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J Polak

Publications and source records attributed to J Polak.

At least 55 records · Page 3Linked to original sources
PubMed1994

Eating patterns of community-dwelling older adults: the Cardiovascular Health Study.

We analyzed eating patterns of 4643 adults (1988 men and 2655 women) aged 65 years and older at the time of their enrollment in the Cardiovascular Health Study. Diet was assessed with a qualitative, picture-sort food frequency questionnaire along with supplemental questions on other eating pattern variables. Consumption of high fat foods and low fiber foods was more frequent in older participants, men, minorities, and persons with body mass index > or = 30 kg/m2 and less common among persons who reported following self-prescribed or medically prescribed special diets. Few associations of consumption of specific food groups with disease status were identified. Participants with coronary heart disease, diabetes, hypertension, and cardiovascular disease were significantly more likely to report following a special diet and using low-calorie or low-sodium food products, however. Although the percentage of participants with prevalent disease who reported following special diets was relatively low from a clinical perspective, it was sufficiently high to suggest that controlling for dietary modifications may be important when attempting to identify associations of diet with prevalent disease in older populations.

Aged↗
PubMed1994

Variance mapping in colour flow imaging: what does it measure?

Flow disturbance is known to occur in association with high grade carotid stenosis and cause spectral broadening and fluttering in the Doppler spectral waveform distal to the stenosis. Colour flow variance mapping has been proposed as a means of documenting its presence. We prospectively evaluated this hypothesis by studying 15 patients with high grade (> 50%) stenotic lesions in the internal carotid artery. In all 15 cases, the site of increased variance on the colour Doppler map corresponded to the point of maximum velocity. In 10 cases of greater than 75% stenosis, the point of aliasing on the traditional colour Doppler map and the site of maximal variance occurred at the stenotic jet (length 7.3 +/- 2.3 mm) and not along the full length of disturbed flow (19.3 +/- 5.5 mm). In five patients with stenoses between 50-75% diameter narrowing, decreasing the colour Doppler pulse repetition frequency (PRF) created a region of abnormal variance corresponding to the site of aliasing. In all 15 stenoses, the site of maximum flow disturbance, defined as fluttering in the Doppler spectral waveform, was not apparent on the variance map. We conclude that the variance map does not reflect flow disturbance and is most likely to occur at sites of aliasing.

Aged↗
PubMed1994

Innervation of recurrent aphthous ulcers.

Specimens from nonkeratinized oral mucosa were obtained from diseased and clinically healthy mucosa from 7 patients with minor recurrent aphthous ulcers. The innervation of the specimens was visualized using antibodies to neuron-specific intermediate cytoskeletal neurofilament fiber, the cytoplasmic protein gene product 9.5 and a 38 kDa integral membrane protein of synaptic vesicles applied in avidin-biotin-peroxidase staining. Mapping with these 3 antibodies revealed dense and basically similar pattern of innervation in the specimens of the clinically healthy oral mucosa. In recurrent aphthous ulcers, all 3 general markers disclosed peripheral nerve fibers also in the lesions, apart from the necrotic area, among the inflammatory cells without signs of retraction from the diseased area. Synaptophysin staining suggested that these peripheral nerve fibers in the inflammatory areas still contained synaptic vesicles. Accordingly, they were shown to contain substance P and calcitonin gene-related peptide, which are known to be released upon stimulation of the nerve and can exert potent paracrine actions, possibly on the local inflammatory cells as suggested by a close spatial relationship between neuropeptide-containing nerves and inflammatory cells.

Adult↗
PubMed1993

Impact of ampicillin and cefuroxime on bacterial colonization and infection in patients on a neonatal intensive care unit.

The impact of ampicillin and cefuroxime on the bacterial flora of neonates was examined in a neonatal intensive care unit (NICU). For the first period of study (January-September 1989), ampicillin plus gentamicin were used as empirical therapy of infection. During this time, 92.6% of all Gram-negative bacilli (GNB) were resistant to ampicillin and 56.6% to cefuroxime. These percentages decreased significantly (P < 0.05) to 60.0% and 16.2% respectively, over the next period of study (October 1989-October 1990) when cefuroxime+gentamicin were used. A decrease in the number of cases of GNB from bacteraemia and meningitis was also significant (from 21.2% to 11.2%), and this correlated with a decline in the occurrence of Klebsiella pneumoniae. However, the number of enterococcal isolates and cases of enterococcal bacteraemia increased. These observations underline the important effect of ampicillin and cefuroxime in modulating the bacterial flora and its antibiotic resistance in patients on a NICU.

