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L Weiss

Publications and source records attributed to L Weiss.

At least 325 records · Page 18Linked to original sources
PubMed1987

The human inactivated X chromosome folds in early metaphase, prometaphase, and prophase.

The inactivated X chromosome has a site of unusually frequent folding in region Xq1, whereas a fold in Xq1 is uncommon on the active X. We investigated the pattern of X chromosome folding in high-resolution GTG- and RBG-stained preparations from four women. In early metaphase cells, slightly more than 50% of late-replicating Xs folded at Xq1----Xq21, compared with about 6% of early replicating Xs. The late-replicating X folded in about 80% of prometaphase cells; the early, in only about 14% of these cells. and the late-replicating X folded in 19 of 20 prophase cells. Occasionally, one X had an omega-shaped loop or apparent physical connection between Xq13 and Xq21.1. It is possible that a segment of Xq1 never completely uncoils and may help to provide continuity for the Barr body from one interphase to the next.

Chromosome Banding↗
PubMed1987

Diminished blood selenium levels in renal failure patients on dialysis: correlations with nutritional status.

Selenium deficiency has been implicated as contributing to the development of cardiovascular disease, skeletal muscle myopathy, anemia, increased cancer risk, and deranged immune function. Since these problems may also be associated with renal failure, and the kidney plays an important role in selenium homeostasis, we measured selenium and compared it with nutritional status in 24 stable hemodialysis patients, 12 chronic intermittent peritoneal dialysis patients, and 29 healthy controls. Whole blood and plasma selenium was determined by a spectrofluorometric method. For whole blood the mean (+/- SD) selenium levels were 0.11 +/- 0.02 micrograms/ml in controls vs. 0.071 +/- 0.01 micrograms/ml in hemodialysis cases and 0.052 +/- 0.006 micrograms/ml in peritoneal dialysis (p less than 0.005). Significant decreases were seen also for plasma and red blood cell selenium in all groups respectively. Pre- and postdialysis plasma and whole blood selenium levels showed no significant changes in both dialysis groups. However, predialysis residual peritoneal fluid did contain selenium (0.029 +/- 0.005 micrograms/ml). Some evidence of protein-energy undernutrition was noted in both dialysis groups compared with controls. However, no significant differences in nutritional parameters were noted between hemodialysis and peritoneal dialysis patients. When all groups were combined, significant correlations were found between whole blood selenium and serum albumin (r = 0.61; p less than 0.001), triceps skin fold in females (r = 0.62; p less than 0.001), and midarm muscle circumference in males (r = 0.71; p less than 0.001). We conclude that low blood selenium is present in renal failure patients undergoing hemodialysis. This abnormality is even greater in peritoneal dialysis cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Blood-to-tissue transport of albumin in rat fibrosarcomas at two different implantation sites.

Albumin clearance and blood flow were measured in normal tissues and in fibrosarcomas by means of a multiple tracer method in intact male rats. Sarcomas implanted in testes had higher albumin clearances than the same tumours implanted in skeletal muscle, 59 and 26 microliters min-1 per 100 g, respectively. Albumin extraction (defined as the ratio of albumin clearance to plasma flow) was found to be 1 x 10(-4) - 14 x 10(-4) in normal tissues. Fibrosarcomas in muscle showed high extractions (24 x 10(-4)), especially in the central portions (96 x 10(-4)), where the extraction was similar to that in tumours implanted in the testes (111 x 10(-4)). The high albumin extraction in poorly perfused central parts of the muscle-implanted tumours and in the similarly insufficiently perfused testicular sarcomas is probably due to an increased endothelial permeability of the exchange vessels and not to an increased capillary exchange surface area compared with the better-perfused peripheral parts of the muscle-implanted tumours. The latter tissue also had a high albumin clearance, however, in the range of that of maximally dilated skeletal muscle vasculature, possibly reflecting a large functional capillary surface area.

