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Biomedical subjects

A Fleischmann

Publications and source records attributed to A Fleischmann.

At least 19 recordsLinked to original sources
PubMed2006

Deaths from pesticide poisoning: a global response.

Self-poisoning with pesticides accounts for about a third of all suicides worldwide. To tackle this problem, the World Health Organization announced a global public health initiative in the second half of 2005. Planned approaches were to range from government regulatory action to the development of new treatments for pesticide poisoning. With broad-based support, this strategy should have a major impact on the global burden of suicide.

Global Health↗
PubMed2004

Novel isotope effects observed in polarization echo experiments in glasses.

In recent years unexpected magnetic field effects have been observed in dielectric measurements on insulating glasses at very low temperatures. Polarization echo experiments have indicated that atomic tunneling systems are responsible for these effects and that the nuclear properties of the tunneling particles are of importance. Subsequently, it was suggested that the magnetic field effects are caused by tunneling systems carrying a nuclear quadrupole moment. Now we have studied the isotope effect in echo experiments on fully deuterated and ordinary glycerol clearly showing the crucial role of the nuclear quadrupole moments for the magnetic field effects. In addition, we have observed a new effect in the decay of spontaneous echoes in zero magnetic field for the deuterated samples which can be explained in terms of a quantum beating involving the quadrupole levels.

Journal Article↗
PubMed2004

[The impact of methodology on the reported prevalence of thyroid pathology: comparison of two autopsy series from Switzerland performed with different methods].

To investigate the impact of methodology on the detection and hence reported prevalence of pathological findings in thyroids, in the geographic area of Kt. Thurgau in Switzerland, we used two different methods in two consecutive autopsy series of 420 patients. In series A, the thyroids were sliced unfixed and only suspect lesions were examined histologically. In series B, the thyroids were fixed in formalin and sectioned in a standardized manner. At least one specimen per lobe was taken for histological examination. Series A revealed that five patients had adenomas, four malignant primary tumors, two metastases and four inflammatory changes in the thyroid. Series B detected ten patients with adenomas, eight with primary malignant tumors, eleven with metastases and twenty-eight with inflammatory changes in the thyroid. These differences were significant (p < 0.001). In conclusion, the methodology has an important impact on the detected prevalence of pathological findings in the thyroid.

Adolescent↗
PubMed2004

Umbilical endometriosis.

We report two women who presented with a recurrent, mildly painful, bluish nodule in the umbilicus. Both patients complained of local tenderness and occasional bleeding that increased during menstruation. Neither patient had had previous pelvic surgery. Excision of the lesions revealed a primary umbilical endometriosis; in one case, a simultaneous laparoscopy showed a pelvic endometriosis. We review the current literature and discuss the possible etiopathogenesis and when a laparoscopy is indicated to diagnose a concomitant pelvic endometriosis. Umbilical endometriosis is a very rare disease but should be considered in the differential diagnosis of umbilical lesions.

Adult↗
PubMed2003

[Rare seminoma metastasis to the corpus spongiosum and urethra].

Anaplastic seminomas account for 5-10% of all seminomas. Their metastatic pattern is similar to the classic form of seminoma. We report on an oligophrenic patient with seminoma pT1 who developed a metastasis to the corpus spongiosum and penile urethra, which was successfully treated by local external radiotherapy resulting in long-term tumor remission over a 4-year follow-up period.

Adult↗
PubMed2001

Pelvic lymph node metastases from bladder cancer: outcome in 83 patients after radical cystectomy and pelvic lymphadenectomy.

PURPOSE: We evaluate the outcome in patients with node positive bladder cancer with particular reference to the effect of individual characteristics of positive nodes on survival after meticulous pelvic lymphadenectomy at cystectomy. MATERIALS AND METHODS: This prospective analysis contains 452 cases of bladder cancer staged preoperatively as N0M0, managed with pelvic lymphadenectomy and cystectomy between 1984 and 1997. A total of 83 (18%) patients with histologically confirmed node positive disease are included in our study. RESULTS: The median overall survival of patients with positive nodes was 20 months. Median 5-year survival was 29%. Patients who survived were found with positive nodes at each site in the pelvis. The median survival of 57 patients with less than 5 positive nodes was 27 months, compared with 15 months for 26 with 5 nodes or more (log-rank test p = 0.0027). Median survival of 26 patients with no lymph node capsule perforation was 93 months, compared with 16 months for 57 with capsule perforation (p = 0.0004). The median survival of 18 patients with a maximum diameter of lymph node metastasis up to 0.5 cm. was 64 months, compared with 16 months for 65 with nodal metastasis greater than 0.5 cm. (p = 0.024). Contralateral positive nodes were found in 16 of 39 (41%) patients with unilateral bladder cancer. CONCLUSIONS: Long-term survival is possible with node positive bladder cancer. Those patients with few as well as smaller and, therefore, unsuspected nodal metastases, and those without lymph node capsule perforation have the best results after removal of pelvic metastatic nodal disease. Because patients who survive may be found regardless of the site of pelvic nodal metastases, meticulous bilateral pelvic lymphadenectomy is warranted in all patients at the time of attempted curative cystectomy for bladder cancer, particularly if there is no clinical evidence of nodal involvement.