Ampicillin↗
PubMed1993

Dilator effect of endothelins in pulmonary circulation: changes associated with chronic hypoxia.

To investigate dilator effects of endothelins (ETs) on the pulmonary circulation and possible changes induced by chronic hypoxia, we examined vascular responses to ET-1 and ET-3 as well as ET binding to receptor subtypes ETA and ETB in the lungs from rats exposed to either room air (controls), hypoxia (10% O2) for 3 wk (3 WH), or 3 WH followed by recovery to room air (3 WH+R). In controls, both ETA and ETB receptor binding was present in smooth muscle of airways and vessels. Infusion of ET-1 or ET-3 (3-100 pM) to isolated perfused lungs preconstricted by U-46619 produced dose-dependent vasodilation with a greater potency of ET-3 (P < 0.01). The vasodilator responses to ET-1 and ET-3 were potentiated by the cyclooxygenase blocker meclofenamate (3 x 10(-6) M) or by the thromboxane synthetase inhibitor R-68070. In meclofenamate-treated lungs, the vasodilator responses to ET-1 and ET-3 remained unaffected by the inhibitor of nitric oxide synthesis, NG-monomethyl-L-arginine (5 x 10(-4) M) or by the guanylate cyclase inhibitor, methylene blue (10(-4) M). Conversely, the K+ channel blockers glibenclamide (10(-4) M) and tetraethylammonium (10(-4) M) attenuated the vasodilator responses to both ET-1 and ET-3. The selective ETA receptor antagonist BQ-123 did not alter ET-induced vasodilation, whereas it attenuated ET-induced vasoconstriction. Vasodilation to both ET-1 and ET-3 was abolished in lungs from 3 WH rats (P < 0.01) but was fully restored in lungs from 3 WH+R rats. Pulmonary vasodilation induced by the K+ channel opener pinacidil, which was suppressed by glibenclamide, did not differ between controls and 3 WH rat lungs. We found no change in ETA and ETB receptor binding from pulmonary vessels in H rat lungs compared with controls. In conclusion, endothelin-induced pulmonary vasodilation which may involve activation of K+ channels is abolished during chronic hypoxia. This abolition does not appear to be related to alterations in ET-receptor subtypes or to unresponsiveness of K+ channels in the pulmonary circulation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Ankle-arm index as a marker of atherosclerosis in the Cardiovascular Health Study. Cardiovascular Heart Study (CHS) Collaborative Research Group.

BACKGROUND: Peripheral arterial disease measured noninvasively by the ankle-arm index (AAI) is common in older adults, largely asymptomatic, and associated with clinically manifest cardiovascular disease (CVD). The criteria for an abnormal AAI have varied in previous studies. To determine whether there is an inverse dose-response relation between the AAI and clinical CVD, subclinical disease, and risk factors, we examined the relation of the AAI to cardiovascular risk factors, other noninvasive measures of subclinical atherosclerosis using carotid ultrasound, echocardiography and electrocardiography, and clinical CVD. METHODS AND RESULTS: The AAI was measured in 5084 participants > or = 65 years old at the baseline examination of the Cardiovascular Health Study. All subjects had detailed assessment of prevalent CVD, measures of cardiovascular risk factors, and noninvasive measures of disease. Participants were stratified by baseline clinical CVD status and AAI (< 0.8, > or = 0.8 to < 0.9, > or = 0.9 to < 1.0, > or = 1.0 to < 1.5). Analyses tested for a dose-response relation of the AAI with clinical CVD, risk factors, and subclinical disease. The cumulative frequency of a low AAI was 7.4% of participants < 0.8, 12.4% < 0.9, and 23.6% < 1.0. participants with an AAI < 0.8 were more than twice as likely as those with an AAI of 1.0 to 1.5 to have a history of myocardial infarction, angina, congestive heart failure, stroke, or transient ischemic attack (all P < .01). In participants free of clinical CVD at baseline, the AAI was inversely related to history of hypertension, history of diabetes, and smoking, as well as systolic blood pressure, serum creatinine, fasting glucose, fasting insulin, measures of pulmonary function, and fibrinogen level (all P < .01). Risk factor associations with the AAI were similar in men and women free of CVD except for serum total and low-density lipoprotein cholesterol, which were inversely associated with AAI level only in women. Risk factors associated with an AAI of < 1.0 in multivariate analysis included smoking (odds ratio [OR], 2.55), history of diabetes (OR, 3.84), increasing age (OR, 1.54), and nonwhite race (OR, 2.36). In the 3372 participants free of clinical CVD, other noninvasive measures of subclinical CVD, including carotid stenosis by duplex scanning, segmental wall motion abnormalities by echocardiogram, and major ECG abnormalities were inversely related to the AAI (all P < .01). CONCLUSIONS: There was an inverse dose-response relation of the AAI with CVD risk factors and subclinical and clinical CVD among older adults. The lower the AAI, the greater the increase in CVD risk; however, even those with modest, asymptomatic reductions in the AAI (0.8 to 1.0) appear to be at increased risk of CVD.

