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We report two cases of multiple fetal anomalies detected by prenatal ultrasound and associated with subtle subtelomeric chromosomal rearrangements. The first case presented at 25 weeks of gestation with an enlarged cisterna magna and ventriculomegaly. Karyotyping of amniocytes showed a subtle terminal abnormality of chromosome 6q. Thereafter, screening of all unique chromosomal subtelomeric regions using a panel of telomere-specific, fluorescence in situ hybridization (FISH) probes revealed an unbalanced reciprocal translocation between 6q and 17p [46,XX.ish der(6)t(6;17)(q25.3;p13)(TelVysion6q-;TelVysion17p+)]. The second case presented at 25 weeks of gestation with tetralogy of Fallot and at 34 weeks of gestation had additional ultrasound findings of an arachnoid cyst and intrauterine growth restriction. Postnatal karyotyping of peripheral blood was performed and appeared normal. However, a cryptic deletion of the subtelomeric region of the long arm of chromosome 14 was identified when the infant's blood sample was used as a control for an oncology FISH probe. Thereafter, screening of all unique chromosomal subtelomeric regions using a panel of telomere-specific FISH probes revealed an unbalanced reciprocal translocation of chromosomes 14q and 20p [46,XY.ish der(14)t(14;20)(q32.3;p13)(IGH-, D14S308-,TelVysion20p+)mat]. These two cases add to a growing number of reports of cryptic subtelomeric chromosomal rearrangements associated with congenital anomalies. This is the first report of multiple, simultaneous FISH screening of the subtelomeric regions in amniotic fluid and has demonstrated the technical feasibility of this technique in the prenatal period.

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The chromosome abnormalities observed in a dedifferentiated chondrosarcoma are reported. A new molecular cytogenetic technique, spectral karyotyping, was used to identify and confirm structural rearrangements in this case. A review of the literature revealed that nine cases have been reported, in eight of which a complete description of the cytogenetic abnormalities was described. Structural aberrations were most frequently reported in chromosomes 1 and 9, and chromosomes 7 and 19 were most frequently observed to be involved in numerical aberrations (trisomy and tetrasomy). In chondrosarcomas, structural aberrations in chromosomes 1 and 9 and trisomy or tetrasomy of chromosome 7 are among the more frequently observed aberrations.

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Congestive heart failure (CHF) is a rapidly growing and expensive cardiovascular disorder. Conventional care for CHF is ineffective and results in a cycle of "crisis management" that includes repeated emergency department visits, hospitalizations, and physician visits. Recently, a number of outpatient coronary care centers that provide consistent, aggressive outpatient therapies and extensive patient education have emerged and are successfully breaking this cycle of dependence on hospital services. One such effort is the Heart Institute's Heart Failure Center, the result of a partnership between a private-practice cardiology group and our tertiary-care medical center. Our program includes not only patient education and outpatient infusions of inotropic agents, but an electronic linkage to the emergency department and home healthcare services. Preliminary data show that 16 months after the program was initiated, hospital admissions decreased by 30%, hospital days by 42% and average length of stay by 17%. An effective outpatient heart failure program can alleviate the economic burden of CHF and improve the quality of patient care.

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Magnocellular neurones in the supraoptic nucleus of the hypothalamus are usually separated by neuropil and glial elements. In lactating animals, however, the surface membranes of many neurosecretory somata and dendrites are frequently in direct apposition, without any glial interposition. A significant number of such neurones are also bridged by the same presynaptic terminal ("double synapses"). As the supraoptic nucleus is composed of two types of neurosecretory cell, secreting either oxytocin or vasopressin, we carried out comparative quantitative analyses on identified supraoptic neurones of virgin and lactating rats to determine which neurones were affected by the structural changes and to what extent. The neurones were identified in: (i) normal and Brattleboro homozygote rats by electron microscopic immunocytochemistry (pre- and post-embedding procedures) using antisera raised against oxytocin, vasopressin and oxytocin-related neurophysin I, and (ii) in homozygous Brattleboro rats by their neuronal content of approximately 170 nm neurosecretory granules. We report here that, in virgin animals under normal conditions, a small proportion of both types of neurone show neuronal appositions. At lactation, neuronal appositions are far more numerous and extensive, as are "double synapses". These changes affect exclusively the oxytocinergic neurones. The increased appositions cannot result solely from glial retraction because the hypertrophied oxytocin cells have a greater absolute, though smaller proportional, coverage by glial processes than cells in the control animals. From the present observations, and those obtained in chronically dehydrated animals (see accompanying article), it is clear that the plastic changes in the supraoptic nucleus are closely related to the activity of its oxytocinergic neurones. During lactation, these structural modifications may serve to facilitate and maintain the characteristic synchronized electrical activity of these neurones at milk ejection. On a few occasions, we also found appositions between one oxytocinergic and one vasopressinergic neurone, which may account for the rare cases of electrophysiological interactions between the two types of cell.