Albumins↗
PubMed1987

The hemodynamic destruction of circulating cancer cells.

The blood-stream is the major disseminative route for metastasizing cancer cells, and metastases are generated when the cancer "microemboli" are trapped in the microcirculation. However, most circulating cancer cells are rapidly destroyed shortly before and/or after arrest. Traditionally, destruction is attributed to the cellular or humoral response of the host defense systems. A novel, non-exclusive mechanism for cancer cell destruction has been proposed by Weiss and Dimitrov in which friction or adhesion between circulating cancer cells and capillary walls causes local vascular blockage, and the blood-pressure differentials normally existing over the entire length of a capillary are consequently applied over the length of the cancer cell. In a simple model, this pressure differential is expected to cause expansion of the cancer cell membrane, resulting in increases in tension above a critical level, with consequent membrane rupture and cell death. In vivo and in vitro experimental tests of this hypothesis are outlined.

Animals↗
PubMed1987

Suppressor T cells in allogeneic bone marrow chimeras.

Immunosuppression is believed to play a role in the maintenance of stable bone marrow (BM) chimeras. This study investigates the nature and specificity of the suppression that lymphocytes from allogeneic BM chimeras exert upon the alloreactivity of donor and recipient lymphocytes. Lethally irradiated CBA/J (H-2k) mice were infused with 10(7) unseparated (WBM) or T cell-depleted BM (TDBM) cells of B10.BR mice (H-2k, disparate at minor histocompatibility antigens). Mixtures consisting of spleen cells (SC) from BM chimeras and SC from either normal donor, recipient, or third party (C3H, H-2k) mice, were sensitized with irradiated BALB/c (H-2d) leukocytes, then assayed for proliferative and anti-H-2d cytotoxic activity and compared with those of appropriate control cultures. The alloreactivity of all three types of normal SC was non-specifically suppressed by SC from both WBM and TDBM chimeras taken 2 weeks post-BM transplantation (BMT). In contrast, at 4 weeks post-BMT, SC from both chimeras suppressed the alloreactivity of recipient-type cells whereas only SC from WBM, but not from TDBM chimeras, suppressed normal donor-type response, and neither could suppress the response of normal third party cells. The suppression of donor-type alloreactivity diminished with time, while that exerted on recipient-type lasted for at least 10 weeks post-BMT. The suppression of donor alloreactivity was mediated by radioresistant Thy1.2+, Lyt1+2+ cells while that exerted upon recipient's alloreactivity was mediated by radiosensitive Thy1.2+, Lyt1+2- cells. Both types of suppressor cells were of donor origin. The potential biological role of the suppressive activity in the engraftment of allogeneic BM is discussed.

Animals↗
PubMed1987

Bone marrow transplantation with T-cell-depleted grafts. II. Reconstitution of immunohemopoietic functions in lethally irradiated mice transplanted with unseparated or T-cell-depleted bone marrow grafts disparate at minor histocompatibility antigens.

Graft-versus-host disease (GVHD), a serious complication of allogeneic bone marrow transplantation (BMT), can be prevented by in vitro depletion of T cells from the bone marrow (BM) prior to transplantation. The purpose of this study was to assess the role of BMT cells in the reconstitution of various immune functions following BMT across minor histocompatibility barriers. Lethally irradiated CBA/J (H-2k) mice were grafted with either 10(7) unseparated or T-cell-depleted BM cells from B10.BR (H-2k, minor-histoincompatible) mice. Blood counts, BM colonies in agar, and various immune functions of spleen cells from the recipient mice were tested 2-12 weeks post-BMT and compared with those of normal donors. The following observations were made: (A) Peripheral blood lymphocyte counts decreased to 30% of normal 2 weeks post-BMT with almost normal recovery at 8 weeks. (B) The percentage of Thy1.2+ splenocytes reached normal levels at 8 weeks post-BMT. (C) The number of BM colonies (GM-CFU) was reduced to 10% at 2 weeks and fully recovered at 12 weeks. (D) Proliferative response to the B-cell mitogen LPS was fully reconstituted after 4 weeks; however, anti-SRBC PFC (following Mishell-Dutton cultures) was restored 50% at 8-12 weeks. (E) Reconstitution of T cell functions including proliferative responses to concanavalin A, phytohemagglutinin, and allogeneic leukocytes, and allocytotoxicity, did not exceed 50% even 12 weeks post-BMT. Overall, depletion of T cells from donor BM allografts incompatible at minor histocompatibility loci, did not seem to significantly alter the rate of immunohematopoietic reconstitution in the lethally irradiated BM recipients.

