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Biomedical subjects

W Hsueh

Publications and source records attributed to W Hsueh.

At least 109 records · Page 6Linked to original sources
PubMed1983

Experimental model of ischemic bowel necrosis. The role of platelet-activating factor and endotoxin.

This report deals with the experimental production of ischemic bowel necrosis in rats by the administration of combined bacterial lipopolysaccharide (LPS) and platelet-activating factor (PAF). Neither LPS alone, nor PAF at a low dose, caused ischemic intestinal necrosis when administered intraaortically. With these two compounds in combination, necrotizing lesions of the gastrointestinal tract developed consistently. The lesions showed marked morphologic similarity to human necrotizing enterocolitis (NEC). There were no thrombi in mesenteric arteries or necrotic lesions in other organs to which these bioactive compounds were delivered. These findings suggest a possible synergistic involvement of PAF and LPS in the pathogenesis of NEC and other forms of ischemic bowel necrosis. The authors further suggest that the pathogenesis of experimental NEC in rats is independent of platelet aggregation.

Animals↗
PubMed1982

Infantile sarcoma with intracytoplasmic filamentous inclusions: distinctive tumor of possible histiocytic origin.

This report describes four malignant tumors originating in infants, (one present at birth), for which a common origin is proposed. The common nature of these tumors was suggested by a remarkable similarity of histologic and ultrastructural features, including the presence of intracellular filamentous aggregates, as well as a shared aggressive clinical course consistent with sarcomatous origin. Two of these neoplasms arose within the kidney and were classified as "rhabdoid" sarcomas, according to the NWTS nomenclature. However, cells from these neoplasms could not be identified as muscular in origin. In culture, these cells demonstrated adherence to substratum, ability to phagocytose particles, and cell surface complement receptors. In addition, the renal tumors contained definite tumor cells positive for muramidase; the liver primary tumor contained only a limited number of such cells, which could not be interpreted as neoplastic. These findings suggest that among the "round-cell sarcomas" of infants and young children, a distinct, highly malignant form may be identified on clinical and morphologic grounds. The possibility that the tumor cells may be linked to the mononuclear phagocyte system was suggested, but not proved, and deserves further study.

Female↗
PubMed1982

Decreased phospholipase A2 activity and prostaglandin biosynthesis in Bacillus Calmette-Guérin-activated alveolar macrophages.

Alveolar macrophages from normal and BCG-infected rabbits were labelled with [14C]arachidonate and its metabolites were measured. It was found that production of both prostaglandins and 12-hydroxyeicosatetraenoic acid was diminished markedly in BCG-primed macrophages. This decrease was due partly to a depression in cyclooxygenase and lipoxygenase activity, but mainly to a decrease in arachidonic acid release, probably due to a suppression in phospholipase A2 activity. This is indicated by a consistent depression of this enzyme activity in BCG macrophage homogenates at a wide pH range, suggesting that both lysosomal an non-lysosomal phospholipases are suppressed in BCG macrophages. However, intracellular lysosomal acid phosphatase and its release were increased markedly in BCG-primed macrophages. Our previous studies have shown a close relationship between lysosomal acid hydrolase release and production of arachidonate-prostaglandins in normal macrophages. The present study shows that in activated macrophages primed by BCG, different mechanisms are operative in the control of synthesis and release of lysosomal acid hydrolases and of the phospholipase for prostaglandin production.

Animals↗
PubMed1981

Wilms' tumor: its morphology in patients under one year of age.

