Search PubMed⌕ Search

Biomedical subjects

S J Li

Publications and source records attributed to S J Li.

At least 91 records · Page 5Linked to original sources
PubMed1989

31P NMR spectroscopic study of bioenergetic changes in radiation-induced fibrosarcoma-1 after radiation therapy.

The effects of localized gamma-irradiation on the in vivo 31P NMR spectra of RIF-1 tumors grown subcutaneously in C3H/HeN mice have been examined before and during the week after treatment. Increases in the ratio of phosphocreatine (PCr) to inorganic phosphate (Pi) and in tumor pH, and decreases in the ratio of Pi to the beta phosphorus resonance of the nucleotide triphosphates (beta NTP) were observed in irradiated tumors. The time course of changes in the 31P spectrum following treatment was the opposite of the pattern during untreated growth, and the magnitude and duration of the changes increased with increasing radiation dose, decreasing clonogenic cell survival and increasing growth delay. To examine the possibility that nontherapeutic systemic effects of the tumor irradiation were responsible for the changes observed, a number of animals bearing two tumors were examined. One tumor on each mouse was selectively irradiated. Changes in tumor volume, Pi/beta NTP, PCr/Pi, the ratio of phosphomonoesters to beta NTP, and tumor pH were all significantly different in the treated compared to the untreated tumor on each animal, indicating that these changes in 31P NMR spectra were a response to radiation therapy and not a systemic response to radiation toxicity.

Animals↗
PubMed1989

Reversal of hepatic steatosis in rats by addition of glucagon to total parenteral nutrition (TPN).

Infusion of total parenteral nutrition (TPN) with excess carbohydrate calories leads to hepatic steatosis in rats that is associated with an elevated portal insulin/glucagon molar ratio. Previously we have shown that adding glucagon to TPN prevents hepatic steatosis in rats. In this study we attempted to reverse the steatosis by adding glucagon to TPN after 1 week of TPN alone. Adult rats (n = 28) received internal jugular catheters: Group 1 (n = 7), saline (3 cc/h) and chow ad libitum; Group 2 (n = 7), 25% dextrose base TPN solution for 1 week; Group 3 (n = 7), 25% dextrose base TPN for 2 weeks; Group 4 (n = 7), 25% dextrose base TPN for 1 week and then glucagon (15 micrograms/100 g/day) added to TPN for the second week. The infusion rate of TPN was 1.2 ml/100 g/hr (40% kcal greater than control). At 7 days (Group 2) and 14 days (Groups 1, 3, and 4) portal and peripheral venous blood levels were drawn for insulin and glucagon radioimmunoassay, blood glucose determination, and liver function tests; livers were removed for histology and lipid content determination. Blood glucose was equivalent among all groups. Liver function tests were within normal limits. Panlobular vacuolization of the hepatocytes was noted on histology in Groups 2 and 3. Hepatic lipid content was significantly elevated in Group 3. The portal insulin/glucagon molar ratio was increased because of excessive portal venous insulin in Groups 2 and 3 (P less than 0.05 by ANOVA). In contrast, portal venous insulin and the insulin/glucagon molar ratio did not increase in Group 4 and hepatic lipid infiltration was absent when glucagon was added to the TPN solution after 1 week of TPN solution alone. The results suggest that the addition of glucagon to hypertonic dextrose TPN is not only protective in preventing hepatic steatosis, but may reverse steatosis, possibly by increasing hepatic lipid export.

Animals↗
PubMed1989

A low hippocampal dynorphin A (1-8) immunoreactivity in spontaneously hypertensive rats.

Dynorphin A (1-8)-like immunoreactivity (DN-LI A(1-8] was determined by radioimmunoassay in the brains of age matched spontaneously hypertensive rats (SHR) and two normotensive control groups consisting of Wistar-Kyoto (WKY) and Sprague-Dawley (SD) strain rats. A significantly lower DN-LI A(1-8) was found in the hippocampus and hypothalamus of the SHR compared with the WKY groups. DN-LI A(1-8) was 24% of control WKY levels in hippocampus and 79% of that in WKY hypothalamus at 16 weeks. Similar lower levels of DN-LI A(1-8) were also observed in SHR at 4, 8, and 12 weeks during the development of hypertension when compared with both WKY and SD groups. We failed to find significant differences in brain stem DN levels between the groups. The relationship between the low hippocampal dynorphin levels in SHR and the hypertension is problematical because the differences were present before (4 wks), during (8 and 12 wks) and after (16 wks) its development.

