Angioplasty-related iliac artery rupture: treatment by temporary balloon occlusion.
A case of nonsurgical treatment of common iliac artery rupture secondary to percutaneous transluminal angioplasty is reported.
Biomedical subjects
Publications and source records attributed to E Levy.
A case of nonsurgical treatment of common iliac artery rupture secondary to percutaneous transluminal angioplasty is reported.
Eight infants presented with a malabsorption syndrome, normal fasting triglycerides, hypocholesterolemia (64.3 +/- 10.0 mg/dl), and deficiency of vitamins A and E. Plasma low-density lipoprotein, apolipoprotein B, and apolipoprotein A-I were decreased. After a fatty meal, plasma triglycerides did not increase and chylomicrons could not be identified. Lipoprotein composition was characterized by normal apoproteins, high phospholipids, and low cholesterol. Increased triglycerides were present in low-density lipoproteins. Immunoperoxidase localization of apolipoprotein B on fasting biopsy specimens showed increased staining of the lipid-laden intestinal epithelial cells compared to normals. On electron microscopy after a fat load, the enterocytes contained large numbers of fat particles vesiculating the endoplasmic reticulum. These particles, morphologically similar to chylomicrons, were also present as aggregates of well-individualized lipid droplets within dilated vesicles in the Golgi zone, but were not seen in the intercellular spaces and lacteals. This recessively transmitted condition differs from abetalipoproteinemia and from the homozygous form of hypobetalipoproteinemia and may be caused by a defect in the final assembly of chylomicrons or in the mechanism of their exocytosis.
Previous studies have reported that the absence of chylomicron, very-low-density lipoprotein, and low-density lipoprotein in abetalipoproteinemia is a consequence of apoprotein B (apo B) deficiency. Although the absence of apo B from the intestine has been shown by immunofluorescence, the antiserum used was raised against low-density lipoprotein apo B. Therefore, the precise nature of the underlying defect remains unknown, given that the postulated gene mutation could prevent the synthesis of the molecular form of apo B specific for chylomicrons, apo B-48, or produce an unstable aberrant form of apo B particle. This report concerns 2 girls aged 5.5 and 4.75 with well-documented clinical and biological manifestations of the disease in whom there was no immunologically detectable plasma apo B-48 and apo B-100. Their cultured jejunal explants incubated with [14C]palmitate showed slight decrease in the esterification of triglycerides, phospholipids, and cholesteryl esters. However, only traces of triglycerides and small amounts of cholesteryl esters were found in the culture medium in contrast to phospholipids, which were readily exported. Protein synthesis as assessed by [3H]leucine incorporation by explants was normal and only modestly diminished in the fat chylomicronlike fraction floated from the sonicated explants. However, there was no radioactivity at the electrophoretic position of apo B-100 and apo B-48. Immunologic confirmation of the absence of these two apoproteins was obtained by Western blots. These data confirm the hypothesis that in certain cases of abetalipoproteinemia the intestinal defect results from the lack of synthesis of apo B-48.
The authors report the case of a 24 year old man with no previous disease who presented with a severe autonomic neuropathy. This included major gastrointestinal dysfunction characterised by decreased peristalsis without distension and paralysis of the gall bladder, and orthostatic hypotension with a normal cardiac tachycardia reflex. There was an associated sensory neuropathy affecting heat sensitivity without motor dysfunction and an increased CSF protein content. The proprioceptive nerve fibre conduction was decreased but another nerve conduction was normal initially. The mesenteric plexuses examined during sigmoidectomy performed for peritonitis due to multiple bowel perforations caused by fecoliths, showed no significant changes. Peripheral nerve biopsy revealed massive rarefaction of myelinated fibres which were of small diameter, and of the unmyelinated fibres, mainly due to axonal degeneration. Only two similar cases with incomplete recovery were found in the literature. In our case, a complete recovery was observed. The cause of the condition is unknown.
