Complementarities and network interactions in AIDS.

The contribution of autoimmune phenomena to the development of AIDS is not fully understood. In this paper we provide new evidence that idiotypic network interactions are operative in the development of AIDS. We furthermore present a model that involves two groups of antibodies and other molecules that are related to each other by a network of specific complementarities. We define Group I molecules to include antibodies and other molecules that have direct or indirect similarities with class I MHC molecules, and Group II substances that have similarities with class II MHC. We observe an inverse relationship between Group I antibodies (including anti-Fab) and Group II antibodies (including anti-anti-gp120, anti-anti-CD8 and anti-rCD4). The potential roles of members of these two groups in AIDS pathogenesis and/or protection are discussed.

Three-month follow-up of 28 dual diagnosis inpatients.

The coexistence of psychiatric and substance abuse problems within the same patient occurs with significant frequency. These patients present serious challenges to a health care system which has traditionally treated mental health and substance abuse in separate venues, with differing and sometimes contradictory treatment modalities. Few studies exist on the treatment of the "dual diagnosis" patient utilizing an integrated approach, where both problems are addressed by the same staff on a single inpatient ward. We describe such a program in which dual diagnosis patients on one ward are separated into two different treatment tracks based upon the severity of their psychiatric illness. Follow-up measures at 3 months after discharge are compared for patients from each treatment track, with no significant difference found for the five outcome variables studied. This suggests that chronically mentally ill inpatients may benefit from integration of attention to their substance abuse problems with psychiatric treatment.

Cocaine-mediated impairment of cardiac conduction in the dog: a potential mechanism for sudden death after cocaine.

Deaths from cocaine abuse continue to increase, while the mechanism of lethality remains unclear. Previous investigations have focused on potential ventricular dysrhythmias and myocardial ischemic events from enhanced autonomic tone or seizure activity from central stimulation. However, cocaine is a local anesthetic and may impair cardiac conduction. To evaluate this, 16 conscious dogs received i.v. cocaine over 30 sec to mimic "recreational" use in doses of 3 mg/kg (n = 6), 5 mg/kg (n = 6) or 7 mg/kg (n = 4). Another group of anesthetized dogs (n = 6) received two infusions of cocaine (5 mg/kg) 1 hr apart. Plasma cocaine levels and His bundle electrograms were obtained at control and at 0.5, 1.0, 1.5, 2.0, 3.0, 4.0, 5.0, 10 and 15 min after cocaine administration. At 0.5 min, plasma cocaine reached peak levels of 30.0, 45.0 and 59.6 micrograms/ml with increasing dose. Cocaine rapidly produced severe prolongation of His to ventricle interval and widening of the R wave. Slowing of conduction was dose-dependent, with maximal increases in His to venticle interval of 37 to 56% (P = .0299) and R wave duration of 34 to 77% (P less than .025). Furthermore, significant conduction impairment developed at cocaine levels that did not produce seizures. Conduction effects were equally pronounced during repeated administration of cocaine. These data indicate that cocaine causes marked conduction slowing, which could play an important role in cocaine death.

Abnormalities in the response of plasma arginine vasopressin during hypertonic saline infusion in patients with eating disorders.

We examined the response of plasma arginine vasopressin (pAVP) to intravenous 5% hypertonic saline in patients with anorexia nervosa (AN) and bulimia nervosa (BN). Patients did not differ from controls in their subjective response for the onset of thirst; however, only 5 patients (3 AN and 2 BN) showed pAVP levels that were within the normal range (0.5-11.0 pg/ml) for this test. With the exception of two eating disorder (ED) patients, all others showed some nonlinear irregularities in the pattern of their secretion of pAVP in response to the hypertonic saline infusion. Seven of the ED patients showed an irregular abnormally high pAVP secretion, and three patients showed abnormally low pAVP responses. Both of these pAVP secretion abnormalities occurred in underweight and weight-recovered AN patients, as well as in BN patients. The cause and pathophysiological consequences of these abnormalities remain unresolved.

Cerebral atrophy in bulimia.

The extent of cerebral atrophy in 8 consecutively chosen unmedicated bulimics and 8 normal controls was determined by magnetic resonance imaging. There was no history of anorexia nervosa or alcoholism in either group. Measures obtained included the ratio of cerebral to cranial area at the midsagittal section, as well as maximum ventricle/brain ratio in the axial plane. Sagittal cerebral/cranial ratio was significantly less in the bulimic group than in controls [0.82 +/- 0.04 (SD) versus 0.90 +/- 0.03, Z = -2.74, p = 0.006, two-tailed Mann-Whitney U-test], whereas ventricle/brain ratio was not significantly different between groups. Implications for the occurrence of cortical atrophy in normal-weight bulimics, as well as for the relative absence of ventricular enlargement in these patients, are discussed.

The anatomy of the pectoral nerves and its significance to the general and plastic surgeon.

It has previously been shown that in 62% of patients the medial pectoral nerve courses through the pectoralis minor muscle to innervate the lower half or two thirds of the pectoralis major muscle. In the other 38% of patients, the medial pectoral nerve exits around the lateral aspect of the pectoralis minor muscle. The lateral pectoral nerve courses on the undersurface of the pectoralis major muscle, innervating the proximal one third or more of the muscle. Consequently, when the pectoralis minor muscle is removed in a modified radical mastectomy, or dissection between the two muscles is performed, there is partial deinnervation of the pectoralis major muscle with partial atrophy and a decrease in size. Further, if the lateral pectoral nerve also is injured or removed, it can result in total deinnervation of the pectoralis major muscle with more severe atrophy and fibrosis of the muscle. In cosmetic augmentations, when the breast implant is placed behind the pectoralis major muscle, that muscle is partially deinnervated. In this clinical situation, this is believed to be advantageous because it allows the breast to project better. This paper details the anatomy of the pectoral nerves and discusses the clinical implications of surgery in this region as it relates to the size and function of the pectoral muscles.

Extended myofascial thigh flaps for repair of large full-thickness abdominal wall defects.

The large, full-thickness abdominal wall defect encompassing the upper and lower quadrants can test the surgeon's ingenuity in providing definitive repair. Two cases are reported of this type of abdominal wall defect closed in one stage using an extended tensor fascia lata myofasciocutaneous flap and an extended rectus femoris myofascial flap, respectively. In addition, a fresh cadaver dye injection study demonstrates the extensive circulatory pattern of these flaps.