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A comparative quantitative analysis was carried out on identified supraoptic neurones of male and female Wistar and Long Evans rats under normal conditions and after chronic osmotic stimulation, and in homozygous Brattleboro rats suffering from diabetes insipidus. The neurones were identified by immunocytochemical or morphological means. Osmotic stimulation resulted in significant increases in the number and extent of direct neuronal appositions and in the number of presynaptic terminals contacting two neurosecretory cells simultaneously ("double" synapses). In the supraoptic nuclei of both sexes these increases were restricted to the oxytocin secreting neurones. In Brattleboro homozygous rats treated with vasopressin, the proportion of oxytocinergic neurones in apposition was not modified, but the number of appositions per soma profile decreased as did the incidence of "double" synapses. In nuclei of osmotically stimulated rats, increase in cell volume affected both types of neurosecretory cell and was accompanied by an increase of the absolute extent of glial coverage. However, the extent of glial coverage of the oxytocinergic neurones did not match the hypertrophy of the cells, resulting in a decrease in their relative glial coverage, compared to normal hydrated animals. The increased neuronal appositions, therefore, cannot result simply from a retraction of glial processes. The structural reorganization of the oxytocinergic system observed during chronic osmotic stimulation was as extensive as that observed at lactation. Moreover, the changes were as extensive in Wistar as in Brattleboro lactating rats, although the latter have an added osmotic stimulus. This implies that lactation and osmotic stimulation do not produce additive effects.(ABSTRACT TRUNCATED AT 250 WORDS)

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Magnocellular neurones in the supraoptic nucleus of the homozygous Brattleboro rat, which are unable to produce vasopressin, were investigated by immunocytochemistry to identify both the oxytocin cells and the abnormal neurones, which in normal animals would produce vasopressin. The abnormal cell profiles were significantly more rounded than those of the oxytocin cells. Both cell types showed evidence of hyperactivity, but the Golgi apparatus was more extensive in the oxytocin cells, probably as a result of the failure of the abnormal cells to produce vasopressin and its neurophysin and the resultant reduction in hormone packaging. Neurosecretory granules (NSG) 160 nm in diameter were found in the oxytocin perikarya but were absent from the abnormal cell bodies. In addition, a population of small dense granules (SDG) 100 nm in diameter was observed in both types of neurone, in numbers equal to the NSG in oxytocin cells. Injection of a low, non-lethal dose of the axonal transport inhibitor colchicine resulted in a rapid and equal accumulation of both NSG and SDG in oxytocin perikarya and of SDG in the abnormal perikarya after one day. The effects of colchicine were reversed 2-3 days after administration. The SDG, which may contain a co-transmitter or co-hormone substance, are thus produced at a similar rate to NSG, and appear to be transported from the perikarya for subsequent release at the nerve endings.

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The possibility that divalent cations may antagonize opiate peptide analgesia and stress-induced analgesia was examined. Intracerebroventricular injection of low doses of Ca2+, Mn2+ and Mg2+ antagonized beta-endorphin and methionine-enkephalin analgesia. Ba2+ and Cd2+ were without effect. The ionophore, A23187, significantly antagonized beta-endorphin analgesia and the effect was increased when a low dose of Ca2+ was injected at the same time as the ionophore. Ethylene glycol tetraacetic acid (but not ethylenediamine tetraacetic acid) significantly potentiated endorphin analgesia. Stress-induced analgesia, as determined by increased tail-flick latencies following intraperitoneal injection of acetic acid, was effectively antagonized by naloxone, Ca2+ and Mn2+. The frequency of writhing following acetic acid injection was increased by both naloxone and divalent metal ions, again suggesting antagonism of endogenous opiates. These results confirm previous findings indicating that divalent metal ions (and especially Ca2+) may be involved in the actions of opiates.

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Intracerebroventricular (i.c.v.) administration of subanalgesic doses of beta- and leucine-endorphin in mice 15 min before subcutaneous morphine injection, significantly enhanced the analgesic effects of the morphine as measured by the tail-flick assay. A similar effect was seen with levorphanol analgesia but not enhancement of leucine- or methionine-enkephalin analgesia by beta-endorphin was observed. The same doses of the endorphins did not affect the development of single-dose morphine tolerance and dependence. Leucine-enkephalin failed to affect morphine analgesia, tolerance or dependence development, while low doses of methionine-enkephalin administered i.c.v. were observed to have an antagonistic effect on morphine analgesia without affecting tolerance or dependence development. Neither endephalin had any effect on beta-endorphin analgesia.

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The surface properties of cells of Pseudomonas aeruginosa which are sensitive to gentamicin are markedly different from those which are resistant to gentamicin. Cells of four out of five strains in which gentamicin-resistance is R-factor-mediated have electrokinetic properties characteristic of gentamicin-sensitive cells. The surface properties of transconjugant strains are indistinguishable from those of the original acceptor strain. Cells of the remaining R-factor donor strain (which transferred very low gentamicin-resistance) exhibited surface properties characteristic of gentamicin-resistant cells. Gentamicin-resistance in cells of this strain is thus the result of at least two different mechanisms. The results are discussed in terms of possible alternative mechanisms of resistance.

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