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J Perez

Publications and source records attributed to J Perez.

At least 127 records · Page 7Linked to original sources
PubMed1995

Effects of fluvoxamine on the protein phosphorylation system associated with rat neuronal microtubules.

We have studied the phosphorylation system associated with the rat cerebrocortical microtubule fraction after short- and long-term administration (15 mg/kg) of fluvoxamine, a selective serotonin reuptake inhibitor with antidepressant activity. Fluvoxamine administered for 5 days significantly enhanced the 32P incorporation stimulated by cAMP into MAP2, while it failed to produce this effect after 12 and 21 days. Moreover, in the same periods of treatment no changes were observed in basal phosphorylation and in the pattern of microtubule proteins. In conclusion, our results suggest that changes in the protein phosphorylation system associated with the microtubule fraction could represent an early neurochemical modification involved in the action of fluvoxamine.

Animals↗
PubMed1995

Neosiphoniamolide A, a novel cyclodepsipeptide, with antifungal activity from the marine sponge Neosiphonia superstes.

A novel cyclodepsipeptide, neosiphoniamolide A [1], has been isolated from the sponge Neosiphonia superstes. The structure of 1, which contains a 12-carbon hydroxy acid, glycine, valine, and a halogenated tyrosine residue in an 18-membered ring, is related to jaspamide and the geodiamolides, previously isolated from sponges. The structure was solved by spectroscopic analysis.

Animals↗
PubMed1995

Abnormalities of cAMP-dependent endogenous phosphorylation in platelets from patients with bipolar disorder.

OBJECTIVE: The aim of the study was to assess cAMP-dependent endogenous phosphorylation in platelets from euthymic bipolar patients. METHOD: Platelets from 10 drug-free euthymic patients with bipolar disorder were compared with those from 10 age- and sex-matched healthy subjects. Basal and cAMP-stimulated protein phosphorylation was examined in each group. RESULTS: Endogenous phosphorylation in both the healthy volunteers and the bipolar patients was significantly stimulated by cAMP; the major polypeptides had apparent molecular weights of 38 and 22 kDa. The cAMP-stimulated 32P incorporation differed between the bipolar patients and the comparison subjects only in the 22-kDa band. CONCLUSIONS: These data suggest a possible role of cAMP-dependent protein phosphorylation in the pathophysiology of bipolar disorder.

Adult↗
PubMed1995

Video conferencing in surgery: an evolving tool for education and preceptorships.

The advent of advanced laparoscopic procedures has provided unquestioned patient benefits but has also engendered some significant concerns about whether surgical team members are able to stay current in this everchanging arena. The interactive video conferencing program at Doctors Hospital in Columbus, Ohio, was developed to improve the education and preceptoring of surgical teams. This article describes the evolution of the program and its basic technology and connectivity. Physicians and other health care professionals began to accept this teaching alternative as usage increased. Based on this initial experience, video conferencing in surgery appears to be a valuable and exciting method of enhancing the educational process and augmenting the preceptorship experience. Further studies need to be conducted to determine the actual cost-effectiveness of this teaching method.

Education, Medical, Continuing↗
PubMed1995

Presynaptic Ca2+/calmodulin-dependent protein kinase II: autophosphorylation and activity increase in the hippocampus after long-term blockade of serotonin reuptake.

