The varied sources of faculae-forming brines in Ceres' Occator crater emplaced via hydrothermal brine effusion.

Before acquiring highest-resolution data of Ceres, questions remained about the emplacement mechanism and source of Occator crater's bright faculae. Here we report that brine effusion emplaced the faculae in a brine-limited, impact-induced hydrothermal system. Impact-derived fracturing enabled brines to reach the surface. The central faculae, Cerealia and Pasola Facula, postdate the central pit, and were primarily sourced from an impact-induced melt chamber, with some contribution from a deeper, pre-existing brine reservoir. Vinalia Faculae, in the crater floor, were sourced from the laterally extensive deep reservoir only. Vinalia Faculae are comparatively thinner and display greater ballistic emplacement than the central faculae because the deep reservoir brines took a longer path to the surface and contained more gas than the shallower impact-induced melt chamber brines. Impact-derived fractures providing conduits, and mixing of impact-induced melt with deeper endogenic brines, could also allow oceanic material to reach the surfaces of other large icy bodies.

Effects of dietary L-arginine on structure and function of flow-restricted vein grafts.

PURPOSE: Experiments were designed to determine effects of dietary supplementation with L -arginine on structure and function of flow-restricted vein grafts. METHODS: Saphenous veins were placed as bilateral interposition grafts in femoral arteries of two groups of adult male mongrel dogs; one group was maintained on a normal diet (control), the other group supplemented with L -arginine (200 mg/kg per day) beginning 1 week before surgery. In each dog, flow was reduced by 50% in one graft by placing an adjustable clamp on the artery distal to the distal anastomosis. Plasma amino acids and oxidized products of nitric oxide (NO(x )) were measured before and after L -arginine feeding. At postoperative week 4, grafts were removed and prepared for organ chamber studies to determine functions of the endothelium or smooth muscle and for histology. RESULTS: Plasma L -arginine increased within 3 hours after feeding and increased from 141 +/- 8 nmol/mL to 169 +/- 11 nmol/mL (n = 6) after 5 weeks of supplementation. Plasma ornithine and citrulline paralleled arginine, whereas circulating NO(x ) was unchanged. Maximal contractions to 60 mmol/L KCl were reduced in grafts from L -arginine-fed dogs. Endothelium-dependent relaxations to the calcium ionophore A23187 and relaxations of the smooth muscle NO were reduced in grafts from L -arginine-fed dogs. Neointimal hyperplasia was increased in grafts with reduced flow and not affected by arginine feeding. CONCLUSIONS: Dietary supplementation with L -arginine did not increase plasma NO in dogs with peripheral vein grafts or increase endothelium-dependent relaxations in control or flow-restricted grafts. Therefore, dietary supplementation with L -arginine may not improve long-term functions of flow-restricted peripheral bypass grafts.

Isolated visceral angioedema: an underdiagnosed complication of ACE inhibitors?

Angiotensin-converting enzyme (ACE) inhibitors are known to cause potentially fatal peripheral angioedema in some patients. ACE inhibitors may also cause isolated visceral angioedema, a rarely reported complication. This article describes 2 patients who experienced this complication. Both patients came to medical attention with episodes of recurrent abdominal symptoms that had occurred while taking ACE inhibitors for hypertension. Each patient had undergone surgical procedures for symptoms that persisted after surgery and were ultimately relieved with cessation of their ACE inhibitors. These cases call attention to what may be an underappreciated cause of abdominal pain in patients presenting to emergency departments.

Rapid upregulation of caspase-3 in rat spinal cord after injury: mRNA, protein, and cellular localization correlates with apoptotic cell death.

Although the precise mechanisms explaining loss of, and failure to regain, function after spinal cord injury are unknown, there is increasing interest in the role of "secondary cell death." One prevalent theme in cell loss in other regions of the CNS involves apoptosis executed by the intracellular caspase proteases. A recent study demonstrated that spinal cord injury rapidly increased the activation of caspase-3. Our previous studies demonstrated peak apoptosis in three of four cellular compartments 3 days after controlled contusion in the rat. We have extended these analyses to include enzyme and substrate studies of caspase subfamilies both in rostral and in caudal adjacent segments compared to the lesion site. Although presumed activation of programmed proenzyme is considered the mechanism for enhanced caspases, our novel analyses were designed to detect upregulation of gene expression. We surveyed traumatically injured spinal cord for caspase family messages with a modified differential mRNA display approach and found that the caspase-3 (CASP3) message was present and upregulated severalfold after injury. Our results clearly demonstrate that cell death in the spinal cord occurs after posttranslational activation of caspases that follow, at least for caspase-3, initial upregulation of CASP3 mRNA levels.

