Correlation of low and high density lipoprotein binding in vivo with rates of lipoprotein degradation in the rat. A comparison of lipoproteins of rat and human origin

These studies were done in the rat to correlate the ability of low and high density lipoproteins of rat (rLDL and rHDL) and human (hLDL and hHDL) origin to bind in vivo to specific tissues with the rates at which these same lipoprotein fractions were cleared from the circulation. The adrenal gland and liver manifested the greatest amounts of rLDL binding in vivo, but activity also was found in spleen, lung, kidney, ovary, and intestine. In contrast, little or no such binding was found utilizing either methyl-rLDL or hLDL. rHDL containing E apoprotein bound to the same group of tissues although in lesser amounts, except in the case of ovary and adrenal gland which bound disproportionately greater amounts of rHDL than rLDL. In keeping with these marked differences in tissue binding, the clearance of rLDL from the plasma equaled 847 +/- 36 microliters/h/100 g of rat while that of methyl-rLDL and hLDL was only 368 +/- 8 and 363 +/- 11 microliters/h/100 g of rat, respectively. When the steady state plasma level of rLDL was raised 2.5-fold, the clearance decreased slightly to 705 +/- 20 microliters/h/100 g of rat. The clearance of hLDL remained constant, however, at about 350 microliters/h/100 g of rat even when the plasma hLDL level was raised to very high values. The clearance of rHDL and hHDL equaled 644 +/- 16 and 408 +/- 13 microliters/h/100 g of rat, respectively, reflecting the more similar rate of binding of rHDL and hHDL to the tissues of the rat. Rates of whole animal sterol synthesis were lowered from 28 mumol/h to 8.8 mumol/h or 13 mumol/h by fasting and cholesterol feeding, respectively, and stimulated to 71 mumol/h by cholestyramine treatment. Under these same conditions, hepatic cholesterol synthesis could be lowered from the normal rate of 15 mumol/h to 4.2 mumol/h and raised to 50 mumol/h. None of these treatments, however, affected the plasma clearance of rLDL and rHDL. In contrast, treatment with ethinyl estradiol increased by 3-fold both the hepatic binding and the whole animal plasma clearance of rLDL. Following resection of approximately two-thirds of the liver under carefully controlled metabolic conditions, there was no change in the rate of hepatic cholesterol synthesis or rLDL binding in the remaining liver, but the clearance of chylomicrons, rLDL, and rHDL diminished by 67%, 26%, and 17%, respectively, suggesting that in the rat the liver was responsible for the degradation of approximately 97%, 39%, and 27%, respectively, of these lipoprotein fractions.     

Structure and function of gastric corpus mucosa in suckling rats after treatment with 16,16-dimethyl prostaglandin E2

Suckling rats were treated every 8 h by intragastric instillation of 16,16-dimethyl prostaglandin E₂ (PG) from postnatal day 7 to 11. As compared to saline control treatment, PG increased the thickness of antral and corpus mucosa, the volume density of parietal cells, the mean individual parietal cell volume and pentagastrin-stimulated acid secretion at the end of the treatment. Plasma gastrin and corticosterone levels were depressed by PG while plasma thyroxine levels were unchanged. These structural and functional changes suggest PG-induced accelerated maturation of gastric mucosa.     

Metabolic Variations of Proteus in the Memphis Area and Other Geographical Areas

The number of strains of Proteus studied was 413, and these were obtained from all clinical materials with the exception of fecal specimens. Lactose was fermented by 37 strains (P. inconstans, 29%; P. rettgeri, 16%; P. mirabilis, 4.2%; P. morganii, 3.6%; and P. vulgaris, 0%) of which 33 were from the genitourinary system. These 33 strains constituted 12.7% of the 260 strains isolated from this source. Biochemically, P. mirabilis was the least variable, and P. rettgeri was the most variable of the five species of Proteus tested. P. inconstans and P. rettgeri resembled each other more closely than any of the other species of Proteus. Comparison of results obtained in the Memphis area with those found in other locations showed that biochemical characteristics varied most with the substances citrate, salicin, xylose, trehalose, and mannitol. In contrast to earlier reports from Israel and England, none of the strains of P. inconstans in the present study was able to attack urea. All five species of Proteus tested (by the disc method) were highly susceptible to methenamine mandelate. P. mirabilis, P. morganii, and P. vulgaris were also highly susceptible to nitrofurantoin. All strains of P. mirabilis were susceptible to ampicillin. P. inconstans was the most resistant species of Proteus. Of the other 356 urease-positive strains tested, 79% were susceptible to chloramphenicol, whereas only 3.8% of the 56 urease-negative strains (P. inconstans) were susceptible. When tested with streptomycin, 61% of urease-positive strains were susceptible and 1.8% of the urease-negative strains were susceptible. Of 36 lactose-positive strains, 33.8% were susceptible to chloramphenicol, whereas 72.8% of all lactose-negative strains were susceptible. Again, of the lactose-positive strains, 17% were susceptible to streptomycin, whereas 56.3% of all lactose-negative strains were susceptible.     

Structure and function of gastric corpus mucosa in suckling rats after treatment with 16,16-dimethyl prostaglandin E2

Suckling rats were treated every 8 h by intragastric instillation of 16,16-dimethyl prostaglandin E2 (PG) from postnatal day 7 to 11. As compared to saline control treatment, PG increased the thickness of antral and corpus mucosa, the volume density of parietal cells, the mean individual parietal cell volume and pentagastrin-stimulated acid secretion at the end of the treatment. Plasma gastrin and corticosterone levels were depressed by PG while plasma thyroxine levels were unchanged. These structural and functional changes suggest PG-induced accelerated maturation of gastric mucosa.     

The necessity of identity assessment of animal intestinal cell lines: A case report

Eight intestinal cell lines, established from different animal species were submitted to DSMZ (German Collection of Microorganisms and Cell Cultures) in order to analyze their species of origin and their microbial contamination. Species identity was determined by PCR targeting mitochondrial genes and hence confirmed by sequencing the amplified PCR products. For three cell lines (CIEB, CLAB, PSI-1) we confirmed the species identity, whereas the species of origin of the three other cell lines (B6, B10XI and IPEC) was not the expected one: B6 and B10XI cells, which were supposed to be of chicken origin were identified as porcine cells. IPEC, allegedly a sub clone of the well-known porcine intestinal cell line IPEC-J2, was of bovine instead of porcine origin. However, two further IPEC-clones, namely IPEC-1 and IPEC-J2, provided by another source were shown to be derived from the correct species (i.e. pig). Furthermore, six out of these eight cell lines turned out to be highly contaminated with mycoplasma. Alerted by this high incidence of infected and false specified cell lines, we feel obliged to inform all those working with animal intestinal cell lines and we strongly recommend verifying the species identity before using them. Also, the presence of mycoplasma should be tested when taking the cells in culture for the first time, and this mycoplasma control should be repeated at regular time intervals (e.g. every 4 weeks).