Aging↗
PubMed1989

Single or repeated electroconvulsive shocks alter the levels of prodynorphin and proenkephalin mRNAs in rat brain.

The effects of single or repeated electroconvulsive shocks (ECS) on the abundance of mRNAs coding for prodynorphin (DYN mRNA) and proenkephalin (EK mRNA) in rat brain were investigated. Rats were given either a single ECS and sacrificed at 0.5, 2, 6, or 12 h post-shock (expt. I), or were subjected to ECS for 1, 3 or 6 days and killed 24 h after the last shock (expt. II). The amounts of DYN mRNA and EK mRNA were measured in several brain regions using RNA blot analysis. In expt. I, a biphasic change in the DYN mRNA level was found in the hippocampus, with an initial 49% decrease at 0.5 h followed by a 51% increase at 6 h after a single ECS. The EK mRNA content in the entorhinal cortex started to increase at 0.5 h, and continued to rise, reaching 260% of the control level at 12 h post-shock. A smaller increase in the EK mRNA level was found also in the hippocampus at 2 to 12 h post-shock. No significant increase in [Met5]-enkephalin or dynorphin A(1-8) immunoreactivity was detected by radioimmunoassay in either area. In expt. II, a dramatic reduction in the DYN mRNA level was observed in the hippocampus 24 h after a single or repeated ECS. In contrast, elevated DYN mRNA levels were seen in the striatum and hypothalamus. The EK mRNA level remained elevated in the entorhinal cortex after 6 daily ECS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Plant regeneration of mesophyll protoplasts from axenic potato (Solanum tuberosum L.) shoot.

Mesophyll protoplasts from commercial potatoes were cultured in shallow liquid media. The regenerated cells divided and formed calli. Regenerant plants of two potato lines (Ke Xin 4; 68-62) were obtained from the regenerated calli after transfer to solid medium. The division frequency of the regenerated cells was influenced by culture protoplast density. Growth of the protoplast-derived colonies was sensitive to sucrose concentration in the liquid medium. The protoplast culture medium obviously affected differentiation frequency for the protoplast-derived calli (P-calli). The P-callus differentiation frequency was raised by supplementing the medium with 3% mannitol, which also shortened the P-callus differentiation.

Cells, Cultured↗
PubMed1988

Response of radiation-induced fibrosarcoma-1 in mice to cyclophosphamide monitored by in vivo 31P nuclear magnetic resonance spectroscopy.

In vivo 31P nuclear magnetic resonance spectroscopy has been used to examine the RIF-1 fibrosarcoma in mice during untreated growth and following chemotherapy with cyclophosphamide. Levels of inorganic phosphate increase relative to phosphocreatine or nucleoside triphosphates during early untreated growth. After the tumor reaches a volume of approximately 1 g, no further decrease in energy level is observed. Following treatment with cyclophosphamide, tumor phosphorus metabolite ratios and pH are significantly altered, compared to untreated age-matched controls. During the growth delay period following chemotherapy there is a significant reduction in the ratio of inorganic phosphate to other phosphate metabolites, compared to age-matched controls. In addition, a more alkaline pH is observed in the tumors of treated animals. When the growth delay period ends, nuclear magnetic resonance spectra return to pretreatment patterns. The magnitude of the differences in 31P nuclear magnetic resonance spectral parameters between treated animals and untreated controls is dose dependent. However, doses of cyclophosphamide above 200 mg/kg do not result in earlier spectroscopic alterations, nor in larger effects by Day 3 after treatment, even though clonogenic cell killing and growth delay are greater at these higher doses.

Animals↗
PubMed1988

Synthesis of acute-phase proteins in perfused liver following administration of recombinant interleukin 1 alpha to normal or adrenalectomized rats.

