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Y Lopez

Publications and source records attributed to Y Lopez.

18 recordsLinked to original sources
PubMed2000

External beam irradiation plus (192)Ir implant after breast-preserving surgery in women with early breast cancer.

PURPOSE: To provide more information for the clinician and to analyze the impact of the boost with brachytherapy on the local disease-free survival (LDFS), disease-free survival (DFS), specific overall survival (OS), and cosmesis, a retrospective study of external radiation therapy and (192)Ir implantation in early breast cancer at Institut Català d'Oncologia has been undertaken. PATIENTS AND METHODS: From 1986 to 1996, 530 patients were selected for this study with a median follow-up period of 39.5 months (range, 10-115 months). External radiation therapy (combined with brachytherapy) was administered postoperatively to the breast in all patients. Mean given dose was 48.7 Gy (range, 42-52 Gy) with external radiation therapy to the breast, and 16.8 Gy (range, 10-27 Gy) was the mean dose with brachytherapy. Variables have been tested for cosmesis. Univariate and multivariate analysis have also been carried out. RESULTS: Mean age of the patients was 54 years (range, 28-81 years). Stages were distributed as follows: 350 patients (66%) in Stage I, 173 in Stage II (32.8%), and 7 in Stage III (1.1%). Pathologic distribution was 445 patients with infiltrating ductal carcinoma (84%), 20 patients with infiltrating lobular carcinoma (4%), and 65 patients (12%) of a miscellaneous group. OS for the entire group was 89.4% and 85.9% at 5 and 7 years respectively. Probability of DFS was 81.7% and 70.1% at 5 and 7 years. The LDFS was 94.9% and 91.7% at 5 and 7 years. The MFS probability was 85.5% and 76.9% at 5 and 7 years, respectively. Univariate analysis demonstrated that age (older than 52 years), premenopausal status, moderate and high histologic grades (Grades II-III), and presence of intraductal comedocarcinoma were prognostic factors for local relapse. Multivariate analysis for local disease-free survival demonstrated that only perineural or muscular infiltration remain as prognostic factors. Tumor dose bed of 70 Gy or higher had a negative impact in breast subcutaneous fibrosis, whereas dose rate lower than 65 cGy/h was better for skin color at 2 years. CONCLUSION: We conclude that patients with early-stage breast cancer undergoing external radiotherapy and LDR brachytherapy can be effectively managed. Overall survival, long-term local control, and cosmetic control are excellent.

Adult↗
PubMed2000

[The temporomandibular joint: recentering...some debate!].

In comparison with hip pathology, the authors emphasize the importance of the biomechanical factor in the stomatognathic systems physiology and pathology. They denounce a syllogism which is set as a reference for the justification of orthodontics and dentistry.

Biomechanical Phenomena↗
PubMed1997

Synergistic antinociceptive interactions of morphine and clonidine in rats with nerve-ligation injury.

