subjects. The PGE content in the plasma is reduced obviously 7-10 days after operation but is increased markedly in recurrent patients. There is no significant difference in extensive metastases, relapse free and normal subjects. The PGE content in the plasma is significantly higher in gastric carcinoma than in chronic atrophic gastritis, but no difference is present between chronic atrophic gastritis and normal subjects.

Adenocarcinoma↗