Of 24 patients aged 1 year or younger, and having conditions diagnosed as Wilms' tumor, only 11 had typical, solid neoplasms with the triphasic histologic composition of blastema cells, epithelial cells, and stromal derivatives. Two of these were bilateral. The remaining 13 cases were distributed among different morphologic categories for which special status has been claimed in recent reports. Chief among these is the rhabdomyomatous form of Wilms' tumor, which accounted for six cases in the present series, three of them bilateral. Two additional cases corresponded to cystic, partly differentiated nephroblastoma (cystic nephroma), and two others to renal sarcomas whose precise relationship with Wilms' tumor is currently a matter of conjecture. No case of typical Wilms' tumor was seen in patients under 6 months of age, but a congenital origin seems certain for the two sarcomas of this series. The cystic form of nephroblastoma accounted for the only other case involving a patient 3 months old or younger.

Humans↗
PubMed1981

Two phospholipase pools for prostaglandin synthesis in macrophages.

Macrophages in culture produce prostaglandins in response to a variety of phagocytic and non-phagocytic stimuli. As prostaglandins are not stored in cells, and mammalian cells contain very little free arachidonic acid, synthesis and release of prostaglandins depends on the release of the precursor, arachidonic acid, from cell lipids. Many agents that stimulate cell prostaglandin production act by releasing arachidonic acid, presumably by activating phospholipase A2 (refs 10, 11) or phospholipase C (refs 12, 13), depending on the cell system used. We have shown previously that rabbit alveolar macrophages secrete arachidonic acid as well as prostaglandins in response to phagocytic stimuli. This secretion depends not on particle attachment, but rather on interiorization of the particles. Furthermore, the time course of prostaglandin and arachidonic acid secretion does not parallel that of particle engulfment per se, but of the release of lysosomal enzymes, indicating that the release of arachidonate and prostaglandin is associated with the latter. We now describe experiments which suggest that these are two independent pools of phospholipases in macrophages, one in the lysosomes and one elsewhere.

Animals↗
PubMed1981

Subepidermal bullous disease and glomerulonephritis in a child.

The infant described in this report had been generalized, subepidermal bullous eruption and concurrent glomerulonephritis. Immunofluorescence studies demonstrating deposition of immunoglobulin and complement in the skin and kidney suggest a common pathogenesis for the two disorders. The elevation of this infant's serum immunoglobulins and depression of serum complement support an immunologic process as the likely mechanism. It is important for clinicians caring for children with bullous skin diseases to search for evidence of renal disease and complement abnormalities.

Abnormalities, Multiple↗
PubMed1981

Prostaglandins in histiocytosis-X. PG synthesis by histiocytosis-X cells.

Histiocytosis-X cells were obtained at autopsy from the lungs and lymph nodes of a patient who died of the disseminated infantile form of this disease (Letterer-Siwe disease). The ability of these cells to synthesize and release prostaglandins was investigated in culture, by prelabeling the cell lipids with [14C] arachidonic acid and measuring the subsequent release of radioactive metabolites. The cells were seen to release primarily PGD2 and thromboxane. Correlative morphologic studies ensured the purity of the cell preparations, ruling out extraneous origin of the prostaglandins from sources other than the lesional histiocytes. Electron-microscopic study confirmed that the same cells that release prostaglandins and are capable of engulfing particles also bear the Langerhans' inclusions considered to be cell markers of histiocytosis-X. The prostaglandin production profile of alveolar macrophages from an infant who died as a result of congestive heart failure, but without histiocytosis, was studied for comparison. These cells produced PGE2 and thromboxane, but not PGD2. The theoretical implications of these findings are discussed.

Arachidonic Acids↗
PubMed1981

Rhabdomyogenesis in renal neoplasia of childhood.

