I read this book the same weekend that the Packers took on the Rams, and the experience of the latter event, obviously, colored my judgment. Although I abhor anything that smacks of being a handbook (like, \"How to Earn a Merit Badge in Neurosurgery\") because too many volumes in biomedical science already evince a boyscout-like approach, I must confess that parts of this volume are fast, scholarly, and significant, with certain reservations. I like parts of this well-illustrated book because Dr. Sj6strand, without so stating, develops certain subjects on technique in relation to the acquisition of judgment and sophistication. And this is important! So, given that the author (like all of us) is somewhat deficient in some areas, and biased in others, the book is still valuable if the uninitiated reader swallows it in a general fashion, realizing full well that what will be required from the reader is a modulation to fit his vision, propreception, adaptation and response, and the kind of problem he is undertaking. A major deficiency of this book is revealed by comparison of its use of physics and of chemistry to provide understanding and background for the application of high resolution electron microscopy to problems in biology. Since the volume is keyed to high resolution electron microscopy, which is a sophisticated form of structural analysis, but really morphology in a modern guise, the physical and mechanical background of The instrument and its ancillary tools are simply and well presented. The potential use of chemical or cytochemical information as it relates to biological fine structure , however, is quite deficient. I wonder when even sophisticated morphol-ogists will consider fixation a reaction and not a technique; only then will the fundamentals become self-evident and predictable and this sine qua flon will become less mystical. Staining reactions (the most inadequate chapter) ought to be something more than a technique to selectively enhance contrast of morphological elements; it ought to give the structural addresses of some of the chemical residents of cell components. Is it pertinent that auto-radiography gets singled out for more complete coverage than other significant aspects of cytochemistry by a high resolution microscopist, when it has a built-in minimal error of 1,000 A in standard practice? I don't mean to blind-side (in strict football terminology) Dr. Sj6strand's efforts for what is \"routinely used in our laboratory\"; what is done is usually well done. It's just that …

Methods in Enzymology.

A nonelectrogenic H+ pump in plasma membranes of hog stomach.

Vitamin B12 deficiency.

Effect of acid and pepsin on blood coagulation and platelet aggregation. A possible contributor prolonged gastroduodenal mucosal hemorrhage.

Electrical resistance of brain microvascular endothelium

Quantitative ultrastructural studies on gastric parietal cells.

https://www.gastrojournal.org/article/0016-5085(92)91790-B/pdf

Two doses of omeprazole versus placebo in symptomatic erosive esophagitis: the U.S. Multicenter Study.

Powerful vagal stimulation of gastric secretion was produced in dogs by the administration of 50–200 mg/kg 2-deoxy-d-glucose (2-DG) The secretion could be entirely prevented or immediately abolished by atropine injection, indicating one link which is apparently cholinergic. Studies with glucose, mannose, fructose, galactose, or 3-O-methylglucose injected before or subsequent to the administration of 2-DG indicated that the vagal secretory center is specifically glucose and mannose dependent. 2-DG appears to act by the formation of nonmetabolized 2-DG-6-phosphate resulting in effective cytoglucopenia. While apparently stimulating gastric secretion in the same way as insulin hypoglycemia, 2-DG appears to have definite advantages of reliability and reproducibility. The vagal center appears to be dose responsive and not an all-or-none system, and stimulates all elements of gastric secretion by a single pathway.

Vagal gastric secretory stimulation by 2-deoxy-D-glucose.

Summary

Background Proton pump inhibitors (PPIs) may cause cyanocobalamin (vitamin B12) malabsorption, but measuring serum B12 alone may underestimate the prevalence. However, B12 deficiency elevates methylmalonic acid and homocysteine, both additional markers of B12 deficiency.



Aim  To determine the true prevalence of B12 deficiency and whether acid suppression by PPI caused it.



Methods  Sixty-one acid hypersecretors (basal acid output >15 mmol/h), 46 with gastrinoma [Zollinger–Ellison (ZE) syndrome] and 15 without [acid hypersecretor without gastrinoma (pseudo-ZE)], were treated with lansoprazole to determine its long-term (up to 18 years) pharmacological and clinical efficacy and safety, particularly as regards malabsorption of B12.



Results  Of 61 patients, six (10%) had low serum B12. Additional tests uncovered B12 deficiency in 13 (31%) of 41 still-available patients, despite normal serum B12. B12 replacement reduced elevated homocysteine and methylmalonic acid, supporting the diagnosis. Also, measuring both basal and stimulated gastric secretion, we found that acid suppression was neither prolonged nor profound enough to explain the B12 deficiency.



Conclusions  In long-term recipients of PPIs, B12 deficiency was more frequent (29%) than detected by measuring only serum B12, and there was not enough acid suppression to explain this deficiency.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2036.2008.03658.x

Vitamin B12 deficiency in hypersecretors during long-term acid suppression with proton pump inhibitors

1. The values of volume, acid, sodium, potassium, chloride, and pepsin in gastric juice in the basal state and following stimulation with histamine given subcutaneously or infused intravenously are reported. Nearly 160 studies were done in five groups consisting of control subjects and patients with duodenal ulcer, gastric ulcer, gastritis, and cancer. 2. The interrelations between a number of the constitutents of human gastric juice are described. With all other conditions the same, changes in one of the major solutes of gastric secretion are accompanied by predictable changes in the others. 3. It is concluded that the process of gastric secretion is a fully integrated mechanism, with the gastric tubule comprising the basic unit of the mucosa. This unit has been named the gastron. Its main actions are tentatively divided into a primary mechanism, the function of which is to secrete [Na+K] Cl and water (and, incidentally, pepsinogen, since the chief cells are thought to perform this function), and in the parietal cells, a secondary mechanism, which exchanges H for Na and so produces HCl.

Basil I. Hirschowitz

Papers

Quantitative ultrastructural studies on gastric parietal cells.

Two doses of omeprazole versus placebo in symptomatic erosive esophagitis: the U.S. Multicenter Study.

Vagal gastric secretory stimulation by 2-deoxy-D-glucose.

Vitamin B12 deficiency in hypersecretors during long-term acid suppression with proton pump inhibitors

Electrolytes in human gastric secretion. Observations and a theory.