Search PubMed⌕ Search

Biomedical subjects

M Segal

Publications and source records attributed to M Segal.

At least 397 records · Page 22Linked to original sources
PubMedDate not supplied

CT of renal densities caused by intravenous infusion of antibiotics.

OBJECTIVE: Patients treated with intravenous antibiotics were seen to have increased attenuation of the renal collecting system on CT scan of the abdomen. To detect whether this was related to certain antibiotics, we undertook a prospective study on patients being treated for sepsis while receiving intravenous antibiotics. In addition, we also tested antibiotics administered to rabbits. MATERIALS AND METHODS: Fourteen patients were tested with cefazolin, gentamicin, cefotaxime, vancomycin, amoxicillin and clavulanic acid (Augmentin), and metronidazole. Ten groups of rabbits received these drugs by intravenous injection. Computed tomography scan of the kidneys was performed prior to and 2 h after intravenous injection of antibiotics. Fourteen patients who underwent CT scan of the abdomen and were treated by intravenous antibiotics were scanned without contrast agent injection. RESULTS: According to our results, cefazolin, cefotaxime, and gentamicin seemed to be the most potent antibiotics in inducing increased attenuation of the collecting system. This effect was synergistic when a combination of drugs was used. CONCLUSION: The elucidation of the potential increase in attenuation of the collecting system by antibiotics in normally functioning kidneys should help to eliminate confusion with other pathologies such as medullary sponge kidney.

Adolescent↗
PubMedDate not supplied

CREB activation mediates plasticity in cultured hippocampal neurons.

Activation of cyclic AMP dependent kinase is believed to mediate slow onset, long-term potentiation (LTP) in central neurons. Cyclic-AMP activates a cascade of molecular events leading to phosphorylation of the nuclear cAMP responsive element binding protein (pCREB). Whereas a variety of stimuli lead to activation of CREB, the molecular processes downstream of CREB, which may be relevant to neuronal plasticity, are yet largely unknown. We have recently found that following exposure to estradiol, pCREB mediates the large increase in dendritic spine density in cultured rat hippocampal neurons. We now extend these observations to include other stimuli, such as bicuculline, that cause the formation of new dendritic spines. Such stimuli share with estradiol the same mechanism of action in that both require activity-dependent CREB phosphorylation. Our observations suggest that CREB phosphorylation is a necessary, but perhaps not sufficient, step in the process leading to the generation of new dendritic spines and perhaps to functional plasticity as well.

Animals↗
PubMedDate not supplied

Refined genetic mapping of juvenile X-linked retinoschisis.

Juvenile X-linked retinoschisis (RS) is an eye disease that causes acuity reduction and peripheral visual field loss typically beginning early in life. In further work towards positional cloning of the RS gene, we restudied our previously reported seven large American families and one additional new family, with a total of 63 affected males. RS linkage analysis using microsatellite repeat markers gave the following results: DXS207 (Z = 24.89, theta = 0.01), DXS987 (Z = 24.04, theta 0.01) and DXS999 (Z = 14.70, theta = 0.00). Recombination events in four individuals were studied further with additional markers (AFM291wf5, DXS443, DXS1052, DXS274 and DXS1226), and a flanking interval was obtained (DXS43, DXS207, DXS987)-RS-(AFM291wf5, DXS443). This study moves the RS centromeric boundary to (AFM291wf5, DXS443), about 5.5 cM closer than the previously reported boundary at DXS274 and narrows the RS inclusion interval to about 3.7 cM (using distances from CEPH family data).

Chromosome Mapping↗
PubMedDate not supplied

Linkage study of Best's vitelliform macular dystrophy (VMD2) in a large North American family.

Best's vitelliform macular dystrophy (VMD2) is an autosomal dominant retinal dystrophy for which the underlying biochemical cause is unknown. We used 11 genetic markers in the vicinity of the VMD2 gene in our study of a large North American family in which macular dystrophy characteristics overlap the broad definition of Best's disease. Significant evidence for linkage was found for markers D11S956 (Z = 5.88, theta = 0.04) and FCER1B (Z = 4.31, theta = 0.00). Recombination events localized the disease gene to the 5-cM interval D11S956-UGB, a genetic inclusion interval that substantially overlaps the VMD2 inclusion interval defined by recombinants at FCER1B and UGB observed by other research groups. The resulting exclusion of ROM1 from the genetic inclusion interval eliminates ROM1 defects as a possible cause of the disease in this family. Linkage studies of many families, including those that share most but not all features with classical Best's disease, will be needed to properly evaluate genetic heterogeneity and the range of phenotypic variation that can result from VMD2 defects.