BACKGROUND: Ligation injury of the L5/L6 nerve roots in rats produces behavioral signs representative of clinical conditions of neuropathic pain, including tactile allodynia and thermal and mechanical hyperalgesia. In this model, intrathecal morphine shows no antiallodynic activity, as well as decreased antinociceptive potency and efficacy. This study was designed to explore the antinociceptive activity of intrathecal clonidine alone or in combination with intrathecal morphine (1:3 fixed ratio) in nerve-injured rats. The aims, with this study, were to use nerve-injured animals to determine: (1) whether the antinociceptive potency and efficacy of intrathecal clonidine was altered, and (2) whether the combination of intrathecal morphine and clonidine would act synergistically to produce antinociception. METHODS: Unilateral nerve injury was produced by ligation of the L5 and L6 spinal roots of male Sprague-Dawley rats. Sham-operated rats underwent a similar surgical procedure but without nerve ligation. Morphine and clonidine were given intrathecally through implanted catheters alone or in a 1:3 fixed ratio. Nociceptive responses were measured by recording tail withdrawal latency from a 55 degrees C water bath, and data were calculated as % maximal possible effect (%MPE). RESULTS: Morphine produced a dose-dependent antinociceptive effect in both sham-operated and nerve-injured rats. The doses calculated to produce a 50 %MPE (i.e., A50) (+/-95% confidence intervals [CI]) were 15 +/- 4.9 micrograms and 30 +/- 18 micrograms, respectively. Though morphine was able to produce a maximal response (100%) in sham-operated rats, the maximal response achieved in nerve-injured animals was only 69 +/- 21.9 %MPE. Clonidine produced a dose-dependent effect, with an A50 (+/-95% CI) of 120 +/- 24 micrograms in sham-operated rats. In nerve-ligated rats, clonidine produced a maximal effect that reached a plateau of 55 +/- 10.9 %MPE and 49 +/- 10.2 %MPE at 100 and 200 micrograms, respectively, preventing the calculation of an A50. In sham-operated rats, a morphine-clonidine mixture produced maximal efficacy, with an A50 (+/-95% CI) of 15 +/- 9.2 micrograms (total dose), significantly less than the theoretical additive A50 of 44 +/- 10 micrograms. In L5/L6 nerve-ligated rats, the morphine-clonidine combination produced maximal efficacy, with an A50 (+/-95% CI) of 11 +/- 5.4 micrograms (total dose), which was significantly less than the theoretical additive A50 of 118 +/- 73 micrograms, indicating a synergistic antinociceptive interaction. The intrathecal injection of [D-Ala2, NMePhe4, Gly-ol]enkephalin (DAMGO) produced A50 values of 0.23 microgram (range, 0.09-0.6) and 0.97 microgram (range, 0.34-2.7) in sham-operated and ligated rats, respectively. Phentolamine (4 mg/kg, intraperitoneally) produced no antinociceptive effect alone and attenuated, rather than enhanced, the effect of morphine in both groups of rats. CONCLUSIONS: These data show that: (1) clonidine, like morphine, loses antinociceptive potency and efficacy after nerve ligation injury, and (2) strongly suggest that a spinal combination of morphine and clonidine synergize under conditions of nerve injury to elicit a significant antinociceptive action when either drug alone may be lacking in efficacy. It is unlikely that the synergy of morphine with clonidine is due to an attenuation of spinal sympathetic outflow by clonidine, because the sympatholytic agent phentolamine produced an opposing effect on morphine antinociception. The data suggest that combinations of morphine and clonidine may prove useful in controlling pain in patients with neuropathic conditions.

Adrenergic alpha-Agonists↗
PubMed1996

Nitric oxide modulates neuropeptide Y regulation of ion transport in mouse ileum.

The possible involvement of nitric oxide in the regulation of intestinal ion transport induced by neuropeptide Y (NPY) was investigated by evaluating the effects of NG-methyl-L-arginine (L-NMA), L-arginine and S-nitroso-N-acetylpenicillamine (SNAP) on NPY activity in mouse ileum mounted in Ussing chambers in vitro. Serosal NPY (10 nM) produced a sustained decrease in basal transmural short circuit current (Isc) and potential difference without altering the tissue conductance. Pretreatment of tissues with L-arginine (3 mM), but not D-arginine (10 mM), blocked the NPY-mediated changes in Isc. This L-arginine effect on NPY activity was reversed by L-NMA (3 mM), and not by NG-methyl-D-arginine (10 mM). The L-arginine effect on NPY activity was concentration-related with an A50 (95% CL) value of 1.6 (0.9-2.3) mM. In contrast to L-arginine, L-NMA (1 mM) pretreatment of tissues produced an enhancement of NPY activity, resulting in a 3.8-fold leftward displacement of the NPY concentration-response curve; NG-methyl-D-arginine was without effect. The effect of L-NMA on NPY activity was concentration-related with an A50 (95% CL) value of 45.3 (23.2-68.8) microM. Serosal application of SNAP, a nitric oxide donor, produced a concentration-related decrease in basal Isc and potential difference without altering tissue conductance with an A50 (95% CL) value of 22.5 (11.1-40.5) microM. Pretreatment of tissue with SNAP (100 microM) reduced the NPY activity with rightward displacement of NPY concentration-response curve. Pretreatment of tissues with L-arginine also blocked the reduction of Isc by [D-Pen2, D-Pen5]enkephalin (10-30 nM), H2N-Tyr-D-Ala-Phe-Glu-Val-Val-Gly-NH2 (10-30 nM) and somatostatin (0.3-1.0 microM), but had no effect on norepinephrine (0.1-0.3 microM)-induced decrease in mouse ileal Isc. These results show that [fgc]l-arginine and SNAP block NPY-mediated changes in ion transport, suggesting that nitric oxide may play a role in the regulation of NPY-mediated ion transport in the mouse ileum.