The object of this study was to ascertain the frequency of postinfectious cow's milk protein hypersensitivity (CMPH). Twenty-four infants less than 3 months old were included in the study. Following hospitalization for acute gastroenteritis, the infants were given a protein hydrolysate formula for a period of 6 weeks, after which an intestinal biopsy was performed. Thereafter, a milk challenge was given. The existence of CMPH was defined as a postchallenge reduction of one or more of the mucosal disaccharidases below the normal levels for our laboratory. A bacterial etiology of the gastroenteritis was found in 10. Nineteen infants had no adverse reaction to cow's milk after 6 weeks on a hypoallergenic formula. Only two could be confidently diagnosed as having developed secondary CMPH; both had been infected by Escherichia coli 0 111. One infant had primary CMPH and one extra-intestinal CMPH. The incidence of secondary CMPH with gastrointestinal manifestations in this series was considerably less than described elsewhere.
Chylomicron retention disease is characterized by fat malabsorption, hypocholesterolemia, normal fasting triglycerides, and marked intestinal steatosis despite the presence of both plasma and intestinal apoprotein B. The defect remains unknown but presumably involves the synthesis or secretion of chylomicrons. The present investigation examines this hypothesis by studying the biosynthesis of chylomicrons in cultured jejunal explants and by defining the quantitative and qualitative abnormalities of plasma lipids and of circulating lipoproteins. Following 2-3 years of a low fat diet supplemented with medium chain triglycerides, six patients with chylomicron retention disease had significantly higher triglyceride (TG) levels coupled with a decrease in both free (FC) and esterified cholesterol (EC) as well as in essential fatty acids and phospholipids (PL) when compared to healthy controls. The low total plasma cholesterol was largely accounted for by low levels of both low density (LDL) and high density lipoprotein (HDL) cholesterol. VLDL and LDL were characterized by a diminished percentage of CE with an increase of TG while HDL contained relatively more FC as well as PL and less CE. The diameter of VLDL was larger whereas those of LDL and HDL were smaller than in normal controls. Jejunal explants, when incubated with [14C]palmitate, were capable of normal biosynthesis of TG, diglycerides, PL, and CE. These lipids, however, except for PL, were retained in the tissue and could not be secreted into the culture medium. Incubation of intestinal biopsies with [3H]leucine and [14C]mannose resulted in normal protein synthesis and reduced glycosylation. The presence of intestinal apoB-48 was confirmed by immunoblot using 2D8 antibodies. These data suggest that the intestinal defect in this disease results from a disorder of the final assembly of chylomicrons or in the mechanism of their exocytosis.
Other presentations to this symposium have indicated that the search at the molecular level for the pivotal regulatory, or structural, gene responsible for determining the development of the undifferentiated gonad has been joined in earnest. It is also clear that genes on the Y chromosome are involved in processes other than primary determination of the testis. In this summary, we will review briefly 'the molecular search for the sex-determining gene' and consider the approaches that are available and the achievements that have been made in the areas relevant to an understanding of the roles and significance of other Y-located genes. The availability of molecular and physical mapping data also allow an examination of the evolutionary relationship of the mammalian X and Y chromosomes and a consideration of the possible homologies between the human and mouse Y chromosomes.
The effect of taurine supplementation on the absorption of a fat meal was evaluated in patients with cystic fibrosis. In a cross-over design study, five patients with cystic fibrosis (12.1 +/- 2.6 years of age) and three control subjects received either placebo or taurine (30 mg/kg/d) for two 1-week periods, a month apart, followed by a fat meal test. Blood samples were drawn 0, 1, 2, 3, 5, 8 hours after the meal. Four patients with cystic fibrosis and severe steatorrhea despite appropriate enzyme therapy showed a significant (P less than .05) improvement in the absorption of triglycerides, total fatty acids, and linoleic acid while receiving taurine supplements. Three control subjects and one child with cystic fibrosis and mild steatorrhea receiving enzyme therapy did not experience such an effect. The difference in triglyceride absorption, when calculated as the area under the curve, receiving and not receiving taurine was significantly (P less than .05) correlated with the degree of steatorrhea. Furthermore, in contrast to control subjects, the fatty acid composition of chylomicrons in these four study patients showed important discrepancies with that of the fat meal and was corrected, in part, by taurine supplementation. These results suggest that taurine supplementation could be a useful adjunct in the management of patients with cystic fibrosis with ongoing fat malabsorption and essential fatty acid deficiency.