Adult↗
PubMed2000

Fra-1 replaces c-Fos-dependent functions in mice.

Structure-function analysis as well as studies with knock-out and transgenic mice have assigned distinct functions to c-Fos and Fra-1, two components of the transcription factor AP-1 (activator protein-1). To test whether Fra-1 could substitute for c-Fos, we generated knock-in mice that express Fra-1 in place of c-Fos. Fra-1 rescues c-Fos-dependent functions such as bone development and light-induced photoreceptor apoptosis. Importantly, rescue of bone cell differentiation, but not photoreceptor apoptosis, is gene-dosage dependent. Moreover, Fra-1 fails to substitute for c-Fos in inducing expression of target genes in fibroblasts. These results show that c-Fos and Fra-1 have maintained functional equivalence during vertebrate evolution.

Animals↗
PubMed2000

The EGF receptor provides an essential survival signal for SOS-dependent skin tumor development.

The EGF receptor (EGFR) is required for skin development and is implicated in epithelial tumor formation. Transgenic mice expressing a dominant form of Son of Sevenless (SOS-F) in basal keratinocytes develop skin papillomas with 100% penetrance. However, tumor formation is inhibited in a hypomorphic (wa2) and null EGFR background. Similarly, EGFR-deficient fibroblasts are resistant to transformation by SOS-F and rasV12, however, tumorigenicity is restored by expression of the anti-apoptotic bcl-2 gene. The K5-SOS-F papillomas and primary keratinocytesfrom wa2 mice display increased apoptosis, reduced Akt phosphorylation and grafting experiments imply a cell-autonomous requirement for EGFR in keratinocytes. Therefore, EGFR functions as a survival factor in oncogenic transformation and provides a valuable target for therapeutic intervention in a broader range of tumors than anticipated.

Animals↗
PubMed2000

Bombesin receptors in distinct tissue compartments of human pancreatic diseases.

Overexpression of receptors for regulatory peptides in various human diseases is reportedly of clinical interest. Among these peptides, bombesin and gastrin-releasing peptide (GRP) have been shown to play a physiological and pathophysiological role in pancreatic tissues. Our aim has been to localize bombesin receptors in the human diseased pancreas to identify potential clinical applications of bombesin analogs in this tissue. The presence of bombesin receptor subtypes has been evaluated in specimens of human pancreatic tissues with chronic pancreatitis (n = 23) and ductal pancreatic carcinoma (n = 29) with in vitro receptor autoradiography on tissue sections incubated with 125I-[Tyr4]-bombesin or the universal ligand 125I-[D-Tyr6, beta-Ala11, Phe13, Nle14]-bombesin(6-14) as radioligands and displaced by subtype-selective bombesin receptor agonists and antagonists. GRP receptors were identified in the pancreatic exocrine parenchyma in 17 of 20 cases with chronic pancreatitis. No measurable bombesin receptors were found in the tumor tissue of ductal pancreatic carcinomas, however, GRP receptors were detected in a subset of peritumoral small veins in 19 of 29 samples. Moreover, residual pancreatic islets in these tissues were shown to express the BB3 receptor subtype. These data demonstrate the presence of bombesin receptors in three distinct tissue compartments of the pancreas, namely GRP receptors in the exocrine parenchyma in chronic pancreatitis and in peritumoral vessels around ductal pancreatic carcinomas, and BB3 receptors in residual pancreatic islets. Such a selective expression of bombesin receptor subtypes in pancreatic tissues may not only be of pathophysiological significance but may represent the basis for potential diagnostic and therapeutic clinical applications of bombesin analogs, including GRP receptor scintigraphy to differentiate chronic pancreatitis from ductal pancreatic carcinoma.

Adenocarcinoma↗
PubMed1999

[A normal thyroid gland upon autopsy: a relatively uncommon finding].

In a series of 420 autopsies the thyroid glands have been weighed, serial sections made and examined histologically with at least one specimen per lobe. There is an age-dependent increase in mean thyroid weight. In the 7th decade the mean weight exceeds 29 g and weights above this are regarded as goitre. Between the 4th and 8th decade the incidence of goitre is 20-30%, after which the incidence rises steadily to 64% in the 10th decade. The commonest thyroid pathology is hyperplastic nodules, which are found in 39% of patients (49.4% of males and 33.4% of females). 2.4% of all patients have adenomas, 1.9% primary carcinomas and 2.8% thyroid metastases. Inflammatory infiltrates are observed in 6.6% of cases (9.4% of females and 4.4 of males). To establish the incidence of normal thyroid glands we have studied 840 serial autopsies. Only 25% of thyroids are normal (19% of females and 30% of males). The incidence of normal thyroid glands tends to decrease with age and in no decade does it reach 50%.

Adult↗
PubMed1999

Chronic treatment with repetitive transcranial magnetic stimulation inhibits seizure induction by electroconvulsive shock in rats.