Animals↗
PubMed1995

Attenuation of gastrin-induced gastric acid secretion by antisense oligonucleotide to the CCKB/gastrin receptor.

The effects of treatment with CCK receptor antagonists or administration of an antisense oligonucleotide to the gastrin receptor, on gastrin-I and cholecystokinin-8-induced acid secretion in mouse stomach were evaluated. Administration of gastrin-I (1 microM) or cholecystokinin-8 (30 nM) stimulated acid output at the rates of 2.6 +/- 0.27 and 1.0 +/- 0.21 microEq h-1, respectively. Gastrin-I-induced acid output was significantly blocked by pretreatment of stomachs with 3R[+]-N-[2,3-dihydro-1-methyl-2-oxo-5- phenyl-1H-1,4-benzodiazepin-3-yl]-N[3-methylphenyl[urea (L-365,260; 1 microM), but not by devazepide (L-364,718; 1 microM). Cholecystokinin-8-induced acid output, on the other hand, was sensitive to both L-365,260 (100 nM) and L-364,718 (100 nM). Administration of antisense, but not mismatch, oligonucleotide significantly reduced gastrin-induced acid output, while antisense oligonucleotide treatment had no effect on cholecystokinin-8-induced acid output. These results of antagonist and antisense oligonucleotide studies suggest that gastrin-I and cholecystokinin-8 may involve different receptor subtypes in stimulating gastric acid secretion in mice, and that antisense oligonucleotide administration may serve an useful tool in characterizing CCK/gastrin receptor subtypes.

Animals↗
PubMed1995

The loss of antinociceptive efficacy of spinal morphine in rats with nerve ligation injury is prevented by reducing spinal afferent drive.

Nerve ligation injury in rats may represent a useful model of some clinical neuropathic pains. Activation of N-methyl-D-aspartate (NMDA) receptors may maintain central sensitivity and contribute to neuropathic pain. Here, nerve injury was produced by unilateral ligation of the L5 and L6 spinal roots of the sciatic nerve of rats. Catheters were inserted for intrathecal (i.th.) or local delivery of drugs at the site of nerve ligation. Acute nociception was measured by the 55 degrees C water tail flick test in sham-operated and nerve-injured rats, and allodynia was determined by measuring response to von Frey filaments. In sham-operated rats, morphine (30 micrograms, i.th.) produced a 60 +/- 14.4% MPE (maximal possible effect). MK-801 pretreatment did not alter tail-flick latency or morphine antinociception in sham-operated rats. In nerve-injured rats, morphine (30 micrograms, i.th.) produced a significantly lower antinociceptive effect than in controls (34 +/- 6.3% MPE). While MK-801 alone did not alter tail-flick latency in nerve-injured rats, it significantly enhanced the antinociceptive effect of morphine to 84 +/- 16.0% MPE. Bupivacaine (0.2 ml, 0.75% w/v) at the site of injury also significantly increased the efficacy of morphine (100 +/- 0% MPE) without affecting tail flick latency alone. Bupivacaine administered at the site of injury also produced a significant antiallodynic effect of 94 +/- 7.4% MPE. The reduction in antinociceptive efficacy of i.th. morphine in nerve injured rats may be due, in part, to an ongoing spontaneous activity initiated by ectopic foci at the site of injury, and possible NMDA receptor-mediated activity of spinal neurons.

Analgesics, Opioid↗
PubMed1995

Inhibition by spinal morphine of the tail-flick response is attenuated in rats with nerve ligation injury.

