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F Lammert

Publications and source records attributed to F Lammert.

45 records · Page 3Linked to original sources
PubMed1998

Biliary secretory immunoglobulin A is a major constituent of the new group of cholesterol crystal-binding proteins.

BACKGROUND & AIMS: Recently we described a new group of lectin-bound biliary proteins that bind to cholesterol crystals, modify crystal morphology, and inhibit cholesterol crystallization. The aim of the current study was to characterize and identify individual members of this group of cholesterol crystal-binding proteins. METHODS: Crystal-binding proteins were purified from human gallbladder bile by lectin affinity chromatography and preparative gel electrophoresis. Purified crystal-binding proteins were characterized by using cholesterol crystal-growth assays, immunoblotting, and amino acid analysis. For comparison, identified biliary proteins were isolated from gallbladder bile by lectin affinity and immunoaffinity chromatography. RESULTS: The individual crystal-binding proteins with molecular weights of 74, 63, and 28 kilodaltons inhibited cholesterol crystallization in a dose-dependent manner (2.5-10 micrograms/mL). Immunoblotting with specific antibodies and N-terminal amino acid sequences revealed that the 74-kilodalton crystal-binding protein is the secretory component, the 63-kilodalton protein is the heavy chain, and the 28-kilodalton protein is the light chain of human secretory immunoglobulin (Ig) A. Isolated biliary IgA showed a potent inhibitory effect on cholesterol crystallization in model bile even at levels less than physiological concentrations (1-100 micrograms/mL). CONCLUSIONS: Biliary secretory IgA is a major constituent of the previously described group of cholesterol crystal-binding proteins. Crystal-binding IgA may be an important modulator of crystal agglomeration into stones and stone growth in vivo.

Amino Acid Sequence↗
PubMed1997

[Hepatic diseases caused by drugs].

Drug-induced hepatotoxicity covers the clinical and pathological expressions of almost any acute or chronic liver disease. Liver damage is due to intrinsic toxicity of the drug (paracetamol) and/or immunoallergic mechanisms (halothane). Acute injury may be cytotoxic or cholestatic. Cytotoxic injury is characterized by necrosis (paracetamol, halothane) or steatosis (valproate). Cholestatic injury can be associated with immune-mediated portal inflammation (chlorpromazine) or solely attributed to inhibition of transport systems (cyclosporin A). Chronic drug-induced disorders include chronic active hepatitis (methyldopa), autoimmune hepatitis (tienilic acid), alcoholic steatohepatitis-like reactions (amiodarone), indolent fibrosis (methotrexate), chronic cholestatic diseases, vascular lesions, and hepatic neoplasms. The clinical and morphological picture of many drug-induced liver diseases is nonspecific. Diagnosis is based on thorough drug history, temporal relationship, time-course of liver dysfunction, and the exclusion of other causes. Treatment consists of instant withdrawal of the suspected drug and administration of acetylcysteine as early as possible in case of paracetamol intoxication. Drug-induced liver diseases are usually reversible, but prolonged treatment leads to progression and liver cirrhosis.

Chemical and Drug Induced Liver Injury↗
PubMed1995

A new subgroup of lectin-bound biliary proteins binds to cholesterol crystals, modifies crystal morphology, and inhibits cholesterol crystallization.

Biliary proteins inhibiting or promoting cholesterol crystallization are assumed to play a major role in cholesterol gallstone pathogenesis. We now report a new group of biliary proteins that bind to cholesterol crystals, modify crystal morphology, and inhibit cholesterol crystallization. Various glycoprotein mixtures were extracted from abnormal human gallbladder bile using lectin affinity chromatography on concanavalin A, lentil, and Helix pomatia columns and were added to supersaturated model bile. Independent of the protein mixtures added, from the cholesterol crystals harvested, the same four GPs were isolated having molecular masses of 16, 28, 63, and 74 kD, respectively. Each protein was purified using preparative SDS-PAGE, and influence on cholesterol crystallization in model bile was tested at 10 microg/ml. Crystal growth was reduced by 76% (GP63), 65% (GP16), 55% (GP74), and 40% (GP28), respectively. Thus, these glycoproteins are the most potent biliary inhibitors of cholesterol crystallization known so far. Evidence that the inhibiting effect on cholesterol crystallization is mediated via protein-crystal interaction was further provided from scanning electron microscopy studies. Crystals grown in presence of inhibiting proteins showed significantly more ordered structures. Incidence of triclinic crystals and regular aggregates was shifted from 30 to 70% compared with controls. These observations may have important implications for understanding the role of biliary proteins in cholesterol crystallization and gallstone pathogenesis.

Analysis of Variance↗
PubMed1982

[Relations between the nasopharynx, eustachian tube distance and maxillary shape].

The results of measurements of the impressions of palate and nasopharynx are compared. While choanes, anterior and medial nasopharynx grow in relation to age, the posterior width correlates with measurements of the maxilla, especially with the distance of molars and premolars. This means that in persons with wide maxillary dimensions, a wide nasopharynx can be expected. This fact may influence the indication for tubal therapy and otosurgery, since a narrow nasopharynx implies poor conditions for the aeration of the Eustachian tube.

Adolescent↗
PubMed1980

[Morphology and growth of the nasopharynx from three years to maturity (author's transl)].

The nasopharynges of 80 adults and children were examined by a specific technique. An impression was taken for a precision plaster model to allow measurement and analysis. In this manner it was possible for the first time to describe spatial relationship and growth of the nasopharynx. The vertical height increases steadily up to the age of 9 years when addition of the adenoids seems to interrupt the growth of the nasopharynx. From then on, the height continues to increase until old age. This increase in mature patients can be attributed to alterations resulting from loss of teeth or maxillary deformation caused by atrophia senilis. The depth shows wide variations, growth was observed with increasing age. The width, i.e., the distance between the eustachian tubes, does not increase. This is due to enlargement of the tubes and increase of the prominentia tubae. The cross-sectional area of the choanae available for air flow increases steadily up to 380 mm2. The volume of the nasopharynx increased in our sample from 2.4 to 6.8 mm3 which represents a factor of 2.8 over the initial size.

Adenoids↗
PubMedDate not supplied

Relationship between bolus transit and LES-relaxation studied with concurrent impedance and manometry.

BACKGROUND/AIMS: Neuromuscular mechanisms regulating esophageal bolus transport are well studied. However, detailed data about the relationship between bolus transit and lower esophageal sphincter (LES)-relaxation during conventional motility testing are still lacking. METHODOLOGY: We performed systematic studies in 25 normal subjects, employing a catheter that integrates the two techniques impedancometry and manometry in a single instrument for simultaneous recording and analysis of the relationship between bolus transit and LES relaxation after swallowing saline or yogurt. RESULTS: 195 swallows were analyzed. LES relaxation occurred frequently later than UES relaxation. The mean latency between bolus entry into the esophagus and LES relaxation was 3.6 +0.2 sec. Two types of swallow-induced LES relaxation were observed: (a) LES relaxation preceding bolus transit (46 cases or 24%) and (b) LES relaxation occurring during bolus transit (149 cases or 76%). In the later case, during 114 (76%) cases of this deglutition, the position of the bolus was very close to the LES. CONCLUSIONS: During deglutition, LES relaxation seems to be modulated by bolus transit and occurs predominantly upon arrival of the bolus in the distal esophagus.

Adult↗