Previous studies on alpha-lactalbumin induced fusion of phosphatidylserine/phosphatidylethanolamine vesicles are extended to vesicles composed of various combinations of phosphatidylserine, phosphatidylethanolamine, phosphatidylcholine and cardiolipin. It was found that inclusion of phosphatidylcholine in the vesicles results in a depression of fusion. This depression of fusion appears to be caused by a reduction in the amount of irreversibly bound alpha-lactalbumin to vesicles containing phosphatidylcholine. It is suggested that in this system fusion is dependent upon the extent by which a particular protein segment penetrates the bilayer.

Hydrogen-Ion Concentration↗

PubMed1989

Penetration and fusion of phospholipid vesicles by lysozyme.

The lysozyme-induced fusion of phosphatidylserine/phosphatidylethanolamine vesicles as studied at a wide range of pH is found to correlate well with the binding of this protein to the vesicles. An identical 6000 molecular weight segment of lysozyme at the N-terminal region is found to be protected from tryptic digestion when initially incubated with vesicles at several pH values. Only this segment is labeled by dansyl chloride, which is partitioned into the bilayer. These results suggest the penetration of one segment of lysozyme into the bilayer. Photoactivated labeling of the membrane-penetrating segment of lysozyme with 3-(trifluoromethyl)-3-([125I]iodophenyl)diazirine ([125I]TID) and subsequent identification of the labeled residues by Edman degradation and gamma-ray counting indicate that four amino acids from the N-terminal are located outside the hydrophobic core of the bilayer. Although treatment of the membrane-embedded segment with aminopeptidase failed to cleave any amino acids from the N-terminal, it appears that a loop of lysozyme segment near the N-terminal penetrates into the bilayer at acidic pH. A helical wheel diagram shows that the labeling is done mainly on one surface of the alpha-helix. The penetration kinetics as studied by time-dependent [125I]TID labeling coincide with the fusion kinetics, strongly suggesting that the penetration of the lysozyme segment into the vesicles is the cause of the fusion.

Amino Acid Sequence↗

PubMed1989

Extracellular potassium activity and axonal conduction in spinal cord of the myelin-deficient mutant rat.

We recorded somatosensory evoked potentials SEPs), extracellular K+ ionic activity ([K+]e), and K+ clearance rates in the spinal cords of 14 myelin-deficient mutant rats and 16 normal male littermates at 16-41 days after birth. Tested under pentobarbital anesthesia (25 mg/kg ip) and hypothermic conditions (32-34 degrees C), myelin-deficient rats had longer cortical SEP latencies (67 +/- 20 ms) compared to those in normal siblings (48 +/- 15 ms; P less than 0.05). Mean baseline [K+]e levels were 2.6 +/- 0.5 mM in myelin-deficient rats and 2.6 +/- 0.8 mM in normal siblings. Clearance times of KCl solutions injected into the spinal cord were biphasic and exponential. The mean initial and secondary exponential half-times were 1.0 +/- 0.5 and 2.7 +/- 1.7 min for myelin-deficient rats and 0.8 +/- 0.4 and 3.8 +/- 3.2 min for normal siblings. Repetitive sciatic nerve stimulation (2-20 Hz, 2- to 6-s trains) produced 1-3 mM transient [K+]e rises in thoracic and lumbar cords of myelin-deficient rats. The [K+]e rises were largest in the dorsal spinal cord at 200-500 microns depth. The normal siblings had smaller or no stimulus-induced [K+]e rises. In myelin-deficient rats, injection of 1 mM 4-aminopyridine (4-AP) solution into the thoracic spinal cord completely suppressed the stimulus-induced [K+]e and markedly increased spinal and cortical SEP amplitudes for several hours. In the normal siblings, the 4-AP injections transiently blocked spinal conduction for 20-30 min but thereafter enhanced cortical SEP amplitudes for 2-3 h. We conclude that sciatic nerve stimulation produces spinal cord [K+]e rises in myelin-deficient rat larger than those in the normal siblings, that the [K+]e transients represent increased K+ release rather than impaired K+ clearance, and that the K+ ions come from 4-AP blockable sources.

4-Aminopyridine↗

PubMed1989

Atrial natriuretic peptide in patients with obstructive uropathy.

Renal response to release of bilateral ureteral obstruction resembles that to intravenous administration of atrial natriuretic peptide. In a prospective study we measured plasma atrial natriuretic peptide levels before and serially after relief of obstruction in 9 patients (mean age 65 +/- 2 years old) with bilateral ureteral obstruction and azotemia. Obstruction was documented by renal ultrasonography. Before relief of obstruction blood urea nitrogen and serum creatinine levels were 85 +/- 18 (mean +/- standard error) and 8.2 +/- 1.3 mg. per dl., respectively, accompanied by metabolic acidosis but not hyperkalemia. Mean plasma atrial natriuretic peptide (measured by radioimmunoassay) was 129 +/- 28, which was markedly elevated compared to 46 +/- 7 pg. per ml. in 7 age-matched control subjects (p less than 0.01). After relief of obstruction, prominent post-obstructive diuresis and natriuresis ensued; the plasma atrial natriuretic peptide level progressively decreased to that noted in the control group, accompanied by improvement in renal function, and diminishing diuresis and natriuresis. These findings were associated with a significant weight loss and an increase in plasma renin activity (from a mean of 1.57 +/- 0.68 to 5.27 +/- 1.82 ng. per ml. per hour, p less than 0.01). These results suggest that atrial natriuretic peptide release is augmented in patients with bilateral ureteral obstruction and azotemia, probably due to hypervolemia, and may contribute to post-obstructive diuresis and natriuresis.