The purpose of this study was to investigate the effects of recombinant interleukin 1 alpha (rIL-1 alpha) on metabolic rate and synthesis of acute-phase proteins in intact and adrenalectomized rats. Animals were housed in metabolic cages with daily recording of food intake and body weight. Twice daily, for 3 days, the rats were injected intraperitoneally with 5000 LAF U of human rIL-1 alpha, purified from Escherichia coli. Control animals were pair-fed and received corresponding injections with saline. In the morning of the fourth day, resting energy expenditure (REE) was determined by indirect calorimetry, and synthesis of total secreted proteins, albumin, complement component C3, and seromucoid fraction was measured by radioimmunological method using rat-specific antisera and [3H]leucine in livers perfused for 2 hr. Food intake decreased by approximately 30% during rIL-1 alpha administration to intact rats. The decrease in food intake occurred later and was less pronounced in adrenalectomized rats receiving rIL-1 alpha. Growth rate was significantly reduced on the first day of rIL-1 alpha treatment in intact rats, while there was no effect on growth rate in adrenalectomized animals. After rIL-1 alpha administration, REE was increased by 26% in intact rats (P less than 0.001) and by 14% in adrenalectomized rats (N.S.). Increased synthesis rates of total secreted proteins, complement component C3, and seromucoid fraction were observed in livers of intact rats following rIL-1 alpha administration. In adrenalectomized rats, only production of C3 was significantly increased after treatment with rIL-1 alpha. Albumin synthesis rate was not changed in either group following rIL-1 alpha injections.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Proteins↗
PubMed1988

Administration of balanced or BCAA-enriched amino acid solution in septic rats. Effects on protein synthesis in the liver.

Total hepatic protein synthesis was measured in vivo with a flooding-dose technique, and the production of total secreted proteins, albumin, complement component C3, and seromucoid fraction was measured in perfused livers of septic rats that received one of three different solutions infused intravenously; Group 1 received 16.4% dextrose; Group 2 received Aminosyn (25% BCAA) in 10.6% dextrose, and Group 3 received Freamine HBC (45% BCAA) in 10.6% dextrose. All solutions were isocaloric, and the amino acid solutions were isonitrogenous. The solutions were administered for 18 or 48 hours after the induction of sepsis. There were no significant differences in mortality rates in the three treatment groups. The negative nitrogen balance seen in the dextrose-infused animals was reversed to the same degree by the two different amino acid solutions. There were no significant differences in hepatic protein synthesis rates in vivo between the three groups of rats. Synthesis rates of secreted proteins in perfused liver were similar in the different treatment groups in the 18-hour experiments, whereas in the 48-hour experiments, synthesis rates of total secreted proteins, C3, and the serumucoid fraction were higher in Group 1 than in Groups 2 and 3. The results suggest that administration of an amino acid solution improves nitrogen balance in sepsis, but that this effect is not caused by stimulated hepatic protein synthesis. The nitrogen-sparing effect during sepsis of a branched chain amino acid (BCAA)-enriched solution does not seem to be superior to that of a balanced amino acid solution.

Amino Acids↗
PubMed1988

Regulation of the metabolism of striatal dynorphin by the dopaminergic system.

The purpose of this study was to explore the dopaminergic control of the striatonigral dynorphin system. Seven daily injections of a dopamine (DA) agonist, apomorphine (APO, 5 mg/kg, b.i.d., s.c.), caused a significant increase of dynorphin A (1-8)-like immunoreactivity (DN-LI) in the striatum (140% over control) and substantia nigra (41% over control) without changing DN-LI in frontal cortex, hypothalamus and hippocampus. Immunocytochemistry revealed intense dynorphin A (1-17)-like immunostaining in striatal "patch" neurons and striatonigral fibers after APO treatment. In order to understand the mechanism of increase in the peptide level, the abundance of preprodynorphin mRNA was quantified by Northern blot hybridization with a 32P-labeled cRNA probe coding for rat preprodynorphin. Seven daily injections of APO increased the abundance of striatal preprodynorphin mRNA by 60%. In another experiment, rats received a single injection of various doses of APO (0.5-2.5 mg/kg s.c.). Striatal DN-LI was decreased by 15% 1 hr after injection of a dose of 2.5 mg/kg of APO. Seven daily injections or a single injection of D-amphetamine produced effects similar to those elicited by APO. These studies reveal that the nigrostriatal DA system plays an important role in modulating the metabolism of striatonigral dynorphin-containing neurons.

Animals↗
PubMed1988

Addition of glucagon to total parenteral nutrition (TPN) prevents hepatic steatosis in rats.

