Demonstration of a narrow-divergence x-ray laser in neonlike titanium.
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Biomedical subjects
Publications and source records attributed to R Epstein.
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This study compares four methods of hepatic denervation and defines the rate and physiological significance of reinnervation. Five groups of rats were prepared: 10 underwent orthotopic liver transplantation. In nine rats a 90% aqueous phenol solution was applied circumferentially to the portal vein. Thirteen rats underwent microsurgical denervation; 28 received different doses of 6-hydroxydopamine (6-HODA) administered as a single intraportal injection [50 (n = 10), 75 (n = 6), and 100 mg/kg (n = 6)]. Twelve rats were studied as controls. Rats were killed 1, 4, and 8 wk after surgery to determine liver tissue content of norepinephrine (NE). Changes in mean arterial pressure (MAP) in response to hepatic nerve stimulation, which was supramaximum in intensity and frequency, were measured before rats were killed. NE content in controls ranged from 121 to 204 ng/g and MAP increased by 30-38 mmHg after electrical stimulation. At 1, 4, and 8 wk after treatment the liver NE content was less than 1, 2.3, and 20.2 ng/g in the transplant group; less than 1, 2.7, 4.1 ng/g in the phenol group; and 17.2, less than 1, and 3 ng/g in the surgically denervated group. In the 6-HODA group, values were 18.9, 47, and 61.5 ng/g (50 mg/kg); 5.7, 20.2, and 15 ng/g (75 mg/kg); and 7.7, 2.5, and 17.5 ng/g (100 mg/kg). When the level of NE was undetectable, MAP increase after stimulation was 0-18% that of controls. When NE content was 15-23% of normal, MAP increased 49-62% regardless of the denervation technique.(ABSTRACT TRUNCATED AT 250 WORDS)
STUDY OBJECTIVE: To determine the long-term risk for colorectal cancer among patients with pernicious anemia. DESIGN: Historical cohort study. SETTING: Population-based inception cohort of Rochester, Minnesota, residents. PATIENTS AND METHODS: We identified 150 Rochester residents who had the onset of pernicious anemia during the 30-year period from 1950 through 1979, and we followed this cohort for 1664 person-years of observation. The observed risk for subsequent colorectal cancer in the cohort was compared with that expected based on incidence rates of colon and rectal cancer for the local population. MEASUREMENTS AND MAIN RESULTS: There were 14 cases of colorectal cancer among the 150 patients with pernicious anemia (where 10.5 cases were expected), and 9 of these cases were found after the diagnosis of pernicious anemia was established (where 5.1 cases were expected). The relative risk for colon cancer at any time after the diagnosis of pernicious anemia was 1.8 (CI, 0.8 to 3.3). The relative risk was greatest (4.1; CI, 1.7 to 8.7) in the 5-year period immediately after the diagnosis of pernicious anemia; during this period, 7 cases of colon cancers were observed but only 1.7 were expected (P less than 0.0001). CONCLUSION: Although the overall risk does not achieve statistical significance, patients with pernicious anemia may have an increased risk for colorectal adenocarcinoma in the 5 years after diagnosis.
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The sperm HOS test was highly predictive of eventual achievement of pregnancy in women in whom other infertility factors had been corrected. No woman conceived whose partner's HOS was less than 50%. The results of spermiograms did not correlate with conception rate.
Four hundred and eighty five students, aged 13-15 years, at nine comprehensive schools in the London borough of Brent completed a questionnaire about health-related behaviours and health concerns. Among general health concerns, most prominent were weight, acne, nutrition and exercise. There appeared to be a considerable unmet need to discuss sexual development, sexually transmitted diseases and contraception. A substantial proportion (16% of the girls and 3% of the boys) reported sexual abuse, but few wished to discuss this with a doctor or nurse. Although a relatively high percentage of the students smoked and a smaller percentage used alcohol or drugs regularly, there was little concern or interest in discussing these matters with a health professional. Most of the schools did not have a formal health education programme, and in none of them were health professionals available for discussion of the issues under study. There appears to be a need for more comprehensive health education in schools and for primary health care professionals, particularly general practitioners to raise these issues opportunistically with their teenage patients.
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A pigeon was trained to peck a small facsimile of a banana placed within its reach, to climb onto a box, to open a door, and to push a box toward targets. When confronted with a new situation-the banana was placed out of reach, and the box was placed behind the door-the four repertoires came together rapidly to produce a humanlike solution to the problem. A tentative account of the performance is offered in terms of empirically validated principles.
The genetic control of the cytotoxic T-cell response to the male histocompatibility antigen, H-Y, was analyzed in BALB/cKe(C) and SJL/J(J) which are both nonresponders. However, the (C X J)F1 hybrid is a responder. Therefore, two dominant complementing genes are involved. Analysis of a set of (C X J) recombinant inbred (RI) lines reveals that these two complementing gene products are a restricting element (R) encoded by the H-2 (MHC) locus on chromosome 17 and a subunit of the T-cell receptor (anti-R) encoded by the Tar alpha-locus on chromosome 14. The order and orientation of gene segments within the Tar alpha-locus has also been established relative to the chromosome 14 marker, Es-10. The existence of two RI strains which are recombinant at chromosome 14 has made it possible to determine that this order is Es-10--v alpha-1--v alpha-2--[C alpha--Np-2]--centromere. The implications of these data for the antigen-specific regulation of immune responsiveness are discussed in terms of the dual recognitive-single receptor model.
The experiments described here delineate the position of the chromosome 16 markers Igl-1 (immunoglobulin lambda 1, light chain), md (mahoganoid), and Bst (belly spot and tail), and suggest their location relative to the endogenous proviral locus Akv-2, which is linked within 5.9 centimorgans to Igl-1 (Epstein et al. 1984). The data from an intercross and a three-point backcross detailed herein show the order of these three genes and distances between them to be: centromere-md-10.4 +/- 1.6-Igl-1-15.6 +/- 2.6-Bst. Using a recombinant chromosome recovered in the intercross, we have constructed a stock homozygous for md and Igl-1b (KpnI-), that will aid in mapping other genes on chromosome 16.
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Numerous economic, legal, and human variables are entangled in the current malpractice crisis. To help governing boards gain perspective on the malpractice situation, James Orlikoff, program director in the American Hospital Association's division of hospital governance, recently spoke with four experts who are familiar with the different areas involved in the crisis: Dixie Arthur, vice-president, Health Providers Insurance Corp.; Richard Epstein, senior vice-president and general counsel, American Hospital Association; James Hughes, partner, Bricker and Eckler, Columbus, OH, and general counsel to the Ohio Hospital Insurance Co.; and William Robinson, AHA senior vice-president and president, Health Provider Insurance Co.
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The restriction enzyme Eco RI reveals DNA cleavage sites that serve to distinguish the gene locus believed to encode the beta subunit of the major histocompatibility complex (MHC)-restricted, antigen-specific receptor of the T cell in BALB/c mice from that of SJL/J mice. A monoclonal antibody, KJ16-133, also distinguishes BALB/c and SJL/J, because it recognizes an allotypic marker present on a cell-surface heterodimer believed to function as the MHC-restricted, antigen-specific T cell receptor. This study has shown that these two markers cosegregate in a set of BALB/c X SJL/J recombinant inbred (RI) mouse strains, permitting the conclusion that they are linked to within 3 centimorgans of each other, and to the kappa locus on chromosome 6. The tight linkage between these independently derived, totally different T cell markers substantially strengthens the argument that they characterize the MHC-restricted antigen-specific receptor of the effector T cell.