Atrial Natriuretic Factor↗

PubMed1989

Ovalbumin-induced fusion of acidic phospholipid vesicles at low pH.

The interactions of ovalbumin (OA) with large unilamellar vesicles (LUV) of phosphatidylserine (PS) and PS/phosphatidylethanolamine (PE) were studied. It was observed that OA induces aggregation, destabilization, and fusion of these LUV composed of acidic phospholipids at low pH levels. The fusion of LUV by OA was monitored by measuring the intermixing of internal aqueous contents of vesicles, by resonance energy transfer assay which follows the mixing of the membrane components, and by thin-sectioning electron microscopy. The pH profile of fusion was found to be similar to the pH-dependent binding of OA to the same phospholipid vesicles. Proteolytic digestion and hydrophobic labeling with dansyl chloride and photoreactive phosphatidylcholine (PC) of the OA-vesicle complex showed that a segment of OA with a molecular weight of approximately 2,500 penetrates the bilayer. The amino acid composition of this segment indicated that it is the 291-322 fragment and not the putative signal sequence.

Amino Acids↗

PubMed1989

Interaction of human apolipoprotein A-I with dipalmitoylphosphatidylcholine in vesicular and micellar complexes.

The interactions of human apolipoprotein A-I (apo A-I) with dipalmitoylphosphatidylcholine (DPPC) in vesicular complexes at low protein concentrations and in micellar complexes at high protein concentrations are compared. The C-terminal segment of this protein, with a relative molecular weight (Mr) of about 11,000, is protected on trypsin treatment of apo A-I-vesicle complexes. A segment within the sequence from Leu-189 to Arg-215 of apo A-I penetrates the hydrophobic interior of the membrane, as found in a hydrophobic labeling experiment involving 3-(trifluoromethyl)-3-(m-[125I]iodophenyl)-diazirine ([125I]TID). No appreciable stretch of apo A-I in micellar complexes was found to be protected from the tryptic digestion. This indicates that the interactions of apo A-I with lipids in the vesicular and micellar complexes are different. The binding equilibrium of apo A-I as to DPPC vesicles at low protein concentrations, as studied by hydrophobic labeling of the bilayer-penetrating segment, is reached within about 1 h, while the formation of micellar complexes at high protein concentrations takes about 24 h at 42 degrees C. Time-dependent labeling studies involving photoreactive phosphatidylcholine (PC) with high apo A-I concentrations suggested an initial interaction with the head group region of the bilayer followed by interaction with the tail ends of the acyl chains of the lipid. A possible mechanism for the micellization process is discussed.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1989

Hepatoma presenting as extrahepatic biliary obstruction due to hemobilia.

A case of hepatoma presenting as extrahepatic biliary obstruction due to hemobilia is reported. The patient, a 49-year-old woman, developed jaundice of the obstructive type after a history of B-viral hepatitis. On laparotomy, the liver revealed macronodular cirrhosis without any noticeable mass. A 4-cm sized friable tissue and blood clots were identified within the distended left hepatic duct. Pathologic examination of this tissue confirmed the diagnosis of hepatocellular carcinoma extended in the hepatic duct.

Biopsy↗

PubMed1989

A case of hyperinfection with strongyloides stercoralis in an immunosuppressed patient.

We experienced a case of hyperinfection with strongyloides stercoralis in a 64-year-old housewife who complained of severe epigastric pain associated with nausea, vomiting and general weakness for the period of one month. She received corticosteroid therapy for several months because of arthritis prior to admission. The diagnosis was confirmed by examination of gastroduodenal juice and gastrofiberoscopic biopsy. Stool examinations disclosed an abundance of the adult form of strongyloides stercoralis. Albendazole was given for treatment. The patient expired on the 79th hospital day.

Adrenal Cortex Hormones↗

PubMed1989

The effects of the alpha 1-adrenergic antagonists terazosin and phentolamine on prostatic adenoma and urethra in vitro.

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Adenoma↗

PubMed1989

Hamartoma of the urachal remnant.

A case of urachal hamartoma occurred in the urinary bladder of a 45-year-old woman, whose presenting symptoms were frequent urination and nocturia. Computed tomographic and contrast radiologic examinations demonstrated a broad-based 5-cm polypoid mass at the dome of the bladder. Grossly the polypoid mass was smooth surfaced and covered by innocent transitional epithelium. The mass and the underlying bladder wall consisted of multiple cystic cavities of various sizes and hyperplastic smooth-muscle bundles. Light microscopy identified numerous tubuloglandular structures, most of them lined by transitional cell epithelium. Simple or ciliated columnar cells and occasional mucous cells were also present, particularly in the epithelium of cystic cavities. Some tubules had communicated with the bladder lumen. Hamartoma of the urachal remnant should be included in the differential diagnosis of urachal and bladder tumors.

Female↗