It is known that long-term treatment with antidepressants induces an enhancement of neurotransmission in the pathway projecting from raphe nuclei to the hippocampus. In the case of selective serotonin (5-HT) reuptake inhibitors, this enhancement is due to a desensitization of presynaptic 5-HT autoreceptors and a concomitant increase in 5-HT release in terminal areas. To investigate whether this effect is accompanied by adaptive changes in the molecular machinery regulating transmitter release at serotonergic terminals, autophosphorylation and activity of Ca2+/calmodulin-dependent protein kinase II were measured in subsynaptosomal fractions from hippocampus and total cortex. Long-term treatment with two selective serotonin reuptake inhibitors (paroxetine and fluvoxamine) and with a nonselective reuptake inhibitor (venlafaxine) induces a large increase of kinase autophosphorylation in synaptic vesicles and synaptic cytosol in the hippocampus but not in synaptosomal membranes. No significant change was detected in total cortex. The change is not reproduced by the direct addition of the drugs to the phosphorylation system and is not elicited by acute treatment of the animals. The increase in autophosphorylation is not accounted for by neosynthesis or translocation of the kinase to synaptic terminals. The change is restricted to the kinase located inside the terminals and is not detected in synaptosomal membranes, containing predominantly postsynaptic kinase, suggesting that only presynaptic kinase is affected. In the same fractions, the kinase activity is increased. These results are in agreement with reports suggesting a presynaptic effect for the SSRIs and disclose a new putative site of action for psychotropic drugs.

Amino Acid Sequence↗
PubMed1995

Synthesis of (+/-)-1-amino-6,7,8,8a-tetrahydro acenaphthene with possible central dopaminergic activity.

We describe the non stereoselective synthesis of (+/-)-1-amino-6,7,8,8a-tetrahydroacenaphthene (14), a novel compound that belongs to the acetanaphtene group, that is presented as a rigid non hydroxylated 2-aminoindan which has a structural disposition of a dopaminergic pharmacophore that possess a phenylethylamine fragment. Intracerebroventricular administration of this compound induces an increase in urinary volume and sodium excretion in conscious rats. The renal actions of 14 were blocked by haloperidol pretreatment, suggesting that 14 acts centrally through a dopaminergic mechanism.

Acenaphthenes↗
PubMed1995

Mesangial cell-derived interleukin-10 modulates mesangial cell response to lipopolysaccharide.

Interleukin (IL)-10 is a novel cytokine produced by a variety of cells, including monocytes/macrophages, upon exposure to lipopolysaccharide (LPS). Recent observations indicate that, in turn, IL-10 exerts suppressive effects on macrophage response to LPS. Because mesangial cells are also a target for LPS, we have examined the potential role of IL-10 in the regulation of mesangial cell response to LPS. To this aim, we have studied the synthesis and the autocrine/paracrine function of IL-10 in cultured mouse mesangial cells. IL-10 mRNA expression and IL-10 protein secretion were determined by a reverse transcription polymerase chain reaction technique and a specific enzyme-linked immunosorbent assay, respectively. No IL-10 mRNA expression was detectable in unactivated cells. LPS induced IL-10 mRNA expression in a dose-dependent fashion (1 to 100 micrograms/ml). In addition, LPS induced IL-10 protein release that was both dose dependent (1 to 100 micrograms/ml) and time dependent (24 to 72 hours). We have also studied the effect of IL-10 on the production of inflammatory mediators by LPS-activated mouse mesangial cells. Whereas recombinant IL-10 inhibited the generation of tumor necrosis factor-alpha (TNF-alpha) and IL-1 beta by 90 and 60%, respectively, it did not affect the formation of nitric oxide-derived nitrite (NO2-) and nitrate (NO3-). As shown by the use of anti-IL-10 monoclonal antibody, endogenously produced IL-10 affected the generation of TNF-alpha but neither that of IL-1 beta nor that of NO2- and NO3-. Finally, we have examined whether conditions known to also reduce the generation of TNF-alpha modified the expression of IL-10. Of all the conditions tested, only the addition of desferrioxamine and transforming growth factor-beta were found to increase IL-10 release. Together, these data demonstrate that mesangial cell-derived IL-10 has important regulatory effects on the inflammatory response of these cells to LPS because of its capacity to blunt TNF-alpha generation.

Animals↗
PubMed1994

Fish oil supplementation and essential fatty acid deficiency reduce nitric oxide synthesis by rat macrophages.