Five different sublines of the BALB/c murine S49.1 T cell lymphoma were found to exhibit distinct patterns of absence of detectable H-2d class I major histocompatibility antigen expression. The results were demonstrated and verified by a) the generation of H-2Kd-, H-2Dd,Ld-, and H-2Ld-specific cytotoxic T lymphocytes that were assayed on S49.1 target cell lines, b) antibody-mediated cytotoxicity with the use of anti-H-2d monoclonal reagents, and c) flow microfluorometry. The five lines investigated were S49.1, T-25, T-25ADH, Thy-1-, and 100/0. None of these lines expressed detectable levels of Ld. S49.1 expressed both Kd and Dd, T-25 and T-25ADH expressed Dd but not Kd or Ld, Thy-1- expressed Kd but not Dd or Ld, and 100.0 did not express any detectable amounts of Kd, Dd, or Ld. These results indicate that K and D (and L) antigens can be expressed independently of each other and suggest that expression of class I antigens is controlled in a locus-specific manner.
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Five murine lymphoma cell lines were assayed for the content and activity of gamma-glutamyltranspeptidase (GTT). All lines [S49; L-12; 230-23-8 (C57 Black); 2M3 and RA3-2C2] contained detectable amounts of GGT. The specific activities of GGT were low and ranged between 1.2 and 2.3 mU/mg protein in cells growth in vitro. A highly malignant variant of the S49 line was also grown in vivo in BALB/c mice. This subline invariably produces both solid and ascitic tumors with infiltrations into the pancreas, liver and spleen. GGT levels in the tumor cells were low and independent of tumor type (solid, ascitic), location, passage number or inoculum size. Infiltrations of S49 tumor cells in liver and spleen were invariably GGT--negative as judged by histochemical examination. GGT activities in suspension cultures prepared from solid, as well ascitic tumors were low. Occasional high GGT activity of solid tumors was due to the presence of pancreas cells in them. The only host tissue significantly responding to the presence of tumors by elevated GGT levels was the liver. Compilation of data from this study and those of others clearly indicates that low GGT level is a typical property of tumors originating in the immune system.
Mutagenesis of Azospirillum brasilense with nitrosoguanidine and selection on ethylenediamine yielded prototrophs which fixed nitrogen in the presence of ammonia. Nitrogenase activity in mutant strains exceeded that of the wild type three- to sixfold. The same mutants were also constitutive for histidine transport. Enzyme activities involved in ammonia assimilation were not affected by the mutation. The data suggest that the mutation occurred at a site which regulates nif and histidine transport functions.
The clinical electromagnetic hyperthermia system has been in use at the Kaplan Hospital since 1980, for treating patients with hyperthermia combined with radio- or chemotherapy. For prostatic tumors, hyperthermia at 43 degrees C is achieved in the prostatic mass using microwaves of 2.45 GHz, with simultaneous cooling of the rectal mucosa and the rectal wall. Thirty-two patients with carcinoma of the prostate have been treated: 4 with heat alone, 20 with hyperthermia combined with radiotherapy, and 8 with hyperthermia combined with hormonal therapy. Follow-up was carried out up to 34 months. Objective local tumor regression was achieved in 3 out of 4 patients treated by heat alone, but the patients relapsed after 6 months. All the 20 patients treated with combined hyperthermia and radiotherapy responded to treatment. Patients treated with combined hyperthermia and hormone therapy responded locally to treatment but died of their metastatic disease, or of unrelated diseases with a follow-up period up to 31 months. Hyperthermia did not increase morbidity beyond that expected for radiation therapy.
