Endovascular stent treatment of cervical internal carotid artery aneurysms with parent vessel preservation

BACKGROUND: Aneurysms involving the cervical portion of the internal carotid artery (ICA) frequently result from prior trauma or dissection. CASE DESCRIPTIONS: Two patients are reported with cervical internal carotid artery aneurysms. In both cases, disease involving the contralateral ICA precluded safe treatment of the aneurysms by ICA occlusion. Endovascular stents placed across the diseased portion of the artery resulted in thrombosis of the aneurysm with preservation of the parent artery. CONCLUSION: Endovascular stent placement should be considered for treatment of aneurysms involving the cervical ICA when preservation of the parent vessel is necessary.     

Reconstruction of the scapholunate ligament in a cadaver model using a bone-ligament-bone autograft from the foot

This study is an investigation of a new procedure in which the scapholunate interosseous ligament (SLIL) is reconstructed using a bone-ligament-bone autograft from the foot. After investigation, the dorsal medial portion of the navicular-first cuneiform ligament (NFCL) was chosen for testing as a potential donor since it is similar in length and thickness to the SLIL and it is easily harvested with minimal potential donor site morbidity. Eight SLILs and NFCLs were harvested from fresh-frozen cadavers. Biomechanical extensometry testing was performed using an Instron 1000 machine. A 5-mm-wide central portion of the NFCL was tested since this width was compatible with the technical aspects of reconstructing the SLIL. Both ligaments were tested for elastic properties, including stiffness, load to failure, and deformation to failure. Mean length of the NFCL was 7.6 mm (range, 5.5-8.5 mm). Stiffness of the NFCL was 10.6 x 10(5) Nm (range, 8.0-13.0 Nm) compared with 14.4 x 10(5) Nm for the SLIL (range, 10.0-19.5 Nm). Peak load to failure for the NFCL was 1,980 N (range, 1,530-2,940 N) compared with 2,940 N for the SLIL (range, 1,780-4,050 N). Total elongation to failure for the NFCL was 2.50 mm (range, 1.7-3.2 mm) compared with 3.2 mm for the SLIL (range, 2.1-5.2 mm). Thus, the biomechanical characteristics of the NFCL were found to be very similar to those of the SLIL. Having established the biomechanical similarities of the 2 ligaments, we are currently using the NFCL to reconstruct the sectioned SLIL in a fresh-frozen cadaver model. Early results suggest that this procedure is feasible for restoration of normal kinematics of the wrist.     

Perceptual errors and negligence

Radiologic errors continue to be made at a rate that has changed little over the past 50 years, despite a variety of methods that have been proposed to reduce such errors. Many of these methods, as well as other steps that can be taken to decrease errors, are described elsewhere [6, 31, 32]. However, the question of whether a missed radiographic diagnosis constitutes malpractice has confounded radiologists, patients, referring physicians, attorneys, jurors, and judges for decades, and it is not likely that the question will be resolved to the satisfaction of any of these parties in the foreseeable future. Against this backdrop, radiologists continue to be subjected to malpractice litigation more for missing radiographic diagnoses than for any other reason. Moreover, radiologists who are sued for missing diagnoses are likely to have more indemnification paid on their behalf to satisfy a settlement or adverse jury verdict than for any other malpractice allegation. Assuredly, it is difficult to defend a radiologist who has failed to perceive a radiographic abnormality that in retrospect can be readily perceived by medical and nonmedical observers alike. Nonetheless, solid defense-supporting data are available that, at times, can be presented to a jury successfully to achieve vindication for a defendant radiologist. These data include statistics regarding the frequency of errors committed by radiologists and other physicians during the course of ordinary everyday practice, the factors that cause varying conspicuity of radiographic densities, the limitations of normal human visual perception, and evidence that the process by which the radiologist originally rendered the interpretation was free of deficiency.     

Apoptosis after traumatic human spinal cord injury

OBJECT: Apoptosis is a form of programmed cell death seen in a variety of developmental and disease states, including traumatic injuries. The main objective of this study was to determine whether apoptosis is observed after human spinal cord injury (SCI). The spatial and temporal expression of apoptotic cells as well as the nature of the cells involved in programmed cell death were also investigated. METHODS: The authors examined the spinal cords of 15 patients who died between 3 hours and 2 months after a traumatic SCI. Apoptotic cells were found at the edges of the lesion epicenter and in the adjacent white matter, particularly in the ascending tracts, by using histological (cresyl violet, hematoxylin and eosin) and nuclear staining (Hoechst 33342). The presence of apoptotic cells was supported by staining with the terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick-end labeling technique and confirmed by immunostaining for the processed form of caspase-3 (CPP-32), a member of the interleukin-1beta-converting enzyme/Caenorhabditis elegans D 3 (ICE/CED-3) family of proteases that plays an essential role in programmed cell death. Apoptosis in this series of human SCIs was a prominent pathological finding in 14 of the 15 spinal cords examined when compared with five uninjured control spinal cords. To determine the type of cells undergoing apoptosis, the authors immunostained specimens with a variety of antibodies, including glial fibrillary acidic protein, 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase), and CD45/68. Oligodendrocytes stained with CNPase and a number of apoptotic nuclei colocalized with positive staining for this antibody. CONCLUSIONS: These results support the hypothesis that apoptosis occurs in human SCIs and is accompanied by the activation of caspase-3 of the cysteine protease family. This mechanism of cell death contributes to the secondary injury processes seen after human SCI and may have important clinical implications for the further development of protease inhibitors to prevent programmed cell death.     