Animals↗
PubMed1987

The effect of T lymphocyte depletion on susceptibility to influenza virus infection and development of anti-viral immunity in lethally irradiated mice reconstituted with syngeneic bone marrow grafts.

Lethally irradiated Balb/c mice reconstituted with syngeneic T cell-depleted or syngeneic untreated bone marrow (BM) were able to produce equal levels of hemagglutination inhibition (HI) antibodies at 4 weeks after bone marrow transplantation (BMT) in response to nasal infection with A/PR8 influenza virus given 1 week after BMT. Likewise, no differences in mortality rates could be observed following influenza virus infection 1 day after BMT. Antibody production was detected in 10-20% of BMT recipients. All animals responded to a secondary infection given 2 months later by production of secondary IgG-type HI antibodies. Mice reconstituted with BM enriched with spleen cells obtained from immune donors showed an improved survival rate as compared with recipients of naïve BM, immune BM or T-depleted BM obtained from immune mice. Our results indicate that T cell depletion by itself does not increase susceptibility of syngeneic BMT recipients to virus infection. However, immune spleen cells may play a significant role in conveying protection against influenza virus infections. Although recipients of both immune and naïve intact BM may mount better anti-influenza titers as compared with T-lymphocyte-depleted BMT recipients, it appears that the proportion of immune donor T cells in the marrow inoculum is insufficient for protection against influenza virus infection. Generation of memory cells to influenza viral antigens in the post-BMT period is not impaired in recipients of T-depleted marrow grafts, suggesting that memory cell precursors are unaffected by the T cell depletion procedure, or else that they were regenerated during the immediate post-BMT period from Thy 1.2-negative precursors.

Animals↗
PubMed1987

[Hyperthyroidism].

Explore the source record for details and available documents.

Graves Disease↗
PubMed1987

Megakaryocytopoiesis: incorporation of tritiated thymidine by small acetylcholinesterase-positive cells in murine bone marrow during antibody-induced thrombocytopenia.

The ability of small acetylcholinesterase-positive (SACHE) cells to incorporate tritiated thymidine (3H-TdR) was studied in the bone marrow of mice made acutely thrombocytopenic by injection of guinea pig antimouse platelet serum (APS) and in control mice injected with normal guinea pig serum (NS). 3H-TdR was administered in vivo, and bone marrow was collected at various time points thereafter. The initial labeling index (LI) for both groups was about 30%. After four hours, the LI increased and reached peak values at 48 hours, but was lower in thrombocytopenic animals. The lower peak LI in APS-treated animals may be the result of both a faster rate of influx of unlabeled cells into the acetylcholinesterase (AChE) positive cell compartment and efflux of more heavily labeled, and probably polyploid, SACHE cells into the compartment of recognizable megakaryocytes. In both groups the increasing LI occurred concomitantly with a decreasing mean grain count. This may indicate cellular division by some fraction of SACHE cells. Heterogeneity in nuclear morphology was also demonstrated, and the frequency of individual morphologies was altered in APS-treated animals. In addition, cells that incorporated 3H-TdR were larger than those that did not. This group of small cells appears to represent a pivotal point in megakaryocytopoiesis in which the switch from mitosis to endomitosis is occurring.

