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C Larsen

Publications and source records attributed to C Larsen.

114 records · Page 7Linked to original sources

Lineage-specific patterns of p21ras proteins in immortalized cell lines derived from mouse teratocarcinoma.

The expression of proteins coded by the ras oncogene family was examined in mouse embryonal carcinoma (EC) cells and in immortalized cell lines derived from EC. These cell lines, which correspond to early stages of differentiation, express the simian virus 40 (SV40) T antigen and still proliferate. By 2-D gel electrophoresis of the immune complexes formed with monoclonal anti-ras antibodies, it was possible to distinguish the products of the Ha-, N- and Ki-ras genes and to correlate the observed patterns with the differentiation state of the cells. We show in this report (1) that the 2-D gel pattern of ras protein is identical for the various EC tested and is not influenced by SV40 transformation, (2) that p21Ki-ras is not detected in EC cells, although some EC cell lines are known to express a Ki-ras transcript, and (3) that the complex patterns of N- and Ha-ras observed in EC cells becomes simpler as differentiation proceeds, with a different, characteristic pattern for neuroectodermal, mesodermal and endodermal derivatives. Such patterns could prove useful as differentiation markers.

Animals↗

Fallopian tube patency demonstrated at ultrasonography.

Fallopian tube patency was assessed in 24 infertile patients by hysterosalpingography (HSG) and ultrasonographic examination of the pouch of Douglas following transcervical injection of a sterile isotonic solution of NaCl. The presence of fluid in the pouch, after the injection, was taken to indicate tubal patency. The results of the HSG and the ultrasonographic diagnosis as to the presence of at least unilateral tubal patency were concordant in 21 patients. Pitfalls consisted of fluid accumulation in periadnexal adhesions, edema in the bowel wall, and spill of the injected saline into a large hydrosalpinx. Ultrasonography is advocated as the initial examination in assessing infertility in young women. If tubal patency is demonstrated, the patient should be recommended a six month trial period, to become pregnant, before invasive procedures are initiated.

Adolescent↗

Ability of ethoxyquin and butylated hydroxytoluene to counteract deleterious effects of dietary aflatoxin in chicks.

The antioxidants ethoxyquin and butylated hydroxytoluene (BHT) were added to diets of chicks in concentrations three and eight times above that usually found in poultry feed beginning 15 days after hatch; the chicks had been placed on feed containing 1000 or 3000 ppb aflatoxin on the day of hatch. These diets were continued until chicks were 6 weeks of age. At that time, deleterious effects of aflatoxin on weight gain, feed efficiency, and organ weights (spleen, bursa) were evident. BHT alleviated these effects, but ethoxyquin did not. Pretreatment with ethoxyquin did not protect chicks either. Ethoxyquin was not able to induce the activities of chick liver enzymes that detoxify aflatoxin and other foreign compounds. Lack of effect of ethoxyquin on these enzymes may hinder ability of this antioxidant to protect chicks from aflatoxin.

Aflatoxins↗

[DNA-RNA hybrids].

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DNA↗

Nitric oxide concentrations and cerebrospinal fluid parameters in an experimental animal model of Streptococcus pneumoniae meningitis.

Streptococcus pneumoniae is a common cause of meningitis. Nitric oxide (NO) has been implicated in causing cerebral edema. Modulating NO production in cerebrospinal fluid (CSF) may have a role in the treatment of bacterial meningitis. Experimental S. pneumoniae meningitis was induced in a rabbit model to determine CSF parameters and NO concentrations. An electrochemical probe in the CSF throughout the 7-hour experiment monitored NO concentrations. The animals had S. pneumoniae (10(5)) injected intracisternally and incubated for 1 hour. Cerebrospinal fluid 200-300 microl was obtained by intracisternal puncture at zero, 2, 4, and 7 hours after drug administration to measure glucose, protein, and lactic acid by standard chemical methods. White blood cell count was measured by hemocytometry. Three groups of five animals were used-control (C), ceftriaxone (CTX), and ceftriaxone plus dexamethasone (CTX+D). Ceftriaxone concentrations in CSF were obtained by microdialysis and analyzed by high-performance liquid chromatography. Mean (+/- SEM) CSF white blood cell count was significantly higher at 2 hours in the C group than in the other two groups (C 7307 +/- 1302, CTX 605 +/- 345, CTX+D 730 +/- 43/mm3, p<0.002). Ceftriaxone induced a significant rise in protein at 4 hours compared with the other groups (C 364 +/- 107, CTX 1158 +/- 797, CTX+D 365 +/- 100 mg/dl, p<0.02). Cerebrospinal fluid lactic acid was significantly different at 4 and 7 hours between C and CTX+D groups (4-hr C 8.0 +/- 2.2, CTX+D 2.0 +/- 0.4 mmol/L, p<0.05; 7-hr C 10.2 +/- 2.4, CTX+D 2.8 +/- 0.8 mmol/L, p<0.01). Median NO concentrations were significantly elevated in the control group compared with the other two groups (C 11.7, CTX 6.8, CTX+D 6.5 micro, p<0.02 C vs CTX, p<0.01 C vs CTX+D). Average (+/- SEM) NO concentrations were significantly higher in the C group at 4 hours (18.1 +/- 0.4, CTX 5.8 +/- 1.8 microM, p<0.05; CTX+D 11.5 +/- 4.0 microM, p>0.05), whereas they did not rise significantly until 7 hours in the CTX group (CTX 18.7 +/- 0.7, C 8.9 +/- 0.4 microM, p=0.055; CTX+D 8.1 +/- 2.2 microM, p<0.05). These results indicate that ceftriaxone with or without dexamethasone significantly decreases lactic acid concentrations and white cell penetration into the CSF in an experimental model of S. pneumoniae meningitis. In addition, ceftriaxone induced a significant elevation in CSF protein. Median NO production in the CSF was significantly attenuated by ceftriaxone.

Animals↗