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Biomedical subjects

L J Marks

Publications and source records attributed to L J Marks.

6 recordsLinked to original sources
PubMed1992

Paralytic shellfish poison (saxitoxin family) bioassays: automated endpoint determination and standardization of the in vitro tissue culture bioassay, and comparison with the standard mouse bioassay.

Mouse neuroblastoma cells swell and eventually lyse upon exposure to veratridine, which, when added together with ouabain, enhances sodium ion influx. In the presence of saxitoxin (STX), which blocks sodium channels, the action of the other two compounds is inhibited and the cells remain morphologically normal. A tissue culture bioassay using mouse neuroblastoma cells, developed by Kogure and colleagues, takes advantage of these principles; in this bioassay, the fraction of the cells protected from the actions of ouabain and veratridine is in direct proportion to the concentration of STX and its analogues. We have modified this bioassay, improving its convenience and speed by eliminating the need to count individual cells to determine the saxitoxin equivalents, and instead have employed a microplate reader for automated determinations of absorbances of crystal violet from stained neuroblastoma cells. When these changes and other minor technical modifications were tested in the tissue culture bioassay systematically, we found the lower detection limit to be around 10 ng STX equivalents (eq) per ml of extract ( = 2.0 micrograms STX eq/100 g shellfish tissue). Our version of the tissue culture bioassay was compared with the standard mouse bioassay using 10 acid extracts of dinoflagellates (Alexandrium excavata and A. fundyense) and 47 AOAC extracts of shellfish tissues. The tissue culture bioassay provided results virtually identical to those obtained with the mouse bioassay (r > 0.96), and moreover, was considerably more sensitive. The results gained from high performance liquid chromatographic (HPLC) analysis of 12 of the same extracts were less consistent when compared with the results from both bioassay methods. The automated tissue culture (neuroblastoma cell) bioassay may be a valid alternative to live animal testing for paralytic shellfish poisoning.

Animals↗
PubMed1977

The Silver-Russel syndrome: a case with sexual ambiguity, and a review of literature.

A 38-month-old patient with Silver-Russel syndrome (SRS) and ambiguous genitalia had a 46,XY karyotype on leukocyte and fibroblast cultures. This is the third SRS child with ambiguous genitalia described in the literature. In a review of the findings in 148 reported cases of the syndrome, abnormalities occurring in over 50% of the cases are short stature, craniofacial dysproportion, low birth weight, term gestation, body asymmetry, incurved fifth digits, normal intelligence, short fifth digits, and down-curved corners of the mouth (shark mouth).

Abnormalities, Multiple↗
PubMed1976

Tumor hypoglycemia: deficient splanchnic glucose output and deficient glucagon secretion.

Fasting hypoglycemia occurred in a patient with a histologically benign mesothelioma; the serum insulin was low (2-4 muU./ml.), as was the glucose utilization rate. Splanchnic glucose output was markedly decreased on direct measurement (21 mg./min.; normal: 108-180 mg./min.). Splanchnic uptake of gluconeogenic substrates plasma glucagon was low normal during hypoglycemia and responded poorly to oral and intravenous alanine. The nonsuppressible insulin-like (NSILA-s) and somatomedin-like activities of the serum were not elevated, and the tumor did not release insulin-like activity on incubation nor did it contain somatostatin. The marked decrease in splanchnic glucose output was the principal cause of hypoglycemia, was associated with an apparent decrease in glycogenolysis, and was at least partly due to deficient glucagon secretion. The relationship of the tumor to these defects is unclear. The tumor may have secreted an unknown insulin-like material affecting primarily the liver and/or pancreatic alpha cell. The approach used here may serve as a paradigm for the analysis of hypoglycemia not caused by excessive insulin.

Glucagon↗
PubMed1975

Vitamin D deficiency rickets. Two cases with faulty infant feeding practices.

Two cases of vitamin D deficiency rickets verify the occurrence of deficiency rickets in the United States in 1973. The two cases demonstrate the need for periodic reviews of feeding practices, especically when the possibility of so-called milk allergy is postulated. This may lead to avoidance of milk products. Fortification of various kinds of food with vitamin D does not ensure the protection from nutritional rickets of all children with peculiar feeding habits.

Alkaline Phosphatase↗