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Biomedical subjects

A Cohen

Publications and source records attributed to A Cohen.

At least 649 records · Page 36Linked to original sources
PubMed1988

Posterior stabilization of cervical spine fractures and subluxations using plates and screws.

Posterior stabilization of cervical spine fractures and subluxations with metal plates and screws is commonly used in Europe, but has rarely been employed by neurosurgeons in North America, where stabilization has usually been achieved with wires supplemented by bone grafts or acrylic. The limitations of the more commonly used stabilization techniques include the failure to achieve rotational stability, the necessity for intact laminae, and the requirement for bone grafting. We therefore examined the efficacy of posterior cervical plating in 19 patients who had posttraumatic instability of the cervical spine between C3 and C7 without residual spinal cord compression and 1 patient who had a subluxation as a result of osteomyelitis. Two patients had no neurological deficit, 4 had partial deficits, and 14 had no neurological function below the level of injury. Operation was performed after patients were medically stable and maximal reduction of fractures was achieved (usually within 48 hours). The plates are made of vitallium and contain two or three holes 13 mm apart through which 16-mm screws are placed bilaterally into the center of the articular masses of two or three adjacent vertebrae to stabilize one or two motion segments. Bone grafting is not performed. Patients are mobilized on the day after operation in a Philadelphia collar, which is worn for 3 months. Fourteen patients had stabilization of one motion segment and 6 had stabilization over two motion segments. The mean follow-up is 9.2 months. In a single patient with ankylosing spondylitis, plate fixation failed when screws pulled out. No patient experienced neurological deterioration as a result of the operative procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Overview of the beta thalassemias: genetic and clinical aspects.

There has been much progress in basic studies of the beta-thalassemia disorders in recent years, as well as in the practical aspects of prenatal diagnosis and clinical management. Alterations in a single or a few nucleotides account for most of the types of beta-thalassemia syndromes that have been characterized, and a variety of deletions have been found associated with beta O thalassemia, delta beta thalassemia, gamma delta beta thalassemia, and hereditary persistence of fetal hemoglobin (HPFH). Studies of nondeletional types of HPFH have revealed several single base changes 5' to the G gamma and A gamma genes, suggesting that these regions may be of major importance in the switchover from fetal to adult hemoglobin synthesis and in the relative production of the G gamma and A gamma globin chains during development. Evaluation of restriction enzyme polymorphisms and the assignment of haplotypes in the beta-like globin region of chromosome 11 have allowed delineation of the origin and distribution of thalassemia mutations, and have provided an important means for prenatal diagnosis. These studies have accumulated much new information about the function and expression of eukaryotic genes, and have served as a model for the investigation of human genetic disorders. The clinical management of patients with Cooley's anemia has benefited greatly from changes in transfusion practice, clear guidelines for splenectomy, and the availability of effective chelation therapy for iron overload. Current basic and clinical studies may lead to new approaches to management, treatment and eventual cures for this disease, including safe bone marrow transplantation, oral chelation treatment, and gene therapy.

Fetal Hemoglobin↗
PubMed1988

[Selective embolization of mycotic aneurysm of the branches of the abdominal aorta].

We report two cases of multiple aneurysm complicating bacterial endocarditis and involving the hepatic, renal and superior mesenteric arteries. The aneurysms were treated by the superselective embolization technique hitherto restricted to cerebral arteries. The first patient had been operated upon for mitral valve endocarditis. Because of a persistent anicteric cholestasis, repeat ultrasonography and computerized tomographic scan were performed which revealed two intrahepatic aneurysms associated, at arteriography, with an aneurysm of the superior mesenteric artery. The patient underwent superselective embolization of one of the intrahepatic aneurysms, then of the superior mesenteric artery aneurysm. Angiographic cure was obtained and persists after a 17-month follow-up. In the second patient, persistent clinical and biochemical hepatic abnormalities after mitral and aortic valve replacements for endocarditis prompted us to perform an ultrasonography which showed a large hepatic aneurysm, and an abdominal arteriography which disclosed the presence of several aneurysms. Because of its size and suspected fissuration, the hepatic aneurysm was treated by superselective embolization, and this was followed by embolization of a renal artery. The immediate post-treatment period was uneventful, and complete angiographic cure was confirmed after 6 months. Superselective embolization seems to give good results at mid-term and should therefore be considered for fragile patients with multiple abdominal aneurysms.

Adult↗
PubMed1988

The stability of uric acid in ammonium hydroxide.

