[Clinical analysis of 15 cases of primary thrombocytosis (author's transl)].
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Biomedical subjects
Publications and source records attributed to A Zhang.
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The acute effects of ethanol on intracellular free magnesium ions ([Mg2+]i) in cultured canine cerebral vascular smooth muscle cells (VSMCs) were studied by digital imaging microscopy using the Mg2+ fluorescent probe mag-fura-2. In 0 mM ethanol, the basal level of [Mg2+]i was between 500-700 microM with a heterogeneous distribution within the cells; [Mg2+]i was greater in the perinuclear than in the peripheral region. Treatment of the cells with 10, 25, and 100 mM ethanol resulted in rapid (within 30 s) concentration-dependent reduction in [Mg2+]i; the greater the concentration and the greater the duration of acute exposure, the greater the fall in [Mg2+]i. Exposure of cerebral VSMCs to 100 mM ethanol resulted in a 57% reduction in [Mg2+]i (i.e., from 510 +/- 40 to 220 +/- 30 microM). These observations are consistent with the tenet that "binge drinking" of ethanol could result in cerebrovasospasm, ischemia, and rupture of cerebral blood vessels as a consequence of depletion of cerebral VSMC [Mg2+]i. Deficits in [Mg2+]i, O2, and nutrient delivery could account in part for some of the behavioral actions of alcohol.
Acute effects of a series of alcohols (methanol, ethanol, n-butanol) on intracellular free magnesium concentration ([Mg2+]i) in canine cerebral vascular smooth muscle cells was studied using mag-fura-2 and digital imaging microscopy. In 1.2 mM [Mg2+]o, basal [Mg2+]i was 500 +/- 30 microM. Exposure of cells to a low concentration (25 mM) of ethanol, but not methanol, for only 30 s resulted in significant loss of [Mg2+]i. Exposure to 100 mM methanol, ethanol, and butanol for 30 s resulted in a relative order of potency for [Mg2+]i depletion, where butanol >> ethanol > methanol. The heterogeneous and relative subcellular compartmented concentrations of [Mg2+]i, where perinuclear > nuclear >> peripheral (cytosolic) region, was not significantly altered by the alcohols. The degree of cellular depletion of [Mg2+]i was directly a function of each alcohol's partition coefficient and chain length. The latter is suggestive of the probability that alcohols promote intracellular depletion of Mg2+ by partitioning in membranes and disordering lipid bilayers.
The influence of chronic treatment of cultured canine cerebral vascular smooth muscle cells, with low concentrations of ethanol, on the intracellular concentrations of free calcium ([Ca2+]i) was studied by use of the fluorescent indicator, fura-2, and digital imaging microscopy. The resting level of [Ca2+]i in the cerebral vascular smooth muscle cells was 89 +/- 3.2 nM. Exposure of these cells to 10 and 25 mM ethanol for 5 days resulted in significant elevation of [Ca2+]i (mean rises to 208 +/- 11.4 and 307 +/- 14.0 nM, respectively), and potentiated the transient rise in [Ca2+]i induced by 10(-7) M PGF2 alpha. However, exposure of these cerebral cells to a high-concentration ethanol (100 mM) resulted in only a slight increase of [Ca2+]i (106 +/- 6.9 nM) and lack of effects on the [Ca2+]i response to PGF2 alpha. Irrespective of the different ethanol treatments, the subcellular distribution of [Ca2+]i was heterogeneous in all the cells tested. Our data suggest that chronic exposure of cerebral vascular smooth muscle cells to ethanol, particularly at low concentrations, results in dramatic increases in [Ca2+]i and the responses of these vascular smooth muscle cells to prostanoids. These results support an hypothesis whereby ethanol induces stroke by causing spasm and rupture of cerebral blood vessels as a consequence of large rises in intracellular Ca2+.
A rare variant of 6q11+ heteromorphism was found in a fetus and the mother during amniocentesis. The G- and Q-banding and DA/DAPI stain were negative. The C-banding was positive and the C-banded segment was 3-fold longer in the variant than in its homologue. Neither of the C-banded regions of chromosomes 6 decondensed when exposed to distamycin A or 5-azacytidine. A DNA replication study indicated that the C-banded variant was late replicating. The lateral asymmetry observed in the 6q11 variant after one replication cycle in 5-bromodeoxyuridine may result from an unequal interstrand distribution of thymidine in the repetitive DNA. Fluorescent in situ hybridization using a chromosome-6-specific alpha-satellite probe (D6Z1) demonstrated hybridization signals on the centromere of chromosome 6. The 6q11 variant showed a signal which was 3-fold larger than its homologue. These results indicate that the 6q11 variant is an amplification of a chromosome-6-specific alpha repeat, and the size of the hybridization signal correlates with the size of the laterally asymmetric and C-banded region.
The authors developed a noninvasive two-channel dynamic dermofluorometer that can quantitatively follow the rapid skin wash-in kinetics of a fluorescent dye to provide an assessment of local skin perfusion. The dermofluorometer was tested in normal subjects and diabetic patients with and without peripheral vascular disease. After an intravenous injection of 1-2 mL of a 10% solution of sodium fluorescein (1.1-2.8 mg/kg), the fluorescent signal was monitored from two sites on the skin surfaces of the forearm and foot. A 3.2-mm-diameter glass fiberoptic bundle was used both to transmit the excitation light (489 nm) and to receive the fluorescent emission (517 nm). Dermofluorometer readings were recorded approximately every second for 10-15 minutes following the injection. The time course of the fluorescein signal intensity was fit to a single exponential curve characterized by a wash-in time constant. There was no significant difference in arm wash-in time constants. Foot wash-in time constants were increased in diabetic patients who had past histories of foot ulcers relative to diabetic patients without a history of foot ulcers (3.2 vs 1.6 min., p < 0.05). Foot wash-in time constants were decreased in diabetic patients who had active infected foot ulcers. This study demonstrates the ability of the dynamic dermofluorometer to measure wash-in constants that reflect the local skin perfusion in less than 15 minutes after a low intravenous dose of sodium fluorescein.