Acetylcholinesterase↗
PubMed1987

The liver in acquired immune deficiency syndrome: emphasis on patients with intravenous drug abuse.

To assess the spectrum of hepatic abnormalities in acquired immune deficiency syndrome (AIDS), we reviewed clinical, biochemical, and pathological material in 32 patients with AIDS. Eight-four percent of AIDS cases had a history of intravenous drug abuse. Ninety percent of AIDS patients has some liver biochemical abnormality at the first presentation of illness. During the course of AIDS, significant (p less than 0.05, paired Student's t test) rises in alkaline phosphatase and bilirubin occurred, without rises in aminotransferases. Mean abnormalities were mild, reflecting approximately 2-fold increases over baseline. Liver failure was not believed to contribute to the death of any AIDS patient. Pathological findings in AIDS included specific infectious diagnosis in 26%, granulomas in 16%, hemosiderosis in 26%, nonspecific abnormalities in 39%, cirrhosis in 23%, and chronic active hepatitis in 3%. AIDS cases were also compared to 10 selected age, sex, and epidemiologically similar non-AIDS patients. Although granulomas or infections were not seen in our comparison group, only the incidence of chronic active hepatitis was significantly different between the groups. If only those with intravenous drug abuse were studied, then none of 24 AIDS patients versus four of eight non-AIDS cases (p less than 0.005) had chronic active hepatitis. AIDS patients with specific hepatic infections tended to have a higher alkaline phosphatase and aspartate aminotransferase (p less than 0.05) than noninfected cases. However, substantial overlap existed, and no difference in hepatomegaly was noted. Ninety percent of AIDS patients were ingesting at least one potentially hepatotoxic drug. We conclude that AIDS patients have a high incidence of underlying hepatic abnormalities. However, clinical and biochemical abnormalities are similar in our selected liver biopsy patients with intravenous drug abuse with or without AIDS. As expected, AIDS patients have a higher incidence of hepatic granulomas and infections, but these patients were not clearly distinguishable from other AIDS cases. Histological examination showed a wide array of changes by light microscopy, but no specific lesion of AIDS was noted. The low incidence of chronic active hepatitis in this AIDS population may imply that the altered T lymphocyte function in AIDS could influence the course of liver disease in these patients.

Acquired Immunodeficiency Syndrome↗
PubMed1986

The stability of kidney-induced selection of Lewis lung tumor cell populations, and their metastasis-related behavior.

The surface charge densities of Lewis lung carcinoma (3LL) cells were measured in tumors transplanted into subcutaneous (s.c.) sites, and into the kidneys (K), as well as in kidney tumors transplanted to, and maintained in, the s.c. site (K.s.c.). K cells showed a significant increase in net negativity in comparison with s.c. cells, which was stable over II passages. On back-transplantation of K cells to the s.c. site, the net negativity of K.s.c. cells was higher than that of the s.c. cells, but the increase was stable for only 7 passages; on subsequent passages the net negativity fell, approaching that of the s.c. cells. Detailed analyses suggest the presence in these tumors of 2 subpopulations of 3LL cells, whose proportions change in the different sites studied to produce changes in the mean electrophoretic mobilities of the whole cancer cell populations. The altered proportions of the 2 cell types in the 3 sites were not associated with major changes either in their general behavior with respect to metastasis, or in differential growth in various organs following s.c., tail vein, and left ventricular injections. Selection induced by growth in the kidney, as evidenced by physiochemical changes at the cancer cell surface, was not associated with kidney preference in metastasis or metastasis-related behavior.

Animals↗
PubMed1986

Mechanical aspects of the lungs as cancer cell-killing organs during hematogenous metastasis.

