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Biomedical subjects

L Weiss

Publications and source records attributed to L Weiss.

At least 289 records · Page 16Linked to original sources
PubMed1989

Continuous arteriovenous hemofiltration in the treatment of 100 critically ill patients with acute renal failure: report on clinical outcome and nutritional aspects.

The clinical outcome for 100 consecutive patients with multiorgan failure including acute renal failure (ARF) was studied. Fifty-eight of the patients had acute renal failure due to complications during and after major surgery. Seventy-three of the patients had a urine output of less than 400 ml/24 hours. The majority of the patients also had complications such as septicemia or respiratory insufficiency and required vasopressor infusions. All patients were treated with continuous arteriovenous hemofiltration (CAVH). The duration of the CAVH treatment varied between a few hours and 90 days, with a mean of 8 days. The mean ultrafiltration volume per 24 hours was, on the average, 12 liters. CAVH resulted in adequate uremic control in 89 cases, but additional treatment with intermittent hemofiltration was necessary in 11 patients. The total survival rate was 45% including survival rates as high as 54% in patients with ARF complicating abdominal aortic surgery. Only three patients were referred for chronic dialysis therapy. In a subgroup of 17 patients with ARF complicating abdominal aortic surgery the nutritional aspects during CAVH were studied. It is concluded that during CAVH therapy it is possible to give adequate nutritional support even to hypercatabolic and anuric patients.

Acute Kidney Injury↗
PubMed1989

The human C3b receptor (CR1).

The human complement system is comprised of 19 plasma components and regulatory proteins and of at least 9 distinct cellular receptors for these proteins or their activation fragments. The important role of complement in host defense against infection is related to its capacity to opsonize microorganisms, lyze target cells, and induce the release of inflammatory mediators from leukocytes. Complement participates in the processing and clearance of immune complexes and in regulation of the immune response. Most of the biologic effects derived from complement activation depend on ligand-receptor interactions between complement proteins or their cleavage fragments and specific receptors on cells. Two types of ligands are generated during complement activation: soluble low-molecular-weight ligands, such as the anaphylatoxins C3a and C5a, and so-called bifunctional ligands that attach both to the target of complement activation (opsonins) and to the appropriate receptor on effector cells. The most abundant complement protein in plasma is C3. Activation of the classic and alternative complement pathways generates C3 convertases that cleave C3 into an anaphylatoxic fragment, C3a, and a major fragment, C3b, which is capable of forming a covalent linkage with the targets of complement activation. Surface-bound C3b is the preferential ligand for the C3b receptor, CR1 (CD 35), which is expressed on most peripheral blood cells. The receptor plays an important role in the processing of immune complexes, the phagocytosis of C3b-bearing microorganisms, and regulation of the immune response. The cellular expression of the molecule is decreased in patients with systemic lupus erythematosus (SLE) and in patients infected with the human immunodeficiency virus (HIV).

Antigen-Antibody Complex↗
PubMed1989

Differential killing of murine B-cell leukemia (BCL1) by photosensitization with merocyanine 540: implications for autologous bone marrow transplantation.

The efficacy of photosensitization by merocyanine 540 (MC540), a lipophilic fluorescent dye, was investigated in the murine B cell leukemia (BCL1). Normal BALB/c mice were injected with BCL1 cells exposed to MC540, followed by photosensitization with white light for 15 min to 2 h. Mice injected with BCL1 cells exposed for 1 or 2 h showed no sign of leukemia. Lethally irradiated mice were successfully reconstituted with mixtures of syngeneic bone marrow (BM) and BCL1 cells treated with MC540 following exposure to white light. Exposure of BM/BCL1 mixtures for 2 h proved to be effective in purging all BCL1 cells without affecting BM viability, as documented by normal hemopoietic reconstitution of all recipients surviving without evidence of leukemia. All recipients of untreated BM/BCL1 cell mixtures developed leukemia within 42 days. Adoptive transfer of 10(6) spleen cells obtained from treated mice into secondary naive syngeneic recipients was carried out in order to test for dormant BCL1 cells in treated recipients. No leukemia developed in any of the secondary recipients. Previous studies indicate that as few as 10, or possibly less, BCL1 cells are sufficient to cause lethal disease in BALB/c recipients. Our results suggest that MC540 may be an extremely potent tool for in vitro elimination of residual tumor cells while leaving uncommitted progenitor hemopoietic cells intact for hemopoietic reconstitution following lethal marrow ablation.

