Cockett syndrome. Initial results with percutaneous treatment in 6 patients

Intimal hypertrophy with venous spur formation caused by compression of the left common iliac vein by the right common iliac artery is advanced as the etiology of the higher incidence of deep venous thrombosis involving the left leg. In most cases of left iliofemoral thrombosis no underlying compression syndrome is detected or treated because the left common iliac vein has to be cleared from thrombi before compression can be identified. A series of 6 consecutive retrospectively analyzed patients with acute left iliofemoral thrombosis is presented. In these patients a left iliac vein compression syndrome was detected after percutaneous intraluminal thrombolysis with Actilyse (rt-PA). This compression was successfully relieved by insertion of a wall stent. Percutaneous treatment of Cockett's syndrome seems an attractive alternative for conservative and/or surgical management.     

The mouse mutation sarcosinemia (sar) maps to chromosome 2 in a region homologous to human 9q33-q34

The autosomal recessive mouse mutation sarcosinemia (sar), which was discovered segregating in the progeny of a male whose premeiotic germ cells had been treated with the mutagen ethylnitrosourea, is characterized by a deficiency in sarcosine dehydrogenase activity. Using an intersubspecific cross, we mapped the sar locus to mouse chromosome 2, approximately 15-18 cM from the centromere. The genetic localization of this locus in the mouse allows the identification of a candidate region in human (9q33-q34) where the homologous disease should map.     

Staff security and work pressure: contrasting patterns of stability and change across five dialysis units

We have previously shown that extracellular ATP, like norepinephrine (NE) and many other hypertrophy-inducing agents, increases expression of the immediate-early genes c-fos and junB in cultured neonatal cardiac myocytes but that the intracellular signaling pathways activated by ATP and responsible for these changes differ from those stimulated by NE. Furthermore, whereas NE increases incorporation of [14C]phenylalanine (14C-Phe) and cell size in neonatal cardiomyocytes, ATP does not. Since ATP is coreleased with NE from sympathetic nerve endings in the heart, we investigated whether ATP could modulate cardiac hypertrophy induced by adrenergic agonists, such as NE. We report in the present study that extracellular ATP inhibited the increase in incorporation of 14C-Phe into cellular protein and the increase in cell size in neonatal rat cardiac myocytes that was induced by NE, phenylephrine (PE), basic fibroblast growth factor, or endothelin-1. This inhibition was dose dependent, occurred predominantly through P2 purinergic receptors, and was observed even when cells were treated with ATP for as little as 1 hour before the addition of the hypertrophy-inducing agent. ATP also selectively affected changes in gene expression associated with hypertrophy. It prevented PE-stimulated increases in atrial natriuretic factor and myosin light chain-2 mRNA levels, while appearing to augment basal and PE-stimulated skeletal alpha-actin mRNA levels. ATP alone increased sarcoplasmic reticulum Ca2+-ATPase mRNA levels but had no effect when added with PE. ATP did not significantly affect the level of the constitutively expressed mRNA for GAPDH. Neither the PE-stimulated increase in immediate-early gene expression nor the initial induction of mitogen-activated protein kinase activity by PE was inhibited by ATP. These results demonstrate that extracellular ATP can inhibit hypertrophic growth of neonatal cardiac myocytes and differentially alter the changes in gene expression that accompany hypertrophy.     

Differences on post-thawing survival between ovine morulae and blastocysts cryopreserved with ethylene glycol or glycerol

Embryos were collected on Days 5 and 6 after breeding to investigate the effectiveness of ethylene glycol (ETG) and glycerol (GLY) as cryoprotectants of sheep morulae and blastocysts and to determine their optimum stage of development for cryopreservation. Only excellent (grade 1) and good (grade 2) embryos (196 morulae and 188 blastocysts) were incubated in increasing concentrations of GLY or ETG and submitted to a slow-freezing and quick-thawing procedure. Both cryoprotectants were removed using 0.25 M sucrose solution, and then embryos were cultured or transferred to determine their viability. Freezing medium containing ETG yielded higher in vitro survival rates (P < 0.01) than medium containing GLY (64.6% vs 16.0%); the difference between cryoprotectants was greater when morulae were used (57.9% vs 4.2%, P < 0.005) as compared with blastocysts (70.4% vs 21.5%, P < 0.05). There was a strong interaction between type of cryoprotectant and embryo stage (P < 0.005). After transfer of morphologically viable embryos, the in vivo development rate of embryos frozen with ETG was also higher than that of embryos frozen with GLY (45.5% vs 27.7%, P < 0.05). There were no significant differences in the number of lambs born among procedures and embryo stage, though the lowest lambing rate was obtained with morulae frozen with GLY (21.4%). Similar lambing rates were produced when blastocysts were frozen with either GLY or ETG (36.6% vs 43.0%). The best embryo survival after thawing was observed when blastocysts were frozen with ETG as cryoprotectant.     

