Isolated atrioventricular discordance. Report of two surgical cases with isolated ventricular inversion

Isolated ventricular inversion is a term used for a congenital heart malformation with the segmental arrangement atrioventricular (AV) discordance and ventriculoarterial concordance. It describes a condition which from a physiological point of view resembles complete transposition of the great arteries. We have recently seen two patients with this anomaly. Both underwent intracardiac repair by means of a Mustard operation at 10 years and 10 months of age, respectively. Associated lesions in the first patient were an AV septal defect with two AV orifices (partial AV canal, ostium primum defect), partial anomalous pulmonary venous return, and anomalies in the systemic venous drainage. A perimembranous ventricular septal defect complicated the condition in the second patient.     

The role of oncogenes, tumour suppressor genes and growth factors in oral squamous cell carcinoma: a case of apoptosis versus proliferation

Mutation, deactivation and disregulated expression of oncogenes and tumour-suppressor genes may be involved in the pathogenesis of oral squamous cell carcinoma (SCC). Deactivation of the p53 tumour-suppressor gene allows cell proliferation and blocks apoptosis of malignant oral keratinocytes. Mutation in the ras oncog-ene results in persistent mitogenic signalling. Upregul-ated c-Myc expression, in the presence of growth factors, provides an additional proliferative signal. Loss of retino-blastoma tumour-suppressor gene (Rb) function may contribute to oral keratinocyte hyperproliferation and recent evidence suggests that simultaneous deactivation of both p53 and Rb is required for tumourigenesis. Enhanced Bcl-2 and reduced Fas expression inhibit tumour cell apoptosis and may convey resistance to cyto-toxic drugs and T cell-mediated cytotoxicity, respectively. Exogenous mutagens such as tobacco, alcohol and viral oncogenes may cause altered expression of oncogenes and tumour-suppressor genes in some cases of oral SCC. The impact of these mechanisms on future therapies for oral SCC is highlighted.     

Intraoperative aortic dissection.

Intraoperative aortic dissection is a rare but potentially fatal complication of open heart operations. If the dissection is promptly recognized and repaired, however, the outcome may be significantly better. In this study, we reviewed the hospital records of patients with dissection of the aortic arch occurring as a complication of a cardiac operation at Massachusetts General Hospital and Mt. Auburn Hospital from January 1980 through June 1990. During this period, 14,877 surgical procedures with the use of cardiopulmonary bypass and aortic cannulation were performed, and 24 patients (0.16%) with iatrogenic aortic dissection were identified. Dissection was discovered intraoperatively in 20 patients and postoperatively after complications developed in 4. Of the 20 patients whose injuries were discovered intraoperatively and repaired, 4 (20%) died. Of the 4 whose injuries were discovered after operation, 2 (50%) died. The primary cause of death was ventricular dysfunction resulting from myocardial ischemia. Dissections originated at the aortic cannulation site in 10 patients, at the cross-clamp site in 8, at the site of the partial-occlusion clamp in 7, at the proximal anastomosis in 1 patient, and as a result of direct injury in 1. Three of these patients had simultaneous injuries at the aortic cannulation site and at the heel of the partial-occlusion clamp. Two techniques of repair were used: primary repair and patch or tube graft insertion. There were two deaths in the patients who underwent primary repair and four deaths in patients requiring graft replacement. Although it is uncommon, intraoperative aortic dissection can be a lethal complication of cardiac operations.(ABSTRACT TRUNCATED AT 250 WORDS)     

Systemic vascular responses to atracurium during enflurane-nitrous-oxide anesthesia in humans

Systemic circulatory responses to atracurium (0.2 and 0.4 mg/kg) were studied in 15 healthy (ASA I or II) adult patients during enflurane (1.0 to 1.25% inspired) and nitrous oxide (70% inspired) anesthesia. All patients were premedicated with intramuscular morphine (10-15 mg) and glycopyrrolate (0.2 mg). Compared with control measurements during enflurane-nitrous oxide anesthesia, heart rate, cardiac and stroke index, central venous pressure, and systemic mean arterial pressure remained unchanged at 2, 5, and 10 min after administration of both doses of atracurium. Systemic vascular resistance was minimally decreased (7% compared to control) (0.01 less than P less than 0.05) at 10 min following both doses of atracurium. No patient demonstrated a decrease in systemic mean arterial pressure greater than 6 mmHg. The authors conclude that atracurium in doses which produce adequate skeletal muscle relaxation during steady-state enflurane anesthesia produces no clinically significant alteration in hemodynamic variables.     

Activation of CD4⁺ Foxp3⁺ regulatory T cells proceeds normally in the absence of B cells during EAE

B cells and regulatory T (Treg) cells can both facilitate remission from experimental auto immune encephalomyelitis (EAE), a disease of the central nervous system (CNS) used as a model for multiple sclerosis (MS). Considering that B-cell-depletion therapy (BCDT) is used to treat MS patients, we asked whether Treg-cell activation depended on B cells during EAE. Treg-cell proliferation, accumulation in CNS, and augmentation of suppressive activity in the CNS were normal in B-cell-deficient mice, indicating that B cells are not essential for activation of the protective Treg-cell response and thus provide an independent layer of regulation. This function of B cells involved early suppression of the encephalitogenic CD4(+) T-cell response, which was enhanced in B-cell-deficient mice. CD4(+) T-cell depletion was sufficient to intercept the transition from acute-to-chronic EAE when applied to B-cell-deficient animals that just reached the peak of disease severity. Intriguingly, this treatment did not improve disease when applied later, implying that chronic disability was ultimately maintained independently of pathogenic CD4(+) T cells. Collectively, our data indicate that BCDT is unlikely to impair Treg-cell function, yet it might produce undesirable effects on T-cell-mediated autoimmune pathogenesis.