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Biomedical subjects

M Hammes

Publications and source records attributed to M Hammes.

6 recordsLinked to original sources
PubMed1995

Laparoscopic Swenson pull-through procedure for congenital megacolon.

Constipation that is unresponsive to conventional remedies is the primary symptom of congenital megacolon (ie, Hirschsprung's disease). The cause of congenital megacolon is lack of ganglion cells in the bowel. The laparoscopic Swenson pull-through procedure involves removing the aganglionic segment of the colon, bringing the normally decompressed bowel through the pelvic floor, and anastomosing the bowel to the anorectal verge. Advantages of the laparoscopic approach include shorter lengths of hospital stay and fewer complications resulting from disruption of skin integrity.

Anastomosis, Surgical↗
PubMed1994

Hypocalcemia in end-stage renal disease: a consequence of spontaneous parathyroid gland infarction.

Advances over the last several years have led to a better understanding of the etiology of hyperparathyroidism in renal disease and to more effective means of medical prevention and therapy. Thus, in most dialysis populations, many of the serious complications, such as bone fractures, refractory hypercalcemia, and hyperphosphatemia with vascular and other extraskeletal calcifications, have diminished. Furthermore, more aggressive medical management has decreased the requirement for parathyroidectomy. Unfortunately, not all patients respond to medical management and few still develop refractory hyperparathyroidism with associated morbidity. Of the many complications of refractory hyperparathyroidism in dialysis patients, the development of life-threatening hypocalcemia has not been described. We describe a patient with severe secondary hyperparathyroidism who presented with the acute development of hypocalcemia. To our knowledge, this represents the fourth case, the first reported in a patient with end-stage renal disease, of parathyroid autoinfarction presenting as acute hypocalcemia.

Adult↗
PubMed1994

Effect of polycations on permeability of glomerular epithelial cell monolayers to albumin.

Polycations can interact with the surface negative charges of the glomerular epithelial cells in the kidney and give rise to metabolic alterations. This study examined whether charge neutralization can affect intercellular junctions and increase macromolecular permeability across epithelial monolayers. We examined this question by studying the effect of polycations on the leakage of albumin across monolayers of glomerular epithelial cells. Cells were grown to confluency on filter-lined cups. They were treated apically with cationic bovine gamma globulin or protamine (100 micrograms/ml) for 2 hours at 37 degrees C. After washing the cells, the monolayers were tested for leakage of albumin by the addition of radioactive bovine serum albumin on the apical side and determining the time course of its appearance on the basal side. Polycation treatment caused significant leakage of albumin in the absence of any toxic effect on viability or lactate dehydrogenase release. The leakage was shown to be through the tight junctions of the monolayer. Permeability alterations were compared at 4 degrees C and 37 degrees C to determine whether impairment was due to the membrane ruffling effect of charge neutralization or due to intracellular metabolic changes. Despite equal bindings of polycations at 4 degrees C and 37 degrees C, significant leak occurred only at 37 degrees C, suggesting the role of active processes in the maintenance of permselectivity. This was consistent with the rapid interiorization of the polycation at 37 degrees C after membrane binding. Further substantiation of this point was obtained by studying the protective effect of removing bound polycation with heparin. Removal of polycation after initial binding failed to protect the monolayer from albumin leakage. The conclusion was that neutralization of glomerular epithelial cell surface charges results in subtle impairment of tight junction control of permeability to macromolecules across the monolayer. The impairment was due to active intracellular processes that ensue after polycation binding to cell surface charges and their subsequent internalization.

Animals↗