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Biomedical subjects

W Jung

Publications and source records attributed to W Jung.

At least 235 records · Page 13Linked to original sources
PubMed1989

Expression of insulin-like growth factor-II mRNA in fetal kidney and Wilms' tumor. An in situ hybridization study.

The pattern of insulin-like growth factor II (IGF-II) mRNA expression in developing kidney and Wilms' tumor was examined with in situ hybridization. In developing kidney, IGF-II was primarily expressed in blastemal cells and lost with their differentiation. In triphasic Wilms' tumor, a similar relationship was found. But in a monomorphous Wilms', tumor cells with epithelial differentiation expressed IGF-II mRNA. These data suggest that IGF-II may be involved in fetal nephrogenesis, that its expression is inversely coupled to normal epithelial differentiation, and that this differentiation may be aberrantly regulated in Wilms' tumor.

Child, Preschool↗
PubMed1988

Synthetic smoke with acrolein but not HCl produces pulmonary edema.

The chemical toxins in smoke and not the heat are responsible for the pulmonary edema of smoke inhalation. We developed a synthetic smoke composed of carbon particles (mean diameter of 4.3 microns) to which toxins known to be in smoke, such as HCl or acrolein, could be added one at a time. We delivered synthetic smoke to dogs for 10 min and monitored extravascular lung water (EVLW) accumulation thereafter with a double-indicator thermodilution technique. Final EVLW correlated highly with gravimetric values (r = 0.93, P less than 0.01). HCl in concentrations of 0.1-6 N when added to heated carbon (120 degrees C) and cooled to 39 degrees C produced airway damage but no pulmonary edema. Acrolein, in contrast, produced airway damage but also pulmonary edema, whereas capillary wedge pressures remained stable. Low-dose acrolein smoke (less than 200 ppm) produced edema in two of five animals with a 2- to 4-h delay. Intermediate-dose acrolein smoke (200-300 ppm) always produced edema at an average of 147 +/- 57 min after smoke, whereas high-dose acrolein (greater than 300 ppm) produced edema at 65 +/- 16 min after smoke. Thus acrolein but not HCl, when presented as a synthetic smoke, produced a delayed-onset, noncardiogenic, and peribronchiolar edema in a roughly dose-dependent fashion.

Acrolein↗
PubMed1988

Purified monocyte-derived angiogenic substance (angiotropin) induces controlled angiogenesis associated with regulated tissue proliferation in rabbit skin.

Angiotropin is a differentiation factor for microvascular endothelial cells isolated from serum-free cultures of lectin-activated, porcine monocytes. We used an ear lobe model in rabbits, single intradermal injection of angiotropin to induce phenotypical changes of the endothelial cells in capillaries and postcapillary venules, vascular engorgement, and subsequent angiogenesis in dose-dependent manner. The vascular changes are associated with epidermal and stromal cell proliferation. Angiogenesis and tissue proliferation occur in the absence of tissue necrosis and do not lead to scar formation. Angiotropin-induced angiogenesis is not inhibited by local dexamethasone although it involves a defined turnover of inflammatory cells. Proliferation is transient and regressive events follow. The overall tissue reaction resembles changes found in the undamaged skin margin of a primary healing wound during the inflammatory/proliferative phase. From these observations we conclude that angiotropin is an important secretory product of activated peripheral macrophages that triggers inflammatory and proliferative reactions in wound healing by activating microvascular endothelial cells.

Angiogenesis Inducing Agents↗
PubMed1987

LTB4 mediated hypoxemia in guinea pigs: relationship to pulmonary and cardiovascular pathophysiology.