Adult↗
PubMedDate not supplied

X-linked juvenile retinoschisis: localization between (DXS1195, DXS418) and AFM291wf5 on a single YAC.

We studied 17 pedigrees with 108 affected males with X-linked juvenile retinoschisis (RS; McKusick No. 31270) and have analyzed all of the known polymorphic markers in the RS region of Xp22.1-p22.2 between DXS987 and DXS41. By haplotype analyses we found 7 individuals who showed crossovers in this interval surrounding RS. We previously reported AFM291wf5 as the centromeric boundary, and this remains unchanged in the present study. A new recombination was identified on the telomeric side at (DXS1195, DXS418). Our data support the locus order Xpter--(DXS987, DXS207, DXS1053, DXS43)--(DXS1195, DXS418)--(RS, DXS257, DXS999)--(AFM291wf5, DXS443)--DXS1052--(DXS1226, DXS274, DXS41)--Xcen; loci grouped in parentheses could not be mutually ordered by our genetic data. Physical mapping has indicated a distance of at most 900-1,000 kb between (DXS1195, DXS418) and AFM291wf5. No recombination was observed between RS and DXS257 which lies in our new interval of interest, but one critical individual was not informative with this marker. Our data now define the smallest RS inclusion interval. This interval is contained on a single YAC from which we have identified expressed sequences as candidate genes for RS.

Chromosomes, Artificial, Yeast↗
PubMedDate not supplied

Clinical utility of monitoring serum cryptococcal antigen (sCRAG) titers in patients with AIDS-related cryptococcal disease.

PURPOSE: The purpose of our study was to define the time course and clinical role of monitoring serum cryptococcal antigen titers (sCRAG) in patients with AIDS-related cryptococcal disease. METHOD: A retrospective chart review was conducted. The medical records for all HIV-infected patients with positive cryptococcal antigen (CRAG) tests from January 1993 to May 1998 at San Francisco General Hospital (SFGH) were reviewed for sCRAG titer levels and clinical outcomes. RESULTS: Out of the 314 patients found to have positive antigen tests, 136 met the inclusion criteria. Twelve (8.8%) had no change in titer from baseline, 6 (4.4%) had an increase, and 118 (86.8%) had a decrease. Examining the association of sCRAG with time to relapse using a variety of Cox models produced largely null results. Rate of change in sCRAG over time (slope) was not significantly predictive of time to relapse nor of time to definite relapse/probable relapse/persistent disease. CONCLUSION: Although in the majority of patients, the sCRAG titers appeared to decrease over time, we could not detect a significant correlation between sCRAG titer results of patients who had a clinical response to treatment and sCRAG titers in patients who experienced persistent disease, probable relapse, or definitive relapse of cryptococcal disease. We conclude that follow-up monitoring of the sCRAG titer is not useful in the management of patients with AIDS-related cryptococcal disease on treatment.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Serotonin and local circuits in rat hippocampus.

Serotonin produces several actions in rat hippocampal neurons recorded in an in vitro slice preparation. These include activation of a voltage-independent potassium current which results in the hyperpolarization of the recorded cells, the blockage of a calcium-dependent slow potassium current underlying the slow after-hyperpolarization (AHP) which follows a burst firing and generation of a slow late depolarization associated with the blockage of a persistent potassium current. An additional effect that we detected recently involves a blockage of inhibitory postsynaptic potentials (IPSP), primarily the slow IPSP, likely to be mediated by activation of potassium currents through a gamma-aminobutyric acid (GABA)-B receptor. The reduction in the IPSPs is produced by a lower concentration of serotonin than that required to produce the hyperpolarization. The lack of reduced sensitivity to GABA indicates that the effect of serotonin on the IPSPs might be presynaptic. Indeed, serotonin has a much larger effect on putative interneurons than on pyramidal neurons. It is suggested that serotonin can enhance reactivity of the hippocampus to afferent stimulation by reducing slow inhibitory synaptic potentials while at the same time reducing the spontaneous activity of the recorded neurons. These effects of serotonin develop relatively late (2-3 weeks postnatally), along with the late appearance of the slow inhibitory potentials.

Animals↗
PubMedDate not supplied

Serotonin, aging and cognitive functions of the hippocampus.