Animals↗
PubMed1989

Parental adjustment to intrapartum and delivery room loss. The role of a hospital-based support program.

Perinatal loss prompts a unique bereavement for parents and their families that is unlike the mourning process experienced at the death of other loved ones. The Support Center For Perinatal and Childhood Death has developed a comprehensive program to provide support, counseling, and information to families who experience miscarriage, stillbirth, fetal anomalies, and therapeutic abortion for genetic or congenital abnormalities. The impact of perinatal loss is felt not only in the real loss of the wished-for child but also in the loss of self-esteem, the role of parent, and the loss of confidence in the ability to produce a healthy child. The emotional experience of miscarriage or stillbirth creates an atmosphere of despair and confusion for families anticipating a joyous event. The presence of a support counselor and medical caregivers at this time can help parents to navigate the crisis surrounding the loss in ways that promote a healthy grieving process and avert pathologic adaptations. Prenatal, intrapartum, and postpartum counseling opportunities are afforded to families as the situation and parental needs dictate. Services also are extended to other family members, with particular attention to surviving siblings who might be vulnerable to the consequences of unresolved or unacknowledged grief. Grief is experienced as a long-term process, which frequently emerges fully after discharge from the hospital and lasts well beyond the interest and stamina of supportive family members and friends. Support groups, which meet the specific needs of families who experience perinatal loss, contemplate subsequent pregnancy, or face the prenatal decision to terminate a genetically or congenitally compromised pregnancy, have been run successfully for a period of several years. Beyond the experience of intrapartum loss in the delivery room, the experience comes full circle for families who enter the delivery room again with a subsequent child. The expressed need for support in acknowledging the rekindled memories of prior loss at this poignant time are matched only by parents' needs to find reassuring ways of differentiating healthy newborns from the memory of those who died. It is often at the time of the subsequent birth that the memory of the lost child can take its proper place in the family. Stein expresses the essence of grief work and resolve: Mourning is not just feeling sad. It is the specific psychological process by which human beings become able to give up some of the feelings they have invested in a person who no longer exists, and extend their love to the living. Mourning is hard, emotional work.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Psychological↗
PubMed1989

Mechanisms of splenic control of murine malaria: tissue culture studies of the erythropoietic interplay of spleen, bone marrow, and blood in lethal (strain 17XL) Plasmodium yoelii malaria in BALB/c mice.

This work characterizes the erythropoietic interplay of the spleen, blood, and bone marrow in a lethal murine malaria, strain 17XL P. yoelii. This malaria runs a fulminant 7 day course in BALB/c/ByJ mice, marked by high levels of parasitized reticulocytes with death likely due to anemia. We have quantitated the levels of burst forming units-erythroid (BFU-E), the early, niche-seeking, largely erythropoietin-unresponsive erythropoietic precursors, and of colony forming units-erythroid (CFU-E), the more differentiated sessile erythropoietin-responsive precursors, in bone marrow, blood, and spleen, through the course of this malaria. A decline in marrow BFU-E began on day 2, but recovered, relatively, after day 3. Marrow cellularity declined, being but 75% normal on day 6. Spleen weight increased about 5-fold within 6 days with enlargement of erythroid, lymphoid, macrophage, and stromal compartments. Splenic BFU-E increased in the first 24 hr and 5-fold by day 6. Splenic CFU-E increased in the first 24 hr and into day 4. They then declined and showed a secondary, large-scale, sustained rise interrupted by death. Because the spleen was enlarging, a greater than 60-fold increase in the absolute number of splenic CFU-E occurred at the time of death. Marrow CFU-E followed the same pattern as splenic CFU-E, but the terminal increase represented but a 4-fold absolute increase because of declining marrow cellularity. High levels of erythropoietin occurred only late in the course of disease, likely in response to profound anemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

A dicentric recombinant 9 derived from a paracentric inversion: phenotype, cytogenetics, and molecular analysis of centromeres.

