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Biomedical subjects

M Case

Publications and source records attributed to M Case.

11 recordsLinked to original sources

Pancreatic ductal bicarbonate secretion: past, present and future.

The pancreatic duct epithelium in the guinea-pig and many other species secretes HCO(3)(-) at concentrations approaching 150 mM. This cannot be explained by conventional models based upon HCO(3)(-) secretion via an anion exchanger at the luminal membrane because: 1) under these conditions, the Cl(-) and HCO(3)(-) concentration gradients would favour HCO(3)(-) reabsorption rather than secretion, and 2) the luminal anion exchanger appears to be inhibited by luminal HCO(3)(-) concentrations of 125 mM or more. There may, however, be a sufficiently large electrochemical gradient to drive HCO(3)(-) secretion across the luminal membrane via an anion conductance. In contrast to earlier studies on rat ducts, the membrane potential E(m) in guinea-pig duct cells does not depolarise appreciably upon stimulation with secretagogues but remains constant at about -60 mV. Consequently, even with 125 mM or more HCO(3)(-) in the lumen and an estimated 20 mM in the cytoplasm, the electrochemical gradient for HCO(3)(-) will still favour secretion to the lumen. Under the same conditions, the intracellular Cl(-) concentration drops to very low levels (approximately 7 mM) presumably because, although Cl(-) may leave freely through the cystic fibrosis transmembrane conductance regulator (CFTR) channels in the luminal membrane, there is no major pathway for Cl(-) uptake across the basolateral membrane. Consequently a HCO(3)(-)-rich secretion may arise as a result of the lack of competition from intracellular Cl(-) for efflux via the anion conductances at the luminal membrane. Whether CFTR, or another anion conductance, provides such a pathway for HCO(3)(-) remains to be seen.

Animals↗

Unsafe sleep practices and an analysis of bedsharing among infants dying suddenly and unexpectedly: results of a four-year, population-based, death-scene investigation study of sudden infant death syndrome and related deaths.

BACKGROUND: Prone sleep and unsafe sleep surfaces increase the risk of sudden infant death. Recent epidemiologic studies also suggest that when an infant's head or face is covered by bedding, or when a sleep surface is shared with others, the risk of dying increases. The inference of a causal role for these risk factors is supported by physiologic studies and by the consistent finding that fewer infants die when risk factors are reduced. The prevalence of most of these risk factors in infant deaths in the United States is uncertain. OBJECTIVE: To describe the prevalence of several important risk factors related to sleep practices among a defined population of infants dying suddenly and unexpectedly. METHODS: In this population-based study, we retrospectively reviewed death-scene information and medical examiners' investigations of deaths in the city of St Louis and St Louis County between January 1, 1994 and December 31, 1997. Because of the potential for diagnostic overlap, all deaths involving infants <2 years old with the diagnoses of sudden infant death syndrome (SIDS), accidental suffocation, or cause undetermined were included. RESULTS: The deaths of 119 infants were studied. Their mean age was 109.3 days (range: 6-350). The diagnoses were SIDS in 88 deaths, accidental suffocation in 16, and undetermined in 15. Infants were found prone in 61.1% of cases and were found on a sleep surface not designed for infants in 75.9%. The head or face was covered by bedding in 29.4%. A shared sleep surface was the site of death in 47.1%. Only 8.4% of deaths involved infants found nonprone and alone, with head and face uncovered. CONCLUSIONS: Using detailed death-scene descriptions, we found that similar unsafe sleeping practices occurred in the large majority of cases diagnosed as SIDS, accidental suffocation, and cause undetermined. Considering these diagnoses together may be useful in public health campaigns during a time when there may be diagnostic overlap. Regardless of the diagnosis, recommendations that infants sleep supine on firm sleep surfaces that lessen the risk of entrapment or head covering have the potential to save many lives. Campaigns are needed to heighten awareness of these messages and of the risks of dangerous bedsharing.

Asphyxia↗

Increased cerebrospinal fluid 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in Kleine-Levin syndrome.

A 17-year-old man with the Kleine-Levin syndrome died unexpectedly of cardiopulmonary arrest during a period of autonomic instability that followed an episode of megaphagia. At autopsy, the only pertinent finding was mild depigmentation of the locus ceruleus and substantia nigra. Premortem CSF levels of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) levels were elevated. These findings indicate that many symptoms of the Kleine-Levin syndrome are a result of a neurotransmitter imbalance in the serotonergic pathway of the brainstem.

Adolescent↗