LTB4 is released in the presence of lung injury and may therefore play a role in the pathophysiology of the lung damage. We therefore, administered LTB4 as an I.V. bolus or as an aerosol to guinea pigs and assessed the physiologic response and the lung histology. After 2 ug of I.V. LTB4 airway pressure (AP) rose transiently by 5 +/- 1 mmHg and at five min was back to baseline while PaO2 fell from 96 +/- 5 mmHg to 78 +/- 3 mmHg and remained low at least 45 min. Static compliance (Cstat) was unchanged. Right ventricular systolic pressure (RVSP) and mean aortic pressure (MAP) rose from 9 +/- 1 to 16 +/- 1 mmHg and 43 +/- 4 to 62 +/- 5 mmHg respectively while cardiac index (C.I.) fell from 266 to 208 ml/kg/min but all values were baseline again by 10 min. Aerosolized LTB4 raised AP by 4.6 +/- 0.2 mmHg while PaO2 fell from 90 +/- 7 to 52 +/- 5 mmHg. AP recovered by 20 min but PaO2 remained low at least for 1 hour. MAP, RVSP and CI and Cstat were unaffected. Both I.V. and inhaled LTB4 increased neutrophil infiltrate in the lung although the water aerosol control did too, preventing us from showing a significant effect with LTB4 aerosol. Indomethacin blocked the airway effects and the hypoxemia after I.V. or aerosolized LTB4 but not the neutrophil infiltrate or the rise in RVSP. It actually enhanced (p less than .05) the rise in MAP after I.V. LTB4. Thus cyclooxygenase released products likely mediated the rise in airway pressure and the prolonged fall in PaO2 after LTB4 in guinea pigs but not the pulmonary and systemic vasoconstriction.

Administration, Inhalation↗
PubMed1986

Ibuprofen prevents synthetic smoke-induced pulmonary edema.

Multiple potentially injurious agents are present in smoke but the importance of each of these agents in producing lung injury as well as the mechanisms by which the lung injury is produced are unknown. In order to study smoke inhalation injury, we developed a synthetic smoke composed of a carrier of hot carbon particles of known size to which a single known common toxic agent in smoke, in this case HCI, could be added. We then exposed rats to the smoke, assayed their blood for the metabolites of thromboxane and prostacyclin, and intervened shortly after smoke with the cyclooxygenase inhibitors indomethacin or ibuprofen to see if the resulting lung injury could be prevented. Smoke exposure produced mild pulmonary edema after 6 h with a wet-to-dry weight ratio of 5.6 +/- 0.2 SEM (n = 11) compared with the non-smoke-exposed control animals with a wet-to-dry weight ratio of 4.3 +/- 0.2 (n = 12), p less than 0.001. Thromboxane B, and 6-keto-prostaglandin F1 alpha rose to 1,660 +/- 250 pg/ml (p less than 0.01) and to 600 +/- 100 pg/ml (p greater than 0.1), respectively, in the smoke-injured animals compared with 770 +/- 150 pg/ml and 400 +/- 100 pg/ml in the non-smoke-exposed control animals. Indomethacin (n = 11) blocked the increase in both thromboxane and prostacyclin metabolites but failed to prevent lung edema.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Effects of Acipimox on plasma lipids and biliary lipids in healthy subjects.

The effects of Acipimox (5-methylpyracine-2-carboxylic acid-4-oxide, 3 X 250 mg/day) on plasma lipids, lipoproteins, and biliary lipids were studied in 14 healthy male volunteers using a double blind cross-over design. There was a significant (P less than 0.05) rise of HDL-cholesterol by 9.8%, while effects on other lipids and lipoproteins were small and insignificant (total cholesterol minus 6.5%, LDL-cholesterol minus 11.8%, free cholesterol minus 4.2%, total triglycerides plus 13.5% and phospholipids plus 3.9%). There was a significant rise of the HDL-cholesterol/LDL-cholesterol ratio by 23.6% (P less than 0.02) and of the HDL-cholesterol/total cholesterol ratio by 16% (P less than 0.05). Apolipoproteins AI, AII, and B were not significantly affected. The ratio of HDL-cholesterol/Apo AI increased significantly (P less than 0.05), and the ratio of HDL-cholesterol/Apo AII rose from 1.22 to 1.32 (P less than 0.05), while the ratio LDL-cholesterol/Apo B fell from 1.96 to 1.73. The composition of HDL and LDL, therefore, must have been altered by Acipimox. The relative cholesterol concentration in bile was significantly (P less than 0.05) increased by treatment with Acipimox, while bile acids and phospholipids were not significantly affected. The lithogenic index rose significantly by 15.1% (P less than 0.02) as calculated according to Admirand and Small, while calculations according to Hegard and Dam yielded a slight insignificant rise (P less than 0.1). The findings suggest that treatment with Acipimox might be associated with an increased risk of cholelithiasis. However, only long-term epidemiologic studies can ultimately demonstrate whether or not Acipimox increases the risk of gallstone formation.