A 4-year-old girl with multiple malformations and severe developmental delay has been shown to have a karyotype of 46,XX-9,+rec(9),dup p,inv(9) (q22.1q34.3)mat, with duplication 9pter-q22.1 and deficiency 9q34.3-qter. This case confirms that a stable recombinant chromosome can result from a paracentric inversion. The recombinant was derived by two crossovers, one within the inversion loop and a second outside the inversion loop, between 9q21 and the beginning of the meiotic inversion at 9q22.1. In 87 cells the rec(9) had one Cd-positive primary constriction. In 13 cells the rec(9) had two primary constrictions; in 12 of these cells there was one Cd-positive centromere, and in one of these cells both primary constrictions were Cd-positive. Nuclear projections were observed in 10% of fibroblast interphase cells harvested in situ, suggesting that there was some spindle-fiber activity of the "latent" centromere. In situ hybridization with a centromere-specific probe (p82H) and a satellite III probe (L6) revealed no differences between the two C-band regions of the rec(9) and the normal 9 or inverted 9 chromosomes.

Abnormalities, Multiple↗
PubMed1988

Effects of metastatic cascades on metastatic patterns: studies on colon-26 carcinomas in mice.

The present studies are based on autopsy data showing that in upper esophageal and lower rectal carcinomas, hematogenous metastasis occurs mainly first to the lungs, and cancer cells from pulmonary metastases generate arterial metastases. In lower esophageal and upper rectal carcinomas, hematogenous metastases occur first in the liver, then in the lungs, and are further disseminated by the arterial route. The arterial metastatic patterns are different in the 2 groups. One possible explanation for these differences in pattern is that liver "residence" is associated with different metastatic behavior; this has been tested in a model system. Experiments with the transplantable colon-26 carcinoma in mice reveal that, when cancer cells from common s.c. transplant sites are grown in the liver, lungs or liver-and-lungs, and then injected into the bloodstream of fresh recipients via the left ventricle, the portal vein or the tail vein, different patterns and degrees of colonization of 11 different target sites are observed. These results are consistent with the hypothesis that growth of cancers in different anatomic sites may modify the subsequent arterial metastatic patterns, due to site-induced changes occurring in cancer cell populations, which influence metastasis from metastases or so-called "cascade" processes.

Animals↗
PubMed1988

Multifocal cytomegalovirus encephalitis in AIDS.

A 43-year-old man with the acquired immunodeficiency syndrome had clinical evidence of multifocal disease of the brain, but computed tomography was negative. Magnetic resonance imaging revealed multifocal lesions, histologically proven to be caused by cytomegalovirus. Therapy with 9[2-hydroxy-1-(hydroxymethyl) ethoxymethyl] guanine (BW B759U) resulted in stabilization of the patient's clinical disease and radiographic improvement of the lesions.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Metastatic patterns of renal carcinoma: an analysis of 687 necropsies.

The metastatic behaviour of renal cell carcinoma has been studied in a series of 687 necropsies. The observations were consistent with the concept of "metastatic inefficiency", in that in 295 cases, including 25 with renal vein invasion, there were no detectable metastases. In the present series, renal vein involvement was not an important prognostic factor in stage 1 or 2 disease. In 73% of cases without lung metastases there were none in other sites, and in 84% of those with lung metastases there were others elsewhere, consistent with a metastatic "cascade" in which metastases first developed in the lungs and were later detected in other organs. However, the observations did not permit discrimination between anatomic cascades, in which other organs were seeded from metastasizing pulmonary metastases, and temporal cascades, in which the other were seeded at the same time as the lungs, but with fewer cancer cells. The patterns of arterial metastasis were consistent with the "seed-and-soil" hypothesis, and a novel index was developed to quantify differential organ "soils". The contralateral kidney was not the best soil for metastases from renal carcinoma. Given the presence of lymph node metastasis, the probability of heamatogenous metastasis is 90%. However, in the absence of nodal metastasis, approximately half the cases had haematogenous metastasis.

Adult↗
PubMed1988

Factors predisposing to seizures in seriously ill infected patients receiving antibiotics: experience with imipenem/cilastatin.

