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  • 1
    Electronic Resource
    Electronic Resource
    Apical membrane endocytosis via coated pits is stimulated by removal of antidiuretic hormone from isolated, perfused rabbit cortical collecting tubule (1988)
    Springer
    The journal of membrane biology 103 (1988), S. 17-28 
    Details
    ISSN: 1432-1424
    Keywords: antidiuretic hormone ; coated pits ; cortical collecting tubule ; endocytosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Antidiuretic hormone increases the water permeability of the cortical collecting tubule and causes the appearance of intramembrane particle aggregates in the apical plasma membrane of principal cells. Particle aggregates are located in apical membrane coated pits during stimulation of collecting ducts with ADHin situ. Removal of ADH causes a rapid decline in water permeability. We evaluated apical membrane retrieval associated with removal of ADH by studying the endocytosis of horseradish peroxidase (HRP) from an isotonic solution in the lumen. HRP uptake was quantified enzymatically and its intracellular distribution examined by electron microscopy. When tubules were perfused with HRP for 20 min in the absence of ADH, HRP uptake was 0.5±0.3 pg/min/μm tubule length (n=6). The uptake of HRP in tubules exposed continuously to ADH during the 20-min HRP perfusion period was 1.3±0.8 pg/min/μm (n=8). HPR uptake increased markedly to 3.2±1.1 pg/min/μm (n=14), when the 20-min period of perfusion with HRP began immediately after removal of ADH from the peritubular bath. Endocytosis of HRP occurred in both principal and intercalated cells via apical membrane coated pits. We suggest that the rapid decline in cortical collecting duct water permeability which occurs following removal of ADH is mediated by retrieval of water permeable membrane via coated pits.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871929
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  • 2
    Electronic Resource
    Electronic Resource
    Changing management of gallstone disease during pregnancy (1998)
    Springer
    Surgical endoscopy and other interventional techniques 12 (1998), S. 241-246 
    Details
    ISSN: 1432-2218
    Keywords: Key words: Gallstones — Cholecystectomy — Pregnancy — Laparoscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Symptomatic gallstones may be problematic during pregnancy. The advisability of laparoscopic cholecystectomy (LC) is uncertain. The objective of this study is to define the natural history of gallstone disease during pregnancy and evaluate the safety of LC during pregnancy. Methods: Review of medical records of all pregnant patients with gallstone disease at the University of California, San Francisco, from 1980 to 1996. Results: Of approximately 29,750 deliveries, 47 (0.16%) patients were treated for gallstone disease, including biliary colic in 33, acute cholecystitis in 12, and pancreatitis in two. Conservative treatment was attempted in all patients but failed in 17 (36%) cases. Two patients required combined preterm Cesarean-section cholecystectomy and 10 required surgery in the early postpartum period for persistent symptoms. Seventeen patients required cholecystectomy during pregnancy for biliary colic (10), acute cholecystitis (six), and pancreatitis (one). Three patients were treated with open cholecystectomy. Fourteen patients underwent LC at a mean gestational age of 18.6 weeks, mean OR time of 74 min, and mean length of stay of 1.2 days. Hasson cannulation was utilized in 11 patients. Reduced-pressure pneumoperitoneum (6–10 mmHg) was used in seven patients. Prophylactic tocolytics were used in seven patients, with transient postoperative preterm labor observed in one. There were no open conversions, preterm deliveries, fetal loss, teratogenicity, or maternal morbidity. Conclusions: In past years, symptomatic gallstones during pregnancy were managed conservatively or with open cholecystectomy. LC is a feasible and safe method for treating severely symptomatic patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004649900643
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  • 3
    Electronic Resource
    Electronic Resource
    The molecular structure of the antidiuretic hormone elicited water channel (1993)
    Springer
    Pediatric nephrology 7 (1993), S. 680-684 
    Details
    ISSN: 1432-198X
    Keywords: Water transport ; Epithelial ; Antidiuretic hormone ; Vasopressin ; CHIP-28
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Measurements of osmotic water permeability (Pf) have shown that the plasma membranes of human red cells and certain epithelial cells possess specialized water channels. Although these water channels have been characterized extensively using biophysical techniques, the proteins that compose these unique channels have only recently been identified. Antidiuretic hormone (ADH) stimulation rapidly increases collecting duct epithelial cell Pf by fusion of water channel-containing vesicles (WCV) with their apical membranes. The proteins of WCV from toad bladder and rodent kidney have been characterized. The principal proteins in toad bladder WCV are 55,000 daltons (55 kDa) and 53 kDa and span the lipid bilayer of these vesicles. Polyclonal antisera raised against the 55-kDa and 53-kDa proteins inhibit ADH-stimulated toad bladder Pf by 80% and recognize protein bands of 46, 38 and 30 kDa in mouse kidney. Purification of WCV from rat kidney reveals enrichment of the 46-kDa protein. Recently, a 28-kDa integral membrane protein (called CHIP-28) has been isolated from human red cells. It forms functional water channels inXenopus oocytes and when reconstituted into proteoliposomes. Large amounts of CHIP-28 protein are present in epithelial cells of the proximal tubule and descending thin limb of Henle's loop. Molecular cloning efforts are underway to elucidate the structure and function of these candidate water channel proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00852578
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    Paper (German National Licenses)
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