Fusiform P1 segment artery aneurysm in a pediatric patient: technical case report

We report a case of cavernous sinus thrombosis in an 8-year-old boy, following a neglected and untreated nasal furuncle. This rare entity is manifested by hyperthermia, with headache, vomiting and involvement of the III-IV & VI cranial nerves. It is usually a complication of a facial infection. The diagnosis is established by CT-Scan or MRI. Without appropriate and early treatment, the prognosis is poor, with a fatal outcome or severe sequelae.     

Radiofrequency volumetric tissue reduction for treatment of turbinate hypertrophy: a pilot study

BACKGROUND: Apoptosis maintains cell homeostasis. Altered apoptosis is involved in carcinogenesis. It was our aim to investigate whether reflux esophagitis may alter apoptosis in the esophageal mucosa and whether antireflux surgery may restore normal apoptosis. METHODS: Apoptosis was studied preoperatively and postoperatively in esophageal biopsies of 39 patients with various grades of reflux esophagitis and in Barrett's mucosa using the TUNEL method. Biopsies were also taken from lesions of the squamous epithelium adjacent to the Barrett's mucosa. RESULTS: Apoptosis increased with the severity of esophagitis. Apoptosis was low in Barrett's epithelium. Squamous epithelium adjacent to Barrett's mucosa showed increased apoptosis. After surgery apoptosis decreased in squamous epithelium, and it remained low in Barrett's epithelium. CONCLUSIONS: Apoptosis in reflux esophagitis may be protective against increased proliferation. Low apoptosis following antireflux surgery indicates that surgery is effective to prevent reflux-induced cell proliferation. Inhibition of apoptosis in Barrett's may promote carcinogenesis. This may not change following surgery.     

Biological and virologic characteristics of primary HIV infection

BACKGROUND: The clinical events surrounding acute HIV-1 infection have been well described, but little is known about whether the virologic course of acute HIV-1 infection influences the subsequent progression of disease. OBJECTIVE: To define the virologic natural history of acute and very early HIV infection. DESIGN: Prospective, longitudinal cohort study. SETTING: University of Washington Research Clinic PARTICIPANTS: 74 adults enrolled soon after acquisition of HIV (mean, 69 days). MEASUREMENTS: Plasma HIV-1 RNA levels; quantitative cell cultures; CD4 cell counts; and detailed clinical assessments done at study entry, biweekly for 1 month, monthly for 2 months, and quarterly thereafter. RESULTS: In the first 30 days after acquisition of HIV, HIV-1 RNA levels varied greatly among participants (range, 27,200 to 1.6 x 10(6) copies per mL of plasma). Levels of HIV-1 RNA decreased by a mean of 6.5% per week for the first 120 days and then increased by a mean of 0.15% per week. CD4 cell counts decreased by a mean of 5.2 cells/mm3 per week for the first 160 days and by a mean of 1.9 cells/mm3 per week thereafter (P < 0.01). Disease progressed faster in participants who sought medical care for their acute seroconversion syndrome (P = 0.01) and those who had high plasma HIV-1 RNA levels 120 to 365 days after acquisition (P < 0.01). Peak levels in the first 120 days were not predictive of disease progression. CONCLUSIONS: The variability in viral RNA levels associated with acute HIV-1 infection is greater than previously appreciated. Within 120 days of acquisition, plasma HIV RNA levels rapidly decrease to an inflection point, after which they gradually increase. Virus-host interactions soon after acquisition seem to have a major influence on the long-term outcome of HIV-1 disease.     

Pre- and postoperative nutritional care in liver transplantation in children

Orthotopic liver transplantation (OLT) is now a definitive treatment option for most cases of endstage liver disease (ESLD) in children. Efforts now focus on active supportive treatment to maintain, if not improve, the patient's clinical status before OLT and to ensure normal patterns of growth and development after OLT. Malnutrition adversely affects the outcome of OLT and is probably the single area in pre-operative management where the largest potential improvement can be made. Our studies indicate significant abnormalities of protein energy metabolism and body composition in children referred for OLT. We have shown that the use of enteral formulae, enriched with branched-chain amino acids, have significant advantages. Other adjunctive therapy, such as growth hormone, is the subject of current investigation. Following transplantation, catch-up weight and growth does occur with the advent of normal liver function, but patients at continuing risk for undernutrition, such as those with rejection and/or chronic infection, need to be targeted for specific nutritional therapy.     

Transgenic animals in toxicology

Recent advances have been made in the characterization of a number of transgenic animal models. These animal models have provided a powerful toxicological tool for studying in vivo chemical effects and have increased our understanding of the role of specific genetic alterations as predisposing factors for chemical carcinogenesis. The goal of this symposium was to introduce the development of transgenic animals and the utilization of transgenics in toxicology research focusing on understanding tissue-specific mutation, chemical effects, and cancer. The production of transgenic animals, including gene insertions and gene knockouts, and the utilization of transgenic technology for studying multistage carcinogenesis and tumor suppressor genes are described. Data on the application and implications of transgenics as a genetic endpoint are also discussed. The use of transgenic animals in toxicology should improve our understanding of the role of specific genetic alterations in the carcinogenic process and lead to improved estimations of human health risks.