Both fish oil-derived omega-3 polyunsaturated fatty acid (omega 3 PUFA) supplementation and essential fatty acid (EFA) deficiency have been shown to exert anti-inflammatory effects and, hence, to ameliorate immune-mediated glomerulonephritis. The mechanisms underlying these effects include alterations in the production of eicosanoids, cytokines (that is, tumor necrosis factor, TNF-alpha) and reactive oxygen species by blood borne cells. Because, in addition to these mediators nitric oxide (NO) is also implicated in glomerular injury, we have examined if both diets affected macrophage NO production as well. Rats were fed a standard chow, an omega 3 PUFA-supplemented diet, or an EFA-deficient diet for six weeks before resident peritoneal macrophages were isolated. These cells were exposed to lipopolysaccharide (LPS) and the NO metabolite, nitrite (NO2-), was measured in the medium using the Griess reagent. Release of NO2- was enhanced by LPS in a dose-dependent manner. With 10 ng/ml LPS challenge, NO2- release was reduced by 37% and 57% by omega 3 PUFA supplementation and EFA deficiency, respectively. NO2- returned to control levels two weeks after the end of diet. Macrophage production of TNF-alpha responded in a similar manner. Diet-induced reduction of NO2- release was neither attributable to a reduction of inducible NO synthase mRNA levels as shown by Northern blot analysis, nor to an increased competition of NO synthase and arginase for the substrate (L-arginine). Indeed, arginase activity of macrophages was even slightly reduced by both omega 3 PUFA-supplemented diet and EFA-deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1994

International pharmaceutical spending controls: France, Germany, Sweden, and the United Kingdom.

France, Germany, Sweden, and the United Kingdom each use different types of policies for controlling prescription drug spending. Until recent years, these policies have relied heavily on regulating prices charged by drug manufacturers, with different systems providing varying degrees of pricing freedom. While these policies appear to have brought some degree of price restraint, they have not prevented continued growth in prescription drug spending. As a result, each country is supplementing its policies with measures aimed at physicians and consumers and targeted at reducing a perceived over-utilization of pharmaceutical products.

Cost Control↗
PubMed1993

Evidence for the existence of cAMP-dependent protein kinase phosphorylation system associated with specific phosphoproteins in stable microtubules from rat cerebral cortex.

Cyclic AMP is a second messenger by which different extracellular signals are transduced into biological responses. Within the cell, most of the effects of cAMP are mediated through the cAMP protein kinase which appears to be localized in specific compartments of the cell near to their substrate proteins. In the present study, we have investigated the possible association of cAMP-dependent protein kinase, its substrate proteins and RII binding proteins in stable microtubules from rat cerebral cortex. The results show that in this fraction there is a cAMP binding protein of 52-54 kDa. This cAMP receptor is in the inactive holoenzyme form, since the addition of cAMP (5 microM) induces an increase in the endogenous phosphorylation of different stable microtubules polypeptides, which is completely inhibited in the presence of a specific protein kinase inhibitor (PKI 5-24 1 microM). Interestingly, overlay binding assay reveals that beside MAP2, 32P/R II is able to bind stable microtubule proteins of M(r) 150 and 75 kDa which, according to their electrophoretic mobility, can also be endogenous substrates for the enzyme. We conclude that cAMP-dependent phosphorylation system is indeed associated with stable microtubules from rat cerebral cortex.

Animals↗
PubMed1993

Cycloheximide mimics effects of oestradiol that are linked to synaptic plasticity of hypothalamic neurons.