Aged↗
PubMed1992

Role of neuromedin B in control of the release of thyrotropin in hypothyroid and hyperthyroid rats.

Neuromedin B (NB) is a recently discovered neuropeptide related to bombesin. It is localized to thyrotropes and we have previously shown that it directly inhibits thyrotropin (TSH) release from the anterior pituitary gland of euthyroid rats. In the current studies, we further evaluated the action of NB and antiserum directed against it in euthyroid rats and compared the actions with those in hypo- and hyperthyroid rats. Rats were rendered hypothyroid by treatment with propylthiouracil and hyperthyroid by treatment with thyroxine. In euthyroid rats, NB suppressed TSH release from hemipituitaries in vitro. Incubation of these pituitaries with highly specific antiserum against NB produced a stimulation of TSH release, whereas normal rabbit serum had no effect on the output of TSH. Thus, in euthyroid animals NB is a physiologically significant inhibitor of TSH release from the pituitary. In hypothyroid as in euthyroid animals, NB inhibited TSH release when microinjected into the third ventricle (3V) in the same dose (0.5 micrograms; 0.44 nmol) as in euthyroid rats. TSH release from hemipituitaries of hypothyroid animals was also suppressed by NB as in euthyroid animals. In hypothyroid animals, anti-NB antiserum was ineffective both in vivo after its microinjection into the 3V and in vitro on hemipituitaries, which suggests that the peptide has little physiologic significance in this condition, presumably because of its reduced release from the thyrotropes associated with diminished NB content in the pituitary of the hypothyroid rat. Intraventricular injection of NB failed to lower plasma TSH in hyperthyroid rats, which suggests that the action of the peptide is already maximal in hyperthyroidism. When antiserum to NB was microinjected twice into the 3V, there was a delayed increase in plasma TSH manifest 24 hr after the initial injection. TSH release from pituitaries of these animals was markedly increased in the presence of NB antiserum. Thus, NB has a physiologically significant TSH release-inhibiting action at the pituitary in the hyperthyroid as well as in the euthyroid rat. We conclude that in the euthyroid animal NB acts in an autocrine fashion to suppress TSH release from the thyrotropes directly. In hypothyroidism, NB synthesis and presumably release from the pituitary is decreased, such that there is no physiologic significance to the residual NB release, although the responsiveness to the inhibitory action of the peptide is increased, possibly via upregulation of its postulated receptors on the thyrotrope. In hyperthyroidism, the concentration of NB in thyrotropes and presumably its release is increased so that it has a physiologically significant TSH release-inhibiting action.

Animals↗
PubMed1992

Transmitter diversity in carotid body afferent neurons: dopaminergic and peptidergic phenotypes.