Of 220 consecutive primary renal tumors of childhood, 17 contained substantial amounts of histologically identifiable striated muscle cells (over 10% of sampled tumor parenchyma). These tumors could be further subclassified into two groups: Wilms' tumors with "massive" rhabdomyogenesis (one-third or more of the tumor parenchyma composed of muscle), and Wilms' tumors with "moderate" rhabdomyogenesis (10-30% muscle composition. The former tumors were invariably seen in young children, under 4 years of age; often the patients were infants 1 year of age, or younger, and more than half of the patients in this group had bilateral tumors. Bilaterality was not seen in patients harboring tumors with "moderate" rhabdomyogenesis, whom in addition, were older children. In both groups, there was a tendency for polypoid intrapelvic growth. All but one of the tumors described in this report were classified as Wilms' tumor; the single exception was considered be be a primary rhabdomyosarcoma of the kidney. Patients with congenital malformations related to Wilms' tumor (one aniridia, one hemihypertrophy) were seen only in the group with"massive" rhabdomyogenesis. However, anatomical lesions consistent with neoplastic multifocal origin were present in both groups. Thus, our findings indicate a definite correlation between extensive rhabdomyogenesis and clinical behavior. This relation is expressed in patterns of age distribution, bilaterality and manner of growth, which are sufficiently consistent to individualize this histologic variant as a cytodifferentiated form of nephroblastoma.

Age Factors↗
PubMed1980

Prostaglandin synthesis in different phases of phagocytosis in lung macrophages.

Macrophages have a central role in bodily defence and inflammatory responses. Prostaglandins (PGs), mediators of inflammation, are secreted by macrophages during phagocytosis. PGE-like activity was first demonstrated in macrophage-rich peritoneal exudate cell preparations from guinea pigs; later, other kinds of PGs were also found to be released by mouse peritoneal macrophages in response to inflammatory stimuli. We have shown that rabbit alveolar macrophages also produce various PGs in response to phagocytic stimuli like zymosan and heat-killed bacteria; however, it was not known precisely which cellular event is associated with PG production. Traditionally, the phagocytic process is considered in three stages: (1) attachment of the particle to the cell membrane; (2) interiorisation (phagocytosis); and (3) fusion of the phagocytic vesicle with intracellular lysosomes (digestion). We show here that PG secretion in response to phagocytic stimuli by macrophages is independent of the first stage, but dependent on engulfment of the particle. Moreover, PG production does not appear to be associated with the process of engulfment per se, but with some event following internalisation.

Animals↗
PubMed1979

Relationship of prostaglandin secretion by rabbit alveolar macrophages to phagocytosis and lysosomal enzyme release.

The phospholipids of rabbit alveolar macrophages were pulse-labelled with [(14)C]-arachidonic acid, and the subsequent release of labelled prostaglandins was measured. Resting macrophages released measurable amounts of arachidonic acid, the prostaglandins E(2), D(2) and F(2alpha) and 6-oxoprostaglandin F(1alpha). Phagocytosis of zymosan increased the release of arachidonic acid and prostaglandins to 2.5 times the control value. In contrast, phagocytosis of inert latex particles had no effect on prostaglandin release. Indomethacin inhibited the release of prostaglandin, and, at high doses (20mug/ml), increased arachidonic acid release. Analysis of the cellular lipids showed that after zymosan stimulation the proportion of label was decreased in phosphatidylcholine, but not in other phospholipids or neutral lipids. Cytochalasin B, at a dose of 2mug/ml, inhibited the phagocytosis induced by zymosan but increased prostaglandin synthesis to 3.4 times the control. These data suggest that the stimulation of prostaglandin synthesis by zymosan is not dependent on phagocytosis. Exposure to zymosan also resulted in the release of the lysosomal enzyme, acid phosphatase. Furthermore, cytochalasin B augmented the zymosan-stimulated release of acid phosphatase at the same dose that stimulated prostaglandin synthesis. However, indomethacin, at a dose that completely inhibited prostaglandin synthesis, failed to block the lysosomal enzyme release. Thus despite some parallels between the release of prostaglandins and lysosomal enzymes, endogenous prostaglandins do not appear to mediate the release of lysosomal enzymes. The prostaglandins released from the macrophages may function as humoral substances affecting other cells.

Acid Phosphatase↗
PubMed1979

Prostaglandin biosynthesis in pulmonary macrophages.