Nerve ligation injury in rats produces increased sensitivity and exaggerated responses to nociceptive stimuli (hyperalgesia) as well as nociceptive responses to normally innocuous stimuli (allodynia) analogous to clinical conditions of neuropathic pain. However, the effect of nerve injury on acute nociception has not been extensively studied. Nerve ligation injury was produced by unilateral ligation of the L5 and L6 spinal roots of the sciatic nerve of male Sprague-Dawley rats. Intrathecal (i.th.) catheters were inserted for spinal drug administration. Response to acute nociception was measured by determining the latency to a rapid flick of the tail (TF) after immersion into a 55 degrees C water bath before (control) and after i.th. morphine administration. No change in baseline response to the nociceptive stimulus was observed in either sham-operated or nerve-injured rats. In sham-operated rats, morphine produced dose-dependent antinociception with a 97 +/- 2.3% maximal possible effect (MPE) at a 60 microgram dose; in these controls A50 (95% CL) was 22 micrograms (17-30 micrograms). Morphine administered to rats with nerve injury also produced dose-dependent increase in TF latency, but an MPE of only 60 +/- 17% was obtained at 100 micrograms; higher doses elicited signs of behavioral toxicity. While it was not possible to produce a proper dose-response curve with i.th. morphine in animals with nerve injury, an estimation of the A50 showed approximately a four-fold loss of potency compared to sham-operated controls. Antinociception was readily reversed by naloxone (5 mg/kg, i.p.) in both groups. These data indicate that nerve ligation injury reduces the potency and efficacy of i.th. morphine. While the reasons for this loss of morphine activity in nerve injured animals are unknown, it is possible to speculate that (a) degeneration of primary afferents subsequent to nerve ligation injury might result in a loss of presynaptic opioid (mu?) receptors in the dorsal horn, thereby reducing the antinociceptive activity of morphine at the spinal level; (b) changes in the efficiency of post-receptor transduction may occur following nerve injury which can reduce opioid efficacy; (c) changes in levels of spinal neurotransmitters (e.g., cholecystokinin) may act to diminish opioid action; or (d) sustained afferent input from the site of the injury may be important in limiting the activity of opioids.

Analgesics, Opioid↗
PubMed1994

Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome.

OBJECTIVE: To measure, and seek clinical correlates with, levels of substance P (SP) in the cerebrospinal fluid (CSF) of fibromyalgia syndrome (FMS) patients. METHODS: CSF from 32 FMS patients and 30 normal control subjects was tested for SP by radioimmunoassay. Clinical measures included tender point examination and standardized questionnaires. RESULTS: CSF SP levels were 3-fold higher in FMS patients than in normal controls (P < 0.001), but they correlated only weakly with tenderness found on examination. CONCLUSION: SP is significantly elevated in FMS CSF, but other abnormalities must exist in FMS to more fully explain the symptoms.

Adult↗
PubMed1991

Central and peripheral control of postprandial pyloric motility by endogenous opiates and cholecystokinin in dogs.

The role of endogenous opiates and cholecystokinin (CCK) in the control of postprandial pyloric myoelectric activity was investigated in conscious dogs with chronically implanted intraparietal electrodes at the gastroduodenal junction. Meals consisted of either 20 g/kg of canned food (standard meal) or the same food supplemented with 0.5 mL/kg of arachis oil (fat meal). During the 6 hours after standard and fat meals, the number of pyloric spike bursts, 2-4 seconds in duration, was 61.8 +/- 15.8 and 49.9 +/- 12.7/15 minutes, respectively. Administered 15 minutes before a fat meal, naloxone (50 micrograms/kg IV) decreased the number of spike bursts by 31.4%, whereas methyl-levallorphan, a peripheral opiate antagonist, increased postprandial spike activity by 22.2% when administered IV (0.5 mg/kg) and decreased it when administered intracerobroventricularly at a dose of 10 micrograms/kg. These two antagonists administered in the same conditions before a standard meal had no effect on the postprandial spike activity. A 1-hour infusion of cholecystokinin octapeptide (CCK-8), 500 ng.kg-1.h-1 IV and 50 ng.kg-1.h-1 intracerebroventricularly, performed 1 hour after a standard meal induced a 19.6% and 15.8% decrease in the number of pyloric spike bursts, respectively. Both naloxone IV (50 micrograms/kg) and methyl-levallorphan intracerebroventricularly (10 micrograms/kg) administered before the infusion of CCK-8 reinforced this pyloric inhibition, which was antagonized by methyl-levallorphan IV (0.5 mg/kg). The CCK antagonist asperlicin, 200 micrograms/kg IV and 20 micrograms/kg intracerebroventricularly, administered before a fat meal increased pyloric spike bursts by 22.0% and 31.5%, respectively. These results indicate that after a fat meal, endogenous opiates exert a peripheral inhibitory and central stimulatory control of pyloric motility; they suggest the involvement of both peripheral and central release of CCK.