The synaptic connectivity of the rat arcuate nucleus, a hypothalamic area rich in oestradiol receptors, is rapidly affected by physiological modifications of hormonal levels. A rise of oestradiol in plasma elicits a coordinated neuronal-glial response that begins with a rapid fall in the number of small (< 10 nm) intramembrane particles and a rapid increase in the number of large (> 10 nm) intramembrane particles in neuronal membranes, followed by a modification in the branching of astrocytic processes and finally results in decreased number of axo-somatic synapses and increased glial wrapping of the neuronal somas. In the course of a series of studies aimed to test possible non-genomic effects of oestradiol on neuronal membranes we analyzed the effect of the systemic administration of the protein synthesis inhibitor cycloheximide on the ultrastructure of arcuate neurons and granule cells of the cerebellar cortex, an area of the brain with low levels of estrogen receptors. Cycloheximide resulted in a significant inhibition of protein synthesis in hypothalmus and cerebellum of ovariectomized rats. Under these circumstances, the number of small intramembrane particles was reduced in hypothalamic and cerebellar neuronal membranes while the number of large intramembrane particles showed a decrease in cerebellar membranes and a transient increase in arcuate neuronal somas. Furthermore, cycloheximide resulted in an increased glial wrapping of arcuate neuronal somas but not of cerebellar granule cells. The ensheathing of arcuate neurons by glial was associated with a 41% decrease in the number of axo-somatic synapses. These results indicate that the protein synthesis inhibitor cycloheximide may elicit the integrated neuronal-glial response that is associated with the hormonally induced remodelling of synaptic contacts on arcuate neurons.

Animals↗
PubMed1993

Laser tomography of heterogeneous scattering media using spatial and temporal resolution.

Time-resolved tomography is performed in transillumination by using 527 nm picosecond pulses from a passively mode-locked doubled Nd/glass laser and a streak camera to select photons according to their flight time. This work reports on the increase in contrast of a time-resolved profile of a 2 mm radius opaque object embedded in a scattering medium, constituted of diluted milk in a 30 mm thick cell. For spatial analysis, the emerging photons are detected through a 6 mm slit at the outlet face of the cell. Transmission profiles obtained as a function of time show that the contrast is enhanced for the shortest flight times, while the 'shadow' of the object is no longer detected after about 100 ps. Moreover, improvements in contrast are studied for different configurations of the model, to analyse separately the role of collimated and scattered photons. It is expected that such a tomographic method based on time-resolved absorption could be applied to imaging for more complex biological structures in the red and near-infra-red range.

Humans↗
PubMed1993

Role of organic acid chelators in manganese regulation of lignin degradation by Phanerochaete chrysosporium.

Nitrogen, carbon, and manganese are potent regulators of lignin degradation, but although nitrogen and carbon elicit a generalizated response when cells are starved, manganese is a relatively specific regulator of lignin and manganese peroxidase (LiP and MnP, respectively). At high manganese levels, MnP is induced, and LiP is repressed. At low Mn levels, MnP is repressed, and LiP is induced. Organic acid chelators are very important in attaining LiP repression with high Mn. Both mineralization and lignin depolymerization are regulated by manganese in the presence of organic acid chelators. As long as the chelators keep Mn(II) and Mn(III) in solution, repression is observed, but eventually, dismutation reactions cause the formation and precipitation of Mn (IV) as MnO2. Repression is immediately relieved, and depolymerization and mineralization proceed at a high rate.

Acids↗
PubMed1993

Hemorrhagic and Mojave toxins in the venoms of the offspring of two Mojave rattlesnakes (Crotalus scutulatus scutulatus).

1. The venoms of two Mojave rattlesnakes and those of their offsprings were analyzed for Mojave toxin and hemorrhagic toxin. 2. The venom of one female, collected in Pima County, Arizona, and the venoms of her six offspring contained hemorrhagic toxin but not Mojave toxin (venom B). 3. The venom of the second female, captured in El Paso County, Texas, contained both toxins (A+B venom). Of her 10 offspring, five contained venom with both toxins, two had hemorrhagic toxin only, and three contained neither toxin. 4. Venoms that caused hemorrhage also inactivated complement. A pool of the venoms of the venom B offspring was less toxic than adult pooled venom A.

Animals↗
PubMed1993

Estradiol induces plasticity of gabaergic synapses in the hypothalamus.

