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Biomedical subjects

J P Judson

Publications and source records attributed to J P Judson.

11 recordsLinked to original sources

A preliminary finding: immunohistochemical localisation and distribution of placental angiotensin II receptor subtypes in normal and preeclamptic pregnancies.

Pre-eclampsia or pregnancy induced hypertension (PIH) affects 6-8% of all pregnancies. Although the underlying mechanism of PIH is still unknown, it is widely believed that the placenta plays an important role. It was thought that an ischemic placenta due to poor perfusion can precipitate the signs and symptoms of PIH. This study aims to investigate the possible role of Type 1(AT1) and Type 2 (AT2) angiotensin II receptor subtypes in the mechanism of PIH. AT1 receptor stimulation causes vasoconstriction and AT2 receptor stimulation causes vasodilatation. Investigating the interactions of these two receptors in the placenta provides an insight as to the balance that may exist between AT1 and AT2 receptors in normal pregnancy. Any disruption to the balance might cause a disruption of the blood flow in the placenta, leading to PIH. Placentas were collected from 11 PIH patients and 11 normal patients. Immunohistochemistry techniques were performed on the placental tissue to determine the distribution of AT1 and AT2 receptors in the placental tissue qualitatively and quantitatively. It was observed that in normal patients, the balance between AT1 and AT2 receptors is that the level of AT2 receptors is higher than the level of AT1 receptors. However in the PIH patient, it was observed that the normal balance was disrupted. In PIH patients the level of AT1 receptors was observed to be higher than the level of AT2 receptors. This study suggests that disruption of the balance between AT1 and AT2 receptors observed in PIH placentas might cause a decrease in blood flow to the placenta, causing it to be poorly perfused. This may cause placental ischemia which may lead to PIH.

Biomarkers↗

Double-outlet right ventricle. Surgical results, 1970-1980.

Between Jan. 1, 1970, and Jan. 1, 1980, 62 consecutive patients underwent repair of classic double-outlet right ventricle (DORV). Patients with subpulmonic ventricular septal defect (VSD), complete atrioventricular canal, atrioventricular discordance, and univentricular heart were excluded. One hundred six associated defects were present in 54 patients. Forty-six patients had pulmonary stenosis. The 36 male and 26 female patients ranged in age from 8 months to 37 years (median age 9 years). The early mortality was 11% for those with pulmonary stenosis, 25% for those without pulmonary stenosis, and 15% for the entire series. The risk of mortality was related to the age of the patient at operation. Causes of early deaths included low cardiac output (three patients), high residual right ventricular pressure (three patients), anomalous coronary artery injury (one patient), infection (one patient), and hemorrhage (one patient). Eleven late deaths occurred among the 53 operative survivors (21%). Ten (91%) of the late deaths were attributed to arrhythmia. All except one of the long-term survivors are in Functional Class I or II. Although the operative mortality for the repair of DORV continues to decrease, the late mortality is of concern, and the problem of late arrhythmia necessitates further study and analysis.

Adolescent↗

Successful repair of coexisting double-outlet right ventricle and two-chambered right ventricle.

Double-outlet right ventricle (DORV) and two-chambered right ventricle (TCRV) are both uncommon cardiac malformations; even more rare is the coexistence of these lesions. This communication describes the first two patients in whom this unusual combination of anomalies was recognized during life and successfully repaired with the aid of extracorporeal circulation. Late results in both patients are excellent.

Child, Preschool↗

Illusions leading to surgical closure of the distal left pulmonary artery instead of the ductus arteriosus.

Illusions, in a collected series of 10 cases, have led to the surgical closure of the distal left pulmonary artery instead of the patent ductus. When the rare, anatomically atypical patent ductus arises from the arch proximal to the subclavian artery, the recurrent laryngeal nerve is found passing under the arch instead of under the ductus. A large ductus creating the illusion of the arch, with the nerve beneath it, can lead to the impression of an anatomically atypical ductus with the resultant surgical closure of the distal left pulmonary in lieu of the ductus. For over two decades the problem has been a recurring one which deserves recognition among the better known complications of ductus operations.

Adult↗