Sand rats (Psammomys obesus) maintained on a diet providing a free choice between laboratory chow and salt bush (Atriplex halimus) were classified into four groups differing in extent of the diabetic syndrome: A, normoglycemic-normoinsulinemic; B, normoglycemic-hyperinsulinemic; C, hyperglycemic-hyperinsulinemic; or D, hyperglycemic with reduced insulin levels. The metabolic pattern of these groups was characterized by measuring the uptake of fatty acid-labeled, very-low-density lipoprotein-borne triglycerides (VLDL-TG) and [3H]-2-deoxyglucose (2-DOG) into muscle and adipose tissues; incorporation of [14C]alanine into glycogen in vivo; gluconeogenesis from lactate, pyruvate, and alanine in hepatocytes; the effect of insulin on glycogen synthesis from glucose; the oxidation of albumin-bound [1-14C]palmitate and [14C]glucose in strips of soleus muscle; activities of muscle and adipose tissue lipoprotein lipase; and activities of rate-limiting enzymes of glycolysis, gluconeogenesis, and fatty acid synthesis in liver. In group A, uptake of VLDL-TG and activity of lipoprotein lipase were higher in adipose tissue and lower in muscle than in albino rats. In the liver, gluconeogenesis and the activity of phosphoenolpyruvate carboxykinase, as well as lipid synthesis and the activity of NADP-malate dehydrogenase, were higher than in albino rats, whereas activity of pyruvate kinase was lower. In group B, uptake of VLDL-TG by adipose tissue and muscle and lipoprotein lipase activity were similar or higher than in group A. Uptake of 2-DOG by muscle and adipose tissue and activity of liver phosphoenolpyruvate carboxykinase were lower than in group A. In groups C and D, uptake of VLDL-TG and lipoprotein lipase activity in muscle were further increased.(ABSTRACT TRUNCATED AT 250 WORDS)
Understanding the sand rat's metabolic responses is necessary in order to employ the animal gainfully in the study of diabetes. Weanlings are most susceptible to the effect of diabetogenic diets. In the present experiment, weanling sand rats were fed diets at 3 levels of energy intake. The diets were based on pellets composed of different ratios of salt bush (Atriplex halimus) and a standard laboratory animal chow pellet. The results showed a significant correlation between the level of energy intake, percent body fat and signs of Type 2 diabetes. Animals with 28-30.6% body fat had blood glucose levels of 260 +/- 66 mg% and plasma insulin concentrations of greater than 558 mu u/ml, and those with 17.9-24.0% body fat had a blood glucose level of 107 +/- 19.8 mg% and a plasma insulin level of 222 +/- 35 mu u/ml. Animals with approximately 10% body fat, had a blood glucose level of 60 +/- 1.9 mg% and a plasma insulin concentration of 35 +/- 10 mu u/ml. The fattest animals had the highest percentage of glycosylated hemoglobin. The animals with the highest quantity of fat receiving high caloric intake had a lower lean body mass than those of similar weight exposed to a lower caloric intake. This result could be accounted for by assuming that the extreme hyperinsulinemia promoted fat production at the expense of lean body mass.
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Colorectal cancer is the second leading cause of cancer death in western populations. As treatment outcome is highly correlated with stage at diagnosis, early detection is a very important task. Three high-risk groups for colorectal cancer (first-degree relatives of colorectal cancer patients; individuals with past history of colorectal neoplasms, polyps, or carcinoma; and patients with ulcerative colitis) were screened for colonic neoplasms. The study program included the leukocyte adherence inhibition test (LAI), a specific immune response test for colorectal cancer antigen; fiberoptic sigmoidoscopy or colonoscopy; and guaiac impregnated slide test. The main finding was the detection of 92 positive LAI tests out of 451 high-risk individuals tested (20%), compared to eight positive tests out of 194 (4.1%) in a control group. Fifty-six colonic neoplasms were found out of 344 (16%) colonoscopies performed, most of them adenomatous polyps and a few carcinomas. Our findings, compared with the expected 2-3% neoplasms in low-risk groups, would prove that the screenees were indeed at high risk. However, only 11/56 (19%) of the polyps identified were LAI positive. The number of polyps found among LAI positive individuals were, so far, 11/92 (11%). The guaiac impregnated slide test for occult blood in the stool was performed in 221 screenees. Of these only 10 were positive (4.5%) compared with the average of 1% positive tests in low-risk groups.
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