The number of axosomatic synapses on arcuate neurons of the adult rat hypothalamus fluctuates following the sequence of increasing circulatory estradiol during the ovarian cycle. To determine whether estrogen is affecting GABAergic synaptic contacts we studied the number of GABA-immunoreactive axosomatic synapses in adult ovariectomized rats injected either with 17 beta estradiol (100 micrograms/100 g body weight) or with sesame oil vehicle. The number of immunoreactive axosomatic synapses was significantly reduced in estradiol-treated rats (77 +/- 8 vs 56 +/- 6 synapses per 1000 microns of perikaryal membrane in control and estradiol-treated rats, respectively) while the number of non-immunoreactive synapses was not significantly affected by the hormonal treatment (44 +/- 6 vs 35 +/- 5 synapses per 1000 microns of perikaryal membrane in control and estradiol-treated rats, respectively). Estradiol administration also resulted in a significant decrease in the percentage of perikaryal membrane covered by immunoreactive synapses. These results suggest that physiological levels of estradiol may induce a remodeling of GABAergic inhibitory inputs on arcuate neurons.

Animals↗
PubMed1993

Heterologous sensitization of adenylate cyclase activity by serotonin in the rat cerebral cortex.

In vitro exposure of rat cerebrocortical slices to microM concentrations of serotonin (5HT) results in an increased response of adenylate cyclase to isoproterenol (ISO). No change in the affinity of the beta-adrenoceptor toward the agonist was found after 5HT exposure when measuring ISO displacement of [3H]CGP 12177 binding. A similar increase of adenylate cyclase response was also found when using VIP as a stimulatory agent. The dose-response curve of adenylate cyclase to the GTP analogue, GppNHp, was modified by 5HT, which promotes a significantly higher maximal response without altering the potency of GppNHp. Forskolin-stimulated adenylate cyclase activity was not affected by 5HT. Serotonergic 5HT2 receptors are involved in the sensitization of adenylate cyclase to GppNHp, since the selective 5HT2 antagonist ketanserin inhibits the effect of 5HT, whereas the 5HT2 agonist DOI mimics 5HT. The involvement of 5HT2 receptor-coupled activation of protein kinase C is also demonstrated: direct protein kinase C activators such as phorbol esters and s,n-dioctanoylglycerol behave in the same manner as 5HT, while the protein kinase C inhibitor CGP 41251 prevents 5HT from increasing adenylate cyclase responsiveness to GppNHp. Moreover, in vitro exposure of cortical slices to 5HT results in reduced inhibition of adenylate cyclase by somatostatin. Since no change was observed at the receptor level and in the direct stimulation of the catalytic subunit of the enzyme, we propose that 5HT might accomplish the sensitization of adenylate cyclase through protein kinase C by inactivating the inhibitory coupling protein Gi and facilitating the interaction of the exogenous GppNHp with the stimulatory coupling protein Gs.

Adenylyl Cyclase Inhibitors↗
PubMed1993

The role for laparoscopic presacral neurectomy.

This study was carried out to determine the efficacy of laparoscopic presacral neurectomy (LPSN) and to define its role in modern gynecology using a prospective consecutive cohort. One hundred three patients underwent LPSN, and 87 were included in this study. After LPSN, 91% of these 87 patients experienced some decrease in pelvic pain, and a majority of patients had 50% or greater reduction in pain score. There was a highly significant difference among the preoperative and postoperative pain levels (p less than 0.0001). Patients with pain of endometriosis (72), primary dysmenorrhea (5), and chronic pelvic inflammatory disease (10) responded with a decrease in pain score to this procedure. Complications included 1 patient with intraoperative bleeding, 2 with postoperative vaginal dryness, and 1 with constipation. We conclude that LPSN is as effective as that performed by laparotomy and should be offered to patients undergoing operative laparoscopy for central dysmenorrhea and pelvic pain. This procedure should be performed only by expert endoscopists experienced in the anatomy of this region.

Cohort Studies↗