Quantitative brain magnetic resonance imaging in attention-deficit hyperactivity disorder

BACKGROUND: Anatomic magnetic resonance imaging (MRI) studies of attention-deficit hyperactivity disorder (ADHD) have been limited by small samples or measurement of single brain regions. Since the neuropsychological deficits in ADHD implicate a network linking basal ganglia and frontal regions, 12 subcortical and cortical regions and their symmetries were measured to determine if these structures best distinguished ADHD. METHODS: Anatomic brain MRIs for 57 boys with ADHD and 55 healthy matched controls, aged 5 to 18 years, were obtained using a 1.5-T scanner with contiguous 2-mm sections. Volumetric measures of the cerebrum, caudate nucleus, putamen, globus pallidus, amygdala, hippocampus, temporal lobe, cerebellum; a measure of prefrontal cortex; and related right-left asymmetries were examined along with midsagittal area measures of the cerebellum and corpus callosum. Interrater reliabilities were .82 or greater for all MRI measures. RESULTS: Subjects with ADHD had a 4.7% smaller total cerebral volume (P = .02). Analysis of covariance for total cerebral volume demonstrated a significant loss of normal right > left asymmetry in the caudate (P = .006), smaller right globus pallidus (P = .005), smaller right anterior frontal region (P = .02), smaller cerebellum (P = .05), and reversal of normal lateral ventricular asymmetry (P = .03) in the ADHD group. The normal age-related decrease in caudate volume was not seen, and increases in lateral ventricular volumes were significantly diminished in ADHD. CONCLUSION: This first comprehensive morphometric analysis is consistent with hypothesized dysfunction of right-sided prefrontal-striatal systems in ADHD.     

Factors which alter the relationship between ventilation and carbon dioxide production during exercise in normal subjects

The slope of the linear relationship between ventilation (V(E)) and carbon dioxide production (VC0(2)) has been thought to indicate that VC0(2) is one of the major stimuli to V(E). A group of 15 normal subjects undertook different incremental treadmill exercise protocols to explore the relationship between V(E) and VCO(2). An incremental protocol using 1 instead of 3-min stages of exercise resulted in an increase in the V E to VCO(2) ratio [26.84 (SEM 1.23) vs 31.08 (SEM 1.36) (P <0.008) for the first stage, 25.24 (SEM 0.86) vs 27.83 (SEM 0.91) (P <0.005) for the second stage and 23.90 (SEM 0.86) vs 26.34 (SEM 0.81) (P = 0.001) for the third stage]. Voluntary hyperventilation to double the control level of V(E) during exercise resulted in an increase in the V(E) to VCO(2) slope [from 21.3 (SEM 0.71) for the control run to 35.1 (SEM 1.2) for the hyperventilation run (P <0.001)]. Prolonged hyperventilation (5 min) during exercise at stage 2 of the Bruce protocol resulted in a continued elevation of VCO(2) and the V(E)/VCO(2) slope. A steady state of V(E) and metabolic gas exchange can only be said to have been present after at least 3 min of exercise. Voluntary hyperventilation increased the slope of the relationship between V(E) and VCO(2). End-tidal carbon dioxide fell, but remained within the normal range. These results would suggest that a non-carbon dioxide factor may have been responsible for the increase we found in V(E) during exercise, and that factors other than increased dead space ventilation can cause an increased ventilation to VCO(2) slope, such as that seen in some pathophysiological conditions, such as chronic heart failure.     

Reconstructive spine surgery in pediatric patients with major loss in vital capacity

The effects of exogenenous monoaminergic neurotransmitters (norepinephrine, NE; epinephrine, E; dopamine, DA and 5-HT) and inhibin alpha N-terminal fragments P32 (1-32), P32-Tyr on P4 production by incubated rat CL cells were studied. The results demonstrated that: (1) alpha fragments caused significant inhibition on P4 production. (2) 0.1 mmol/L NE (or E) and 10 mumol/L DA produced a marked increase in both basal and hCG induced P4 production by CL cells (P < 0.001). The rank orders of potency of the catecholamines in stimulating P4 production were different, for basal P4 production, NE > E > DA; but for hCG induced P4 production, DA > E > NE, i.e. the order just reversed. Addition of P32-Tyr significantly neutrolized the stimulatory action of E, but only slightly increased the action of NE. (3) alpha receptor blocker phentolamine and beta receptor blocker propranolol were effective in decreasing basal and hCG-induced P4 production, the latter being more effective than the former. It was further shown that both blockers augmented the inhibitory effect of alpha-fragments on P4 production. (4) Unlike NE, E, and DA, 5-HT at 0.5 mumol/L exerted inhibitory effect on the basal and hCG-induced P4 production, but profoundly supressed the inhibitory effect of alpha-fragments on P4 production. The above results suggested: (1) Adrenergic, DA and 5-HT receptors are present in rat CL, where catecholamine might exert a stimulating effect on basal and hCG-induced P4 production via different pathways. (2) The inhibitory effect of P32, P32-Tyr on P4 production might be related to their inhibition by partial blocking alpha/beta receptors, which were antagnized by 5-HT. (3) The action of P32, P32-TYr on P4 production is brought on the participation of neurotransmitters NE, E, DA and 5-HT.