Hypoxic stimulation of carotid body chemoreceptors is conveyed to the brainstem by primary sensory neurons whose peripheral axons run in the carotid sinus nerve. While considerable attention has focused on defining chemical neuroregulators released by glomus cells in the carotid body, our understanding of the morphology, distribution and transmitter phenotype of these carotid body afferent neurons remains limited. Carotid body afferent neurons were labeled by microinjection of the retrograde tracer, Fluorogold, into the vascularly isolated rat carotid body. In addition, immunoelectron microscopy was used to correlate transmitter phenotype with ultrastructural features of afferent terminals in the carotid body. Our results indicate that 41% of all carotid body afferent neurons express tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, whereas 7% contain substance P. Tyrosine hydroxylase- and substance P-positive neurons constitute separate subpopulations of carotid body afferents, as these two phenotypes were not colocalized. Most of the tyrosine hydroxylase-containing carotid body afferent neurons were small- or medium-sized (mean cell diameter 15-20 microns) and located in the distal petrosal ganglion, whereas the majority of substance P-containing carotid body afferent neurons were medium- to large-sized (mean cell diameter 20-29 microns) and located in the proximal petrosal ganglion and jugular ganglion. These differences strengthen the notion that these catecholaminergic and peptidergic carotid body afferent neurons give rise to functionally distinct subsets of chemoafferent fibers. To further characterize the catecholaminergic phenotype expressed by tyrosine hydroxylase-positive cells in the petrosal ganglion, we examined the colocalization of tyrosine hydroxylase and DOPA decarboxylase, the dopamine-synthesizing enzyme. Eighty-six per cent of tyrosine hydroxylase-positive neurons in the distal petrosal ganglion also contained DOPA decarboxylase; as these cells do not express the norepinephrine-synthesizing enzyme, dopamine beta-hydroxylase, these data indicate that the catecholaminergic carotid body afferent neurons are dopaminergic. Finally, ultrastructural analysis of the peripheral processes of tyrosine hydroxylase-positive afferent terminals in the carotid body demonstrated endings in close opposition to Type I glomus cells, consistent with a role for dopaminergic afferent neurons in carotid body chemoreception. One possibility is that these cells, in addition to their role as afferents, constitute a morphologic substrate for dopaminergic "efferent" inhibition in the carotid body.

Animals↗
PubMed1992

Hypoxic-ischemic brain damage in term neonates--the relation of neurodevelopmental handicap to cranial ultrasound findings.

This study presents ultrasound findings and neurodevelopmental follow-up in ten infants born at term suffering most severe grade of hypoxic-ischemic encephalopathy. Early ultrasound findings showed in nine of these ten neonates signs of cerebral edema accompanied in two children by intraventricular haemorrhage. Late ultrasound findings in all infants examined demonstrated severe cerebral atrophy, predominantly affecting the cortico-subcortical area. In three children multiple subcortical cysts were also present, corresponding to ultrasound findings of subcortical leukomalacia. Cranial computerized tomography was performed in six of the ten children, showing more precisely the predominant site of cortical atrophy, whereas in children with ultrasound findings of subcortical leukomalacia extensive low density areas in the subcortical white matter were present. All children had neurodevelopmental follow-up for between two and seven years. Six of the ten children have multiple disabilities suffering from spastic quadriparesis, epilepsy, mental retardation and/or visual disability. Among these six were all three children with subcortical leukomalacia. All the children demonstrated poor head growth and became markedly microcephalic. We consider ultrasonography to be very useful in the diagnosis of hypoxic-ischemic brain damage in term neonates as well in predicting the neurodevelopmental outcome in asphyxiated term infants.

Atrophy↗
PubMed1990

Lack of benefit from semi-annual screening for cancer of the lung: follow-up report of a randomized controlled trial on a population of high-risk males in Czechoslovakia.

Cigarette-smoking males (6,364), aged 40-64, were randomized into an intervention group which received 6-monthly screening by chest X-ray and sputum cytology, and a control group which received no asymptomatic investigation. After 3 years, both groups entered a follow-up period during which they received annual chest X-rays. Lung cancer cases detected by screening were identified at an earlier stage, more often resectable, and had a significantly better survival than "interval" cases diagnosed mainly because of symptoms. Comparison of the 2 groups showed a higher incidence of lung cancer in the intervention group, despite the follow-up period when both groups received annual examinations. There was no significant difference in mortality between the 2 groups.

Adult↗
PubMed1990

Motor nerve terminal restoration after focal destruction in young and old mice.