Effects of dietary L-arginine on the reactivity of canine coronary arteries.

Experiments were designed to determine the effects of supplemental dietary L-arginine on the endothelial and smooth muscle function of canine coronary arteries. One group of dogs was fed the standard laboratory chow while another group was supplemented with 250 mg/kg per day L-arginine. All dogs had undergone bilateral reversed interposition saphenous vein grafting and received 325 mg/day oral aspirin. After 5 weeks of arginine feeding, left circumflex coronary arteries were removed, cut into rings, and suspended for the measurement of isometric force in organ chambers. Concentration-response curves were obtained to L-arginine, UK-14,304 (alpha2-adrenergic agonist) and A23187 (calcium ionophore) in the absence and presence of N(G)-monomethyl-L-arginine (L-NMMA) and tetraethylammonium (TEA) alone or in combination. Serum concentrations of L-arginine increased by about 20% following 2 weeks of arginine feeding and remained elevated throughout the study. In rings with and without endothelium contracted with prostaglandin F2alpha, L-arginine caused concentration-dependent contractions in rings from control animals but no significant change in tension in rings from arginine-fed animals. Contractions to L-arginine in control animals were reduced by either L-NMMA or TEA. Endothelium-dependent relaxations to the alpha2-adrenergic agonist were decreased with arginine feeding while relaxations to the calcium ionophore and the endothelium-derived factor nitric oxide were similar among groups. Relaxations to UK-14,304 were reduced by L-NMMA in both groups but by TEA only in rings from control animals. These results suggest that dietary supplementation with L-arginine modifies reactivity of endothelium and smooth muscle by at least two mechanisms: one associated with activation of potassium channels and the other with receptor-coupled release of nitric oxide.

Long-term survival and late complications after repair of ruptured abdominal aortic aneurysms.

PURPOSE: Long-term survival and late vascular complications in patients who survived repair of ruptured abdominal aortic aneurysms (RAAA) is not well known. The current study compared late outcome after repair of RAAA with those observed in patients who survived elective repair of abdominal aortic aneurysms (AAA). METHODS: The records of 116 patients, 102 men and 14 women (mean age: 72.5 (8.3 years), who survived repair of RAAA (group I) between 1980 to 1989 were reviewed. Late vascular complications and survival were compared with an equal number of survivors of elective AAA repair matched for sex, age, surgeon, and date of operation (group II). Survival was also compared with the age and sex-matched white population of west-north central United States. RESULTS: Late vascular complications occurred in 17% (20/116) of patients in group I and in 8% (9/116) in group II. Paraanastomotic aneurysms occurred more frequently in group I than in group II (17 vs. 8, p = 0.004). At follow-up, 32 patients (28%) were alive in group I (median survival: 9.4 years) and 53 patients (46%) were alive in group II (median survival: 8.7 years). Cumulative survival rates after successful RAAA repair at 1, 5, and 10 years were 86%, 64%, and 33%, respectively. These were significantly lower than survival rates at the same intervals after elective repair (97%, 74%, and 43%, respectively, p = 0.02) or survival of the general population (95%, 75%, and 52%, respectively, p < 0.001). Coronary artery disease was the most frequent cause of late death in both groups. Vascular and graft-related complications caused death in 3% (3/116) in group I and 1% (1/116) in group II. Cox proportional hazards modeling identified age (p = 0.0001), cerebrovascular disease (p = 0.009), and number of days on mechanical ventilation (p = 0.01) to be independent prognostic determinants of late survival in group I. CONCLUSIONS: Late vascular complications after repair of RAAA were higher and late survival rates lower than after elective repair. These data support elective repair of AAA. As two-thirds of the patients discharged after repair of RAAA are alive at 5 years, aggressive management of RAAA remains justified.