The cholinergic hypothesis of senile dementia /18/ does not provide a sufficient explanation for age-dependent spatial learning deficits; these are observed before an appreciable reduction of cholinergic markers can be detected. Behavioral deficits similar to those observed in old rats cannot be induced in young rats by comparable cholinergic lesions but do occur following combined cholinergic/serotonergic lesions. Serotonergic raphe grafts in the hippocampus (but not in the entorhinal cortex or hypothalamus) prevent such combined lesion-induced spatial learning deficits. The behavioral deficits are associated with a reduction of hippocampal commissure feed-forward inhibition. Similar reduced inhibition is found in old rats, deficient in their performance of a spatial learning water-maze task. Finally, treating old rats with the serotonergic precursor 5-hydroxytryptophan (5-HTP) reduces the age-dependent spatial learning deficits and restores hippocampal commissure feed-forward inhibition. Serotonin may act in parallel to the cholinergic innervation of the hippocampus by affecting inhibitory interneurons but in addition it may act by modulating acetylcholine release. Acetylcholine release is modulated by serotonin and the enhancing effects of serotonin releasing drugs on dentate granule cell excitability are mediated by acetylcholine. We thus propose that a reduction of serotonergic modulation of hippocampal interneuron activity and impaired modulation of cholinergic effects in the hippocampus contribute to age-dependent cognitive deficits.

Aging↗
PubMedDate not supplied

Overview of drugs used in treating drug-induced dependence: a treatise interrelating existing hypotheses in order to attain maximal therapeutic benefits.

Despite the fact that we do not yet completely understand the physiology of physical dependence, many treatment modalities are available. In this overview, an attempt is made to discuss available treatments and mechanisms to possibly attain a better understanding of the complex interactions that occur between systems. An attempt is also made to understand interrelations between drug misuse and mental disorders as one aspect of the treatment process--the ultimate goal being more efficacious and safer therapy.

Clonidine↗
PubMedDate not supplied

A moving target: financing Medicare for the future.

Since 1997, there has been a steady downward trend in projected Medicare spending as a share of the gross domestic product (GDP), substantially improving the long-run outlook for Medicare. But even with improvements in outlook, the required share of GDP will rise by more than 70%, and the question remains as to who will pay for Medicare in the future. This report examines a limited set of tax options and a flat beneficiary premium to illustrate the size of contributions necessary to achieve several different goals, and to explore the difference that multiple years of projections can make on these requirements.

Aged↗
PubMedDate not supplied

A comparison of black and white family caregivers experience with dementia.

The chronicity of dementia and the ever-increasing need for care of those afflicted, places tremendous burden on the family and those individuals who assume primary responsibility for caregiving. In this descriptive study, the investigators report findings comparing Black and White families' experiences with dementia, specifically, the problems associated with caregiving, the coping strategies used by the caregivers and the various forms of supportive modalities that help family caregivers provide care. Study findings indicated differences between the Black and White caregivers in identifying the single most difficult problem that they had in caring for their confused relative. Differences in coping strategies between the two groups of caregivers are noted as well. Black caregivers of all ages used religious faith as a primary means of coping with the stresses of caregiving while White caregivers tended to seek help from professionals and use problem-solving methods. The implications of the study findings for structuring interventions are discussed. Implications of this study concern three areas: 1) respite services; 2) individual and family counseling; and 3) education.

Adaptation, Psychological↗
PubMedDate not supplied

Chloride conductances in central neurons.

Two types of chloride conductances--gamma-aminobutyric acid (GABA)-activated and Ca2+-voltage dependent--were studied in tissue-cultured central neurons. Cultured hippocampal neurons contain identified GABA-mediated perisomatic synaptic connections. Activation of these synapses evokes, in voltage-clamped neurons, an inhibitory postsynaptic current (IPSC) that rises within 3 to 5 msec and decays exponentially with a time constant of 15 to 20 msec. The decay of the IPSC is voltage-dependent, and is altered by drugs known to act on GABA receptors. The kinetics of the IPSC appears to be determined by that of the GABA-activated Cl- ion channel. Ca2+ and voltage-dependent Cl- conductance is best seen in cells where K conductances are blocked. It usually follows a Ca spike and is blocked by Ca antagonists. Analysis of tail currents in voltage clamped hippocampal, hypothalamic and spinal cord neurons indicates that the current decays slowly (200 msec) and passively and reverses a function of [E]C1 (equilibrium potential for Cl-). Chloride conductance functions to suppress excitability of these neurons. The pharmacological and physiological properties of this conductance in vivo are not as yet known.

Animals↗