Regeneration of soleus motor nerve terminals after focal destruction by black widow spider venom (BWSV) or its active factor alpha-latrotoxin (LTx) was compared in young and old CBF-1 mice. The object was to determine whether previously reported delayed regeneration after nerve injury in old rodents was due to altered removal of debris, or delay or aberrancy in structural or functional restoration of the neuromuscular junction. In addition, the use of a new fluorescent technique permitted for the first time quantitation of the accuracy of early nerve terminal regeneration in mammalian muscle. Immunohistochemical and electron micrographic studies showed no age difference in destruction of terminals and removal of debris 2 days after toxin application. The indirect twitch and structural reinnervation (measured with flourescent techniques) returned to an equal extent in young and old mice beginning at 3 days after LTx treatment. BWSV (as opposed to LTx) delayed regeneration 1 day in young but not in old mice. On the first day of reinnervation, there was perisynaptic outgrowth in both young and old mice, although in the latter, there was a higher incidence of aberrant outgrowth. The relation between return of twitch strength and recovery of nerve terminal area (measured in teased zinc iodide-stained preparations) showed no age dependency. We conclude that factors cited to explain altered reactive sprouting in the aging CNS do not apply to regeneration of peripheral motor nerve terminals. However, it is possible that the aberrant regrowth observed at the neuromuscular junction in old mice will pertain to the aging CNS. Altered axonal rather than nerve terminal regeneration is the likely source of delayed peripheral nerve regeneration in old animals.

Aging↗
PubMed1989

Role of neuromedin B in the control of the release of thyrotropin in the rat.

Neuromedin B (NB), a bombesin-like peptide, was first isolated from porcine spinal cord and subsequently found in the central nervous systems of rat, cat, and human. Immunocytochemical studies have shown that NB is present in hypothalamus and various other regions of the brain and in thyrotrophs of the anterior pituitary of the rat. The possible physiological role of NB in the hypothalamic-pituitary axis is not known. Therefore, we studied the in vivo effect of this peptide on the plasma levels of thyrotropin (TSH) after administering NB to conscious freely moving adult male rats. When injected i.v., only the highest dose of NB (50 micrograms, 44.2 nmol) significantly lowered plasma TSH levels relative to levels in saline controls. When injected intraventricularly, NB doses of 0.5 and 5 micrograms (0.44 and 4.42 nmol, respectively) lowered plasma TSH levels with a 15-min latency period. Responsiveness of the pituitary to TSH-releasing hormone (TRH) was tested after the effective dose of NB was administered i.v. The increase in plasma TSH levels after the i.v. injection of 1 microgram of TRH was not altered by NB. NB at 10(-9) to 10(-7) M also reduced TSH release from hemipituitaries incubated in vitro without decreasing the response to TRH. Consequently, NB appears to have a direct inhibitory effect on TSH release from thyrotrophs. Since the response to TRH was not depressed, NB appears to act on a separate NB thyrotroph receptor that suppresses TSH release by a TRH-independent mechanism. After antiserum directed against NB was injected into the third ventricle, there was a highly significant elevation of the plasma level of TSH, beginning at 4 hr and increasing at 6 hr, relative to initial levels and levels in normal rabbit serum-injected controls. These results indicate that NB has a tonic suppressive effect on TSH release and is a physiologically significant TSH-release-inhibitory factor.

Animals↗
PubMed1989

[Computerized tomography and ultrasound in the early diagnosis of brain damage].

Eighty-one neonates were evaluated clinically by ultrasound and/or CT with the aim of assessing diagnostic possibilities of both methods in the cases of pathomorphologic findings linked with perinatal risk factors and subsequent neurologic deficits. In perinatal at-risk infants (N = 11), premature infants (N = 6) and term infants (N = 5) ultrasound is a reliable diagnostic method in the detection and follow-up of intraventricular hemorrhage and perivascular leukomalacia in preterm infants, while for the diagnosis of hypoxic-ischemic lesions, especially focal cortico-subcortical changes in term infants, besides ultrasound it is necessary to perform CT. In perinatal infants (N = 50) with neurologic deficits at the age of 2-5 years, on CT scanning, atrophic changes were found in 50% of cases, while in 10% vascular lesions were observed, and a combination of atrophic and vascular lesions was found in 28% of the cases examined. In the group of infants (N = 20) with neurologic deficits (II and III trimenon) without risk factors, on CT scanning the pathomorphologic finding was identified as a vascular or atrophic lesion. In the authors' opinion, CT is the only objective method in the detection of the precise localization and evaluation of lesions in children with neurologic deficits after their first year of life.