We examined the stability of uric acid in dilute aqueous ammonium hydroxide solution by mass spectrometry. Uric acid decomposes in ammonium hydroxide even as dilute as 15 mmol/L when the mole ratio of ammonium hydroxide to uric acid is 50:1. There are at least four products of the decomposition, two of which have been identified as allantoin and urea. The slope of the decomposition curve indicates that uric acid is destroyed at an initial rate of 2-3% per hour. In ammonium hydroxide at a concentration of 1 mmol/L and a mole ratio of ammonium hydroxide to uric acid of less than or equal to 3.4, uric acid is not detectably decomposed. Evidently, any method for determination of uric acid that involves treating the analyte with ammonium hydroxide before analysis may destroy it. Therefore, a published method described as being "definitive" for uric acid (J Clin Chem Clin Biochem 1985; 23:129-35) could produce incorrect results because it involves storing the uric acid in 15 mmol/L ammonium hydroxide at a mole ratio of ammonium hydroxide to uric acid of greater than 120:1.

Ammonium Hydroxide↗
PubMed1988

[Lutenyl and menstrual disorders. A hospital study].

The efficacy of nomegestrol acetate in the treatment of menstrual cycle disorders and dysfunctional uterine bleedings was confirmed on 66 cases in this study conducted by three hospital departments. The study also confirmed the perfect clinical tolerance of nomegestrol acetate. One knows that the same is not true with Nortestosterone derivatives which were used up to now in these indications.

Adult↗
PubMed1987

Roles of globotriosyl- and galabiosylceramide in verotoxin binding and high affinity interferon receptor.

The cellular specificity of the Escherichia coli-derived verotoxin is of particular interest because of its extreme toxicity and high selectivity toward certain primate cells. The human Burkitt lymphoma cell line (Daudi) is highly susceptible to the cytotoxicity of verotoxin and contains large amounts of the verotoxin-binding glycolipids on its surface. A mutant selected from Daudi cells for verotoxin resistance was found to be deficient in the verotoxin-binding glycolipids, globotriosylceramide and galabiosylceramide, and failed to bind verotoxin to its surface; interestingly, these mutant cells were found to be cross-resistant to inhibition of growth by alpha-interferon. Mutant cells also lack the high affinity component of alpha-interferon binding. These observations suggest that, in addition to providing the functional cell-surface receptor for verotoxin, these glycolipids may also play a role in the modulation of the affinity of alpha-interferon for its membrane protein receptors.

Bacterial Toxins↗
PubMed1987

Metabolic consequences of DNA damage: alteration in purine metabolism following poly(ADP ribosyl)ation in human T-lymphoblasts.

The effect of DNA damage caused by N-methyl-N'-nitro-nitrosoguanidine (MNNG) on poly(ADP-ribose) synthesis, NAD levels, and purine nucleotide metabolism was studied in human T-lymphoblasts. Excessive DNA breaks caused by MNNG activated poly(ADP-ribose) polymerase and rapidly consumed intracellular NAD. NAD depletion was followed by rapid catabolism of ATP as well as induction of total purine nucleotide catabolism leading to excretion of purine catabolic products. MNNG-treated cells were not able to replenish the intracellular nucleotide pools due to the depletion of intracellular ATP and phosphoribosylpyrophosphate pools which are required for de novo purine biosynthesis. Inhibition of poly(ADP-ribose) polymerase by 3-aminobenzamide prevented both the depletion of NAD pools and the associated changes in purine nucleotide metabolism.

Adenine↗
PubMed1987

Impairment of nucleotide metabolism by iron-chelating deferoxamine.

The effect of deferoxamine on nucleotide metabolism in HL-60 leukemic cells was studied to explore the mechanism of its antiproliferation activity. It was found that in intact cells deferoxamine markedly inhibited the ribonucleotide reduction and incorporation of bases (adenine, hypoxanthine), ribonucleosides (inosine, guanosine) and deoxyribonucleosides (thymidine, deoxyadenosine, deoxyguanosine) into nucleic acids. Although deferoxamine did not inhibit thymidine and uridine incorporation into free nucleotides, inhibition of hypoxanthine and adenine incorporation into nucleotides as well as inhibition of nucleotide biosynthesis de novo was found. Nucleotide catabolism, protein synthesis, and intracellular levels of ribonucleotides were not affected significantly by deferoxamine. These results showed that deferoxamine selectively affects several specific reactions of nucleotide metabolism. Inhibition of ribonucleotide reduction, inhibition of ribonucleotide and deoxyribonucleotide incorporation into nucleic acids, as well as inhibition of purine biosynthesis, may alter significantly cellular physiology and, therefore, contribute significantly to the antiproliferative activity of deferoxamine.

Cell Division↗