Cultured rabbit alveolar macrophages, prelabeled with 14C-arachidonic acid (AA), released into the medium a trace amount of labeled prostaglandins (PG) as well as their precursor, AA. Phagocytosis of zymosan, heat-killed Staphylococcus, or bacille Calmette-Guérin (BCG) increased the AA and PG release to 2--2.5 times control values. The released PGs consisted of PGE2, D2, F2 alpha, and 6-keto F1 alpha. Phagocytosis of latex particles had no effect on PG release. Indomethacin inhibited release of PGs but did not affect AA release at low doses. Analysis of the cellular lipids showed that zymosan decreased the radioactive label in phosphatidylcholine (PC), but not in other phospholipids or neutral lipids, suggesting that PC is the main source of AA for PG synthesis in pulmonary macrophages. Cytochalasin B (CB) at phagocytosis-inhibiting doses or below, markedly increased PG synthesis by zymosan-treated macrophages. These data suggest that PG release is not dependent on engulfment of the particles. Phagocytosis of zymosan (but not latex) also resulted in the release of two lysosomal enzymes, acid phosphatase and beta-glucuronidase, which appeared temporally associated with the release of PGs (but not to phagocytosis). Furthermore, CB augmented the zymosan-stimulated release of these enzymes at the same doses stimulating PG synthesis. However, indomethacin, at a dose completely inhibiting PG synthesis, failed to block lysosomal enzyme release. Thus, the coincidental release of PGs and lysosomal enzymes is not the result of a regulatory role of PGs in the release of lysosomal enzymes, but probably is the result of a common pathway of stimulation. (Am J Pathol 97:137--148, 1979).

Animals↗
PubMed1978

Thyrotoxicosis in a patient with secondary hypothyroidism.

We have described a patient with panhypopituitarism who developed thyrotoxicosis. There is a widespread belief that pituitary thyrotropin (TSH) is not a pathogenetic factor in most patients with thyrotoxicosis. Due to technical reasons, however, it has been difficult to entirely exclude the role(s) of TSH in the development of thyrotoxicosis. In this report hyperthyroidism appeared in a patient with TSH deficiency proved by the lack of response to TRH administration. This is the first known case in which TRH stimulation demonstrated total abscence of TSH before the onset of thyrotoxicosis. We cannot exclude the possibility that factors of adenohypophyseal origin play some role in the pathogenesis of thyrotoxicosis, but TSH per se does not play a role in the development of Graves' thyrotoxicosis.

Humans↗
PubMed1977

Hormone selective lipase activation in the isolated rabbit heart.

The synthesis and release of PGs by the isolated perfused rabbit heart upon bradykinin stimulation results from lipase stimulation which liberates arachidonic acid for PG biosynthesis. The [14C]-labelled fatty acids, arachidonate, linoleate, and oleate, when infused into the heart preparation, were efficiently incorporated into the phospholipid pool in the heart mostly in the 2-position of phosphatidylcholine. On the other hand, [14C]-palmitate was esterified into both the 1- and the 2-position. Bradykinin released bioassayable PG when injected into the rabbit hearts, regardless of which fatty acid label was incorporated into the phospholipid pool. However, only [14C]-arachidonic acid (but not [14C]-linoleate, oleate or palmitate) was liberated from the variously labelled hearts upon hormone stimulation. This selective bradykinin effect on fatty acid release suggests that hormone stimulation either activates a specific lipase that distinguishes different fatty acids in the 2-position or activates lipase which is selectively compartmented with arachidonate-containing phospholipids. Ischemia, on the other hand, appeared to non-specifically stimulate tissue lipases, resulting in a non-selective release of oleic as well as arachidonic acid. A disproportionally large release of arachidonic acid was observed accompanying a relatively small PG (10:1 arachidonate: PG ratio) production during ischemia, as compared to bradykinin (3:1 ratio), suggesting distinct mechanisms for PG biosynthesis induced by bradykinin and ischemia.

Animals↗