Brain↗
PubMed1988

Synaptic analysis of amacrine cells with neuropeptide Y-like immunoreactivity in turtle retina.

Neuropeptide Y-like immunoreactivity has been localized previously within three classes of amacrine cells in the turtle retina. We have used the avidin-biotin with horseradish peroxidase technique to label these neurons for examination at the ultrastructural level to answer the following questions. Where are the synaptic contacts of these neurons made? What types of neurons are involved pre- and postsynaptically? What is the intracellular distribution of the immunoreactivity? Processes with neuropeptide Y-like immunoreactivity were located primarily within three regions of the inner plexiform layer: stratum 1, stratum 3, and at the border between strata 4 and 5. In all three regions the processes with neuropeptide Y-like immunoreactivity received synaptic contacts from both unlabeled amacrine and bipolar cells, but the majority of the synaptic input in all three regions was from unlabeled amacrine cells. Processes with neuropeptide Y-like immunoreactivity were presynaptic to unlabeled amacrine cells in all three regions, but also formed contacts onto unlabeled bipolar cells in the region between strata 4 and 5. The immunoreactivity within these cells gave rise to a diffuse reaction product that was distributed throughout the cytoplasm and within large vesicles. This localization of neuropeptide Y-like immunoreactivity within large vesicles suggests that this peptide may play a neuromodulatory role. Such a role would be consistent with previous studies of neuropeptides in the turtle retina.

Animals↗
PubMed1988

Filopodia, lamellipodia and retractions at mouse neuromuscular junctions.

In order to determine if mature motor nerve terminals retain structures associated with development such as filopodia and lamellipodia, we studied whole mounts of mature mouse neuromuscular junctions stained with both fluorescent-labelled tetanus toxin C-fragment and alpha-bungarotoxin, and employed electron microscopy in parallel. The rapid fluorescent stain may be of general usefulness. Both filopodia and lamellipodia were found, extending beyond the border of the established postsynaptic receptors. Filopodia often appeared in clusters, were devoid of a synaptic vesicle antigen, and many withdrew in response to cytochalasin D. Control experiments demonstrated that filopodia were not induced by the toxin treatment. The mean number of filopodia per endplate varied from about one in phasic muscle to three in tonic muscle, and was twice as great in immature mouse muscle. Postsynaptic receptor-rich regions without overlying terminals were less numerous than filopodial and lamellipodial projections without underlying receptors. Electron microscopy showed that lamellipodia contained actin-like filaments and immunoreactivity to actin, but no neurofilaments, microtubules, mitochondria or vesicles. Therefore, these structures would not be visualized by in vivo mitochondrial stains. The lamellipodia protruded into the gap between muscle and a closely overlying Schwann cell process. Lamellipodia occupied about 5% of the linear extent of the terminal arbor in whole mounts, but appeared in 16% of random electron micrographic fields. Thus, the lamellipodia and filopodia typical of developing terminals are present in adulthood and represent a distinctive specialization of the nerve terminal, which may interact with the adjacent Schwann and muscle cell. The frequency of filopodia is a function of age and of muscle or motoneuron type. We suggest that some of the factors known to regulate growth of filopodia and lamellipodia in vitro or in development may continue to act at adult presynaptic nerve terminals.

Animals↗
PubMed1988

Ultrasonography in hereditary degenerative diseases of the cerebral white matter in infancy.

Ultrasonography of the brain, performed on two female infants who were clinically suspected of having leukodystrophy, demonstrated markedly increased echoes in the periventricular regions bilaterally and indistinct visualization of sulci and gyri on sagittal and coronal scans. The same sonographic features present on subsequent US examinations corresponded to progressive low density areas and atrophy on CT scans. Increased periventricular echogenicity which shows no evolution, in a clinical context, may contribute to the early recognition of neurodegenerative disorders affecting white matter.

Brain↗