Animals↗
PubMed1991

Action of endogenous prostaglandins on postprandial pyloric motility: a possible modulation by fats.

The involvement of endogenous prostaglandins (PGs) and the effect of exogenous PGs on the myoelectrical activity of the pylorus were examined for 6 hours after a meal in dogs chronically fitted with intraparietal electrodes on the gastroduodenal junction. The animals received either a standard meal or a fat meal which consisted of canned food added or not (standard meal) with arachis oil. The cyclooxygenase inhibitors, indomethacin (1 mg/kg) and piroxicam (0.2 mg/kg) given prior a fat meal significantly increased the frequency of pyloric spike bursts but did not modify the pyloric motility associated with a standard meal. Synthetic derivatives of PGE1 (misoprostol, 5-10 micrograms/kg) or PGE2 (enprostil 0.5-1 micrograms/kg) reduced the frequency of pyloric contractions after a fat but not a standard meal. It is suggested that both endogenous and exogenous prostaglandins may modulate postprandial pyloric motility when fats are present in sufficient amount into the meal.

Administration, Oral↗
PubMed1987

[An orbitocranial foreign body. Diagnostic reflections].

The authors demonstrate how a delay in diagnosis, in the case of an orbito-cranial foreign body, serves to underscore importance of CT in even minor, orbito-facial injuries, when there is some suspicion of intracranial penetration. This examination, which should be requested as soon as possible in such cases, usually permits detection of the intracranial foreign body. However, if the image is much clearer than those of conventional X-rays, it can in certain cases, remain a matter of subtle interpretation, particularly in cases of less dense materials such as wood.

Adult↗
PubMed1983

Ileal varices revealed by recurrent hematuria in a patient with portal hypertension and Mekong Schistosomiasis.

This present report describes a unique case of a patient with ileal varices revealed by recurrent bleeding from vesical varicosities. Ileal varices were associated with portal hypertension secondary to portal thrombosis. An unusual ileovesical shunt was demonstrated by the venous phase of the superior mesenteric arteriogram. This shunt was favored by adhesions between an abnormal ileal loop, which was infiltrated with ova of schistosoma mekongi, and the superior vesical wall. The patient was treated successively by lysis of adhesions and ileal resection. No portacaval shunt was performed.

Adult↗
PubMedDate not supplied

[Pneumatosis cystoides intestinalis manifested by pneumoperitoneum].

We report the case of a female patient, suffering from chronic respiratory insufficiency and treated with steroids, in whom the discovery of pneumoperitoneum led to exploratory laparotomy. The plain abdominal X-rays demonstrated gas in the walls of the stomach as well as in the peritoneal cavity. Intraoperative exploration revealed the existence of pneumatosis cystoides of the stomach and small intestine. This observation is a reminder that not all cases of pneumoperitoneum are surgical, and notably this is the case for cystic intestinal pneumatosis.

Female↗
PubMedDate not supplied

[Inflammatory pseudo-tumors of appendiceal origin. Study of twelve cases (author's transl)].

The authors relate their experience concerning twelve cases of inflammatory pseudo-tumors of appendiceal origin treated during the last five years. Their personal acquisitions are confronted with the literature and they propose a protocole of clinical, roentgenological and intra-operatory diagnosis thus permitting rational and adapted management.

Adolescent↗