A substantial proportion of many different types of circulating cancer cells appear to be killed during their interactions with the pulmonary microcirculation. Different tensions exist during respiration within alveolar units, and hence the pulmonary capillaries. We have calculated the effects of these tensions on the entry and subsequent fate of circulating cancer cells. Our calculations indicate that during expiration, when tension in the capillary walls is low, cancer cells can enter and travel along the capillaries without damage, because the vessels are deformed by the cells and the hydrodynamic field surrounding them. During normal inspiration when the alveoli are stretched, the increased tension within the capillary walls serves to compress the contained cancer cells. This compression, together with previously calculated blood pressure differentials between the ends of the cells, is thought in some cases, to increase their membrane tensions above the critical level for rupture, resulting in cytolysis, in accord with experimental observations. In deep inspiration, when a very substantial increase in capillary wall tension occurs, cancer cells already within the capillaries, entering them and in transit along them are expected to develop membrane tensions greatly exceeding the critical values for rupture. It is suggested that these respiration-induced effects may act as an important rate-regulating step in the metastatic process, where the development of pulmonary metastases plays a central role. Furthermore, induced deep inspiration may conceivably be utilized in the inhibition of pulmonary metastasis.

Animals↗
PubMed1986

The management of extranodal head and neck lymphomas.

The results from 156 patients with extranodal head and neck lymphomas treated at Stanford (Calif) University School of Medicine are combined with the experience of other investigators to recommend the management of these lymphomas. The tonsil and sinuses were the most common sites of presentation, and the most common histology was diffuse histiocytic lymphoma. The histologic classification systems are described as well as the use of immunohistochemistry in diagnosis. The appropriate staging procedures and the Ann Arbor staging system are discussed. Following the staging of 948 patients, 66% were found to have stage I or stage II disease and 34% had more widespread disease. Treatment with radiotherapy is discussed. Patterns of relapse following local radiotherapy for 360 relapsing patients with stage I and II disease showed a 73% distal relapse rate. Various treatment programs are recommended based on site, stage, and histology.

Combined Modality Therapy↗
PubMed1986

Mechanisms of splenic control of murine malaria: reticular cell activation and the development of a blood-spleen barrier.

By complex stromal responses, the spleen controls the course of nonlethal Plasmodium yoelii murine malaria. The course of disease may be divided into four phases. In the immediate postinfective phase, lasting several days, the filtration beds of the spleen are open. Parasitized and nonparasitized erythrocytes, many plasma cells, lymphocytes, and macrophages are sequestered from the blood; and most or all of the parasitized erythrocytes are phagocytized. In the following precrisis phase, approximately 1 week long, there is increasing parasitemia and anemia. The filtration beds of the spleen support large-scale erythropoiesis, lymphopoiesis, plasmacytopoiesis, and monocyte-to-macrophage differentiation. Reticular cells, the stromal cells which form the splenic filtration beds, become activated, showing signs of intense protein secretion and increased branching and mitosis. The locules of the filtration beds appear sealed off from the blood by branches of activated reticular cells. A blood-spleen barrier is thereby formed, protecting splenic hematopoiesis from the parasite. Factors are produced, moreover, which damage intraerythrocytic parasites, producing crisis forms. Crisis follows. It may occur over several days, presaged by the appearance of circulating crisis forms. The filtration beds are opened to the blood. Circulating crisis forms are trapped within the locules of the filtration beds and phagocytized while the stores of reticulocytes produced there in the precrisis period are released to the blood. The malaria, as a result, is no longer patent and the anemia is relieved. In the fourth or postcrisis phase, lasting many months, the normal structure of the spleen is approached. We postulate that reticular cells, normal and activated, have the following functions: to fabricate the locules of the filtration beds; to control the migration of free cells through these beds; to trap free cells, including parasitized erythrocytes, by cell-surface adherence; to open or close the filtration locules, creating a dynamic blood-spleen barrier; to control the circulation of the spleen--by contraction and alignment in normal spleens and by activation and closing of locules in enlarged spleens; to synthesize collagen III; to synthesize factors which influence marrow release of monocytes; and to secrete antiplasmodial substances.

Animals↗