Adult↗
PubMed1985

Primary culture of rat hepatocytes as a model system of canalicular development, biliary secretion, and intrahepatic cholestasis. V. Disturbance of the cellular membrane and bile canalicular ultrastructure induced by chlorpromazine.

In the present paper rat hepatocytes in primary monolayer culture were used to investigate the adverse effects of chlorpromazine (CPZ) at the cellular level. As revealed by thin sectioning many of the ultrastructural alterations were comparable to those described for the isolated perfused rat liver under the influence of CPZ. Alterations comprised short-term effects, such as dilation of the rough endoplasmic reticulum and the nuclear envelope, and long-term effects including huge accumulations of myeloid bodies within the cytoplasm as well as dilation and diverticulation of bile canaliculi. Freeze-fracturing revealed the dislocation of intramembrane particles in the sinusoidal plasma membrane which could be detected as early as 30 min after exposure to CPZ. As judged from filipin cytochemistry, alterations in the cholesterol content seems to play a minor role in the process of membrane damage except at the sinusoidal surface where a reduction of cholesterol content may contribute to the impairment of membrane functions. It is concluded that CPZ exerts its cholestatic effect primarily by a rapid disturbance of the membrane architecture of the sinusoidal surface and secondarily by other interactions with the bile secretory apparatus.

Animals↗
PubMed1985

Uptake of 59Fe and 239Pu by rat liver cells and human hepatoma cells.

The accumulation of 59Fe and 239Pu was studied in rat hepatocytes in primary culture and in human hepatoma cells (Hep-G2 cells) and was compared with the uptake in isolated perfused rat liver and in rat liver in vivo. With respect to iron uptake from citrate both cell types react similarly: time and concentration dependence as well as the influence of temperature point to a non-specific but energy-dependent uptake mechanism. Pu shows similar behaviour except that a relatively large fraction remains bound to the cell membrane and uptake is lower. This is much more pronounced in Hep-G2 cells than in hepatocytes. If the metals are bound to transferrin, uptake into both cell lines, as well as into isolated perfused rat liver, is very low. After intravenous injection of 239Pu-citrate, accumulation in the rat liver is very rapid during the first 10 min and much slower after that. The role of citrate in metal uptake is discussed.

Animals↗
PubMed1985

Studies on human scar tissue proteoglycans.

The proteoglycans (PGs) in pooled normal scars and pooled hypertrophic scars were extracted with 4 M guanidinium chloride and isolated by DEAE-cellulose chromatography. The PG samples were then fractionated further by dissociative CsCl density gradient sedimentation. Following cleavage of the density gradient PG fractions with alkaline NaB3H4, the glycosaminoglycan (GAG) constituents were isolated and analyzed by quantitative cellulose acetate electrophoresis. In addition, single samples of normal skin and a keloid scar were also analyzed. The results showed that the hypertrophic scars had a higher average content of extractable and also residual PGs than did the normal scars but a wide range of values was obtained for each type of scar. Some differences were noted in the amounts and distribution of the GAGs in CsCl gradient fractions, in the different types of scar tissue. The PGs in tissues were distributed in low-, medium-, and high density fractions and are, therefore, heterogeneous. Dermatan sulfate (DS) was the major GAG in each tissue and smaller quantities of chondroitin sulfate (CS), heparan sulfate (HS), and heparin (HP) were also present. In addition, 2 other GAG constituents were also detected. Based on the susceptibility of these GAGs to enzymes and nitrous acid treatments, one was a HS or HP while the second was a DS. The major differences in the PG composition of the scar tissues were the higher proportions of low-density CS-PGs in the keloid scar and of low density DS-PGs in hypertrophic and keloid scars.

Chromatography, DEAE-Cellulose↗
PubMed1983

Compartment analysis of the potassium fluxes in the cochlea.

The results obtained from tracer kinetics, measured by Konishi et al. (1978) and June (1979), are combined to construct a two-compartment model of the guinea-pig cochlea. The potassium fluxes are calculated using a mathematical two-compartment theory. For the basal turn, one finds a circulating flux between the endolymphatic and perilymphatic spaces of 190 pMol/min and 1 mm cochlea, whereas a minor value of 100 pmol/min/mm is calculated for the flux from the perilymphatic scales out of the cochlea.