Observations on 1,754 patients treated with imipenem/cilastatin in phase III dose-ranging studies in the United States were reviewed to determine risk factors for seizures. The patients were moderately to severely ill with numerous background disorders known to be associated with an increased risk of seizures. Fifty-two patients (3 percent) had seizures and in 16 (0.9 percent) of them the seizures were judged by the investigators to be possibly, probably, or definitely related to imipenem/cilastatin. An incidence of seizure of 2 to 3 percent was noted among patients treated with other antibiotics (usually including a beta-lactam in the regimen) at times when imipenem/cilastatin was not being given. The average time of onset of seizures for patients receiving imipenem/cilastatin was seven days after start of therapy. As with other beta-lactam antibiotics, central nervous system lesions and disorders including seizures and renal insufficiency were found to be strong risk factors for seizures. Imipenem/cilastatin dosages in excess of those currently recommended by the manufacturer, particularly in patients with renal insufficiency, were also associated with an increased risk of seizures. There was an association with Pseudomonas aeruginosa infection that remained statistically significant even after controlling for imipenem/cilastatin dosage as well as for the other factors indicated. A high background incidence of seizures in general in a group of severely ill patients makes it both difficult to assess the etiology of a seizure and important to consider the risk factors when choosing the appropriate dose of an antibiotic. Guidelines are presented for appropriate dosing of imipenem/cilastatin in relation to renal function, body weight, and infecting pathogen.

Anti-Bacterial Agents↗
PubMed1988

Cephalosporin-induced alterations in erythroid (CFU-E) and granulocyte-macrophage (CFU-GM) colony-forming capacity in canine bone marrow.

Cephalosporins are among the safest antibiotics. Nevertheless, hematologic abnormalities ranging from mono- to pancytopenia do occur, albeit infrequently, following their therapeutic use. Similar abnormalities to those reported in people have been seen in dogs given high doses of cephalosporins. As part of a study to define the latter thoroughly, we explored the effects of long-term, high-dose cephalosporin administration on canine marrow erythroid (CFU-E) and granulocyte-macrophage (CFU-GM) progenitor cells. Cefazedone (Refosporen, E. Merck, Darmstadt) was administered intravenously at doses of 540 to 840 mg/kg daily to 14 healthy beagle dogs for up to 4 months, or less if hematologic effects were evident earlier. Within 6 to 10 weeks, treated dogs developed pancytopenia (5/14), thrombocytopenia (11/14), moderate to severe neutropenia (8/14), and/or normocytic anemia (8/14). There was evidence of immune-mediated destruction of peripheral blood cells. All treated dogs exhibited a significant reduction in marrow colony-forming capacity, irrespective of whether peripheral cytopenia was present, with 12/14 showing decreased CFU-GM and 14/14 decreased CFU-E activity. Within a week following cessation of dosing, all affected dogs achieved hematologic remission as defined by restoration of the peripheral blood counts. However, despite this apparent recovery, both CFU-E and CFU-GM activities of the bone marrow remained depressed for at least another 8 months. We conclude that in dogs prolonged administration of high doses of cefazedone induced a persistent deficit of CFU-E and CFU-GM progenitor cells. The clinical relevance of this, if any, remains to be established.

Animals↗
PubMed1988

Haematogenous dissemination of cells from human renal adenocarcinomas.

Estimates were made of the rates at which cancer cells were released directly into the renal vein in patients undergoing radical nephrectomy for primary renal cancer. Cancer cells were counted in blood samples taken from the renal vein using a density gradient centrifugation procedure, and identified using immunocytochemical techniques, on the basis of their cytoskeletal intermediate filament proteins. Cancer cells were released as single cells and multicell emboli in 8/10 patients, in numbers varying widely between 14-7509 emboli ml-1 of blood. Despite a calculated median input into the metastatic process of 3.7 x 10(7) cancer cells per day for at least 180 days, only 3/10 patients had extraperitoneal metastases prior to surgery and only 1 of the remaining disease-free patients subsequently developed distant metastases over a maximum 35 month period. These results are discussed in terms of primary tumour kinetics and metastatic inefficiency.

Adenocarcinoma↗
PubMed1988

Interactions of cancer cells with the microvasculature during metastasis.

Metastasis of cancer via the bloodstream is a major factor in the diagnosis, treatment, and prognosis of patients with cancer. Key events in hematogenous metastasis occur in the microvasculature. This is a brief, selective review of some interactions involving cancer cells and the microvasculature in pathological sequence, specifically: 1) intravasation of cancer cells; 2) the arrest of circulating cancer in the microvasculature; 3) cancer cell trauma associated with arrest; 4) microvascular trauma; 5) the inflammatory and 6) coagulative responses associated with arrest; and 7) the fate of arrested cancer cells. The evidence shows that in addition to providing routes for cancer cell dissemination and arrest sites for cancer cell emboli, the microvasculature, through a series of complex interactions with cancer cells, controls the efficiency of and acts as a rate regulator for the metastatic process.

Blood Coagulation↗