Hepatic steatosis is one of the two principal hepatic complications of total parenteral nutrition (TPN), the other being cholestasis. While the cause is uncertain, an excess of carbohydrate calories in rats leads to an elevated portal insulin/glucagon (I/G) molar ratio, periportal fatty infiltration, and increased total hepatic lipid content. Insulin causes fatty acid biosynthesis, whereas glucagon causes hepatic release and inhibition of fatty acid synthesis. Thus we attempted to add glucagon to lower the I/G to see if this would affect the degree of hepatic fatty infiltration by encouraging hepatic fat mobilization. Adult rats (n = 21) received internal jugular catheters; Group 1 (n = 7) was given saline solution (3 ml/h) and chow ad libitum; Group 2 (n = 7), 25% dextrose-base (D25W) TPN solution; Group 3 (n = 7), D25W TPN + 33 micrograms/100 gm/day glucagon. At 7 days portal and peripheral venous blood samples were drawn for insulin and glucagon radioimmunoassay and blood glucose determination; livers were removed for histologic study and lipid determination. Blood glucose did not differ in any group. Hepatic lipid and peripheral and portal venous I/G were increased and periportal fatty infiltration was extensive in Group 2, whereas hepatic lipid and I/G were decreased and periportal fatty infiltration was absent in glucagon-infused rats (Group 3). An abnormally high I/G ratio in portal blood elicited by high-glucose TPN may be responsible, at least in part, for hepatic steatosis. By increasing hepatic lipid export, addition of glucagon to TPN may play a major role in decreasing hepatic steatosis.

Animals↗
PubMed1987

500-MHz proton homonuclear Overhauser evidence for additional base pair in the common arm of eukaryotic ribosomal 5S RNA: wheat germ.

A "common-arm" fragment from wheat germ (Triticum aestivum) 5S RNA has been produced by enzymatic cleavage with RNase T1 and sequenced via autoradiography of electrophoresis gels for the end-labeled fragments obtained by further RNase T1 partial digestion. The existence, base pair composition, and base pair sequence of the common arm are demonstrated for the first time by means of proton 500-MHz nuclear magnetic resonance. From Mg2+ titration, temperature variation, ring current calculations, sequence comparisons, and proton homonuclear Overhauser enhancement experiments, additional base pairs in the common arm of the eukaryotic 5S RNA secondary structure are detected. Two base pairs, G41 X C34 and A42 X U33 in the hairpin loop, could account for the lack of binding between the conserved GAAC segment of 5S RNA and the conserved Watson-Crick-complementary GT psi C segment of tRNAs.

Base Composition↗
PubMed1987

Dopaminergic regulation of tachykinin metabolism in the striatonigral pathway.

The influence of the dopaminergic system on the striatonigral tachykinin pathway was studied in male Fischer 344 rats. Activation of dopamine receptors by subacute administration of apomorphine (APO; 5 mg/kg s.c. twice daily for 7 days) significantly increased striatonigral substance P-like immunoreactivity (SP-LI; 73% over control in striatum, 63% over control in substantia nigra) and substance K-like immunoreactivity (49% over control in striatum, 15% over control in substantia nigra). The changes in striatonigral SP-LI were dose dependent (0.5-5 mg/kg), time related (one, three or seven daily injections) and region specific as changes were not observed in frontal cortex, hippocampus and hypothalamus. The increase of SP-LI and substance K-like immunoreactivity was completely prevented by the dopamine receptor blocker, haloperidol, which, by itself, caused a slight decrease of both peptide levels. Immunocytochemical staining revealed enhanced SP-LI in neurons restricted to striatal patches and fibers in substantia nigra pars reticulata after APO treatment as compared with SP-LI intensity in control. In order to understand the molecular mechanism underlying the APO-induced increase in the level of tachykinins, the abundance of messenger RNA coding for preprotachykinin was quantified by blot hybridization. It was found that subacute administration of APO increased the abundance of preprotachykinin messenger RNA in the striatum. These results suggest that stimulation of dopaminergic receptors leads to an acceleration of tachykinin biosynthesis. A single dose of APO (2.5 mg/kg s.c.) induced a slight but significant reduction in striatal SP-LI (82% of control). This result suggests that APO triggers the release of tachykinins.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