Animals↗
PubMed1983

The orally active thia-imino-prostacyclin Hoe 892: antiaggregatory and cardiovascular activities.

The short chemical half-life limits the potential therapeutic value of Prostacyclin (PGI2). Replacement of the acid-labile enolether structure of PGI2 by a beta-thia-imino group resulted in the orally active and chemically stable analogue Hoe 892. Incubation of rabbit platelet rich plasma with PGI2 and Hoe 892 caused a dose dependent inhibition of collagen and arachidonic acid (AA) induced platelet aggregation with ID50 of 4.2 and 20.1 ng/ml for PGI2 respectively 43.3 and 170.2 ng/ml for Hoe 892. These effects could be potentiated by the phosphodiesterase inhibitor theophylline. Single oral administration of Hoe 892 in conscious rabbits inhibited platelet aggregation for more than 3 hrs with an ID50 of 0.2 mg/kg using collagen and 1.5 mg/kg using AA. These doses were without influence on systemic blood pressure (BP) in conscious rabbits. Intravenous injection of Hoe 892 induced a dose dependent decrease of systemic BP in anesthetized rats (ED25 of 2.2 micrograms/kg) and in the rats with acute renal hypertension. Hoe 892 stimulated renin release in anesthetized rats. The hemodynamic profile in anesthetized dogs (0.5 micrograms/kg/min i.v.) was characterized by a decrease of systemic BP, left ventricular pressure, pulmonary artery pressure, total peripheral resistance and in increase in heart rate, cardiac output and dp/dt max, thus demonstrating arteriolar vasodilation. In conscious dogs with two kidney, two wrapped hypertension oral treatment for 1 or 5 days resulted in a marked reduction of BP.

Animals↗
PubMed1983

[Centrally caused achromatopsia].

A 65-year-old patient sustained a transient left-sided sensomotoric monoparesis with homonymous hemianopsia. One day later there was an acute deterioration in the patient's vision and he developed achromatopsia, prosopagnosia, disturbance of spatial orientation and a homonymous upper hemianopsia. Six months later the findings are about the same. The CT shows a bioccipital lesion with left-sided accentuation, extending dorsocaudally. The origin of the cerebral infarct is presumably a vertebrobasilar insufficiency due to congestive cardiomyopathy and atrial fibrillation.

Aged↗
PubMed1982

Intracerebroventricular angiotensin II increases arterial blood pressure in rhesus monkeys by stimulation of pituitary hormones and the sympathetic nervous system.

Intracerebroventricular injections of angiotensin II in anesthetized rhesus monkeys increase systemic blood pressure and heart rate. These effects are accompanied by an increase in plasma ADH, cortisol, adrenaline and noradrenaline. Angiotensin II may participate in central mechanisms of blood pressure regulation by its stimulatory effect on the sympathetic nervous system, on ADH and on ACTH release in primates.

Angiotensin II↗
PubMed1982

A microsphere study on the effects of somatostatin and secretin on regional blood flow in anesthetized dogs.

The endogenous peptides somatostatin and secretin are effective in the therapy of upper gastrointestinal tract bleeding and acute pancreatitis. The clinical effects may be partly brought about by changes in the regional blood flow. To evaluate the effects of somatostatin (50 and 100 micrograms/min over 6-8 min) and secretin (0.1 and 0.5 U X kg-1 X min-1 over 3-5 min) on tissue blood flow, particularly of the gastrointestinal tract, the tracer microsphere reference sample method was used in anesthetized dogs. Infusion of somatostatin significantly diminished gastric and pancreatic blood flow whereas no changes of duodenal and ileal blood flow could be obtained. Blood flow through spleen, kidneys and adrenal glands was increased but no changes were observed in the blood flow of other tissues. Cardiac hemodynamics remained unchanged. Secretin increased the blood flow of the duodenum, the kidneys and the adrenal glands and diminished gastric blood flow without changing pancreatic, ileal, hepatic, pulmonary and muscle blood flow. Cerebral, pituitary and myocardial blood flow was increased by a higher dose of secretin. It also evoked a slight but significant positive ino- and chronotropic effect. Since secretin and somatostatin differ in their respective effects on gastrointestinal blood flow it is suggested that the previously reported beneficial effects of both peptides on upper gastrointestinal bleeding cannot solely be attributed to changes in regional blood flow.

Animals↗