BACKGROUND: Studies in laboratory animals suggest that repetitive transcranial magnetic stimulation (rTMS) and electroconvulsive shock (ECS) increase seizure inhibition acutely. This study was designed to explore whether chronic rTMS would also have seizure inhibition properties. METHODS: To this purpose we administered rTMS (Magstim Rapid) and sham rTMS twice daily (2.5 T, 4-sec train duration, 20 Hz) to two groups of 10 rats for 16 days. The rTMS coil was a 50-mm figure-8 coil held directly over the rat's head. Raters were blind to experimental groups. On days 11, 17, and 21 (5 days after the last rTMS) ECS was administered with a Siemens convulsator using three electrical charge levels. Variables examined were the presence or absence of seizures and seizure length (measured from the initiation of the tonic contraction until the end of the limb movement). RESULTS: At day 11 rTMS had no effect on seizures, and both rTMS and sham rTMS animals convulsed equally. At day 17, however, rTMS-treated animals convulsed significantly less (both at presence/absence of seizures, and at seizure length) than sham rTMS animals. At day 21 the effects of rTMS had disappeared. CONCLUSIONS: These findings suggest that rTMS administered chronically leads to changes in seizure threshold similar to those reported for ECS and ECT; however, these effects were short-lived.

Animals↗
PubMed1996

Transcranial magnetic stimulation downregulates beta-adrenoreceptors in rat cortex.

Recently, a method for transcranial magnetic stimulation (TMS) of the brain has been developed. Thus, it is possible to explore neurochemical and behavioral effects of TMS in rats. Repeated TMS (9 days) reduced beta-adrenergic receptor binding in cortex, as does electroconvulsive shock (ECS) and other antidepressant treatments. Thus TMS appears to be a potential antidepressive treatment.

Adrenergic beta-Agonists↗
PubMed1995

The effect of transcranial magnetic stimulation of rat brain on behavioral models of depression.

Magnetic stimulation of the brain in unanesthetized humans and animals can painlessly induce motor movements and has recently been reported to have antidepressant properties. In behavioral models of depression and electroconvulsive therapy including enhancement of apormorphine-induced stereotypy, reduction of immobility in the Porsolt swim test and increases in seizure threshold for subsequent stimulation, magnetic stimulation of rat brain had effects similar to those of electroconvulsive shock.

Animals↗
PubMed1995

GABAA receptor activation induces GABA and glutamate release from preoptic area.

The effect of GABA receptor agonists on release in vitro of radiolabeled GABA and glutamate was studied using a crude preparation of isolated nerve terminals (neurosomes). GABA agonists were incubated (2 min, 37 degrees C) with neurosomes prepared from hypothalamus, preoptic area (POA) and frontal cortex tissues. Under these conditions, GABA and the GABAA receptor agonist muscimol, but not the GABAB receptor agonist baclofen, stimulated 3H-GABA and 3H-glutamate release from POA but not hypothalamic or cortical neurosomes of gonadally intact male rats. These effects were inhibited by the GABAA receptor antagonists picrotoxin, bicuculline and SR-95531. Significant efflux of 3H-glutamate could be elicited from cortical neurosomes following longer (5 min) incubations with 500 microM GABA and 400 microM muscimol. Muscimol-induced release of 3H-glutamate and 3H-GABA was dependent on extracellular calcium. Muscimol and GABA failed to release 3H-GABA or 3H-glutamate from POA neurosomes of ovariectomized female rats. However, administration of estradiol and progesterone to ovariectomized females prior to sacrifice caused the appearance of muscimol induced-release of amino acids from POA neurosomes comparable to that obtained in male rats. GABA-induced release of 3H-glutamate was similarly dependent on pretreatment of ovariectomized rats with ovarian steroids. GABAA receptor-induced release of amino acids is therefore brain region-specific and modified by hormonal status.

Animals↗
PubMed1993

Tail-pinch induced analgesia and immobility: altered responses to noxious tail-pinch by prior pinch of the neck.

Noxious pinch to the scruff of the neck using a metal clip produces profound immobility and analgesia. Noxious pinch delivered to the tail fails to induce immobility and results in nociceptive behavior directed at the pinched tail. However, when administered shortly after neck-clip removal, noxious tail-pinch reinstated immobility without any nociceptive response. Prior neck-clip also enhanced the antinociception induced by the tail-pinch as measured by nociceptive response to a leg pinch. Immobility, as well as antinociception, decreased as the time interval between neck-clip removal and the tail-pinch application increased. Pharmacological manipulations which reduce nociception produced a similar alteration in the response to tail-pinch. Thus, following local injections antinociceptive doses of lidocaine to the base of the tail and systemic morphine administration tail-pinch produced marked immobility. Transection of the brain at the intercollicular level provides evidence for supraspinal involvement in post-neck pinch effects. Not only was the ability of prior neck-pinch to confer antinociceptive properties on tail-pinch abolished, but increased responsiveness to noxious tail-pinch was seen. We, therefore, propose that prior neck-pinch confers new stimulus properties on noxious pinch of other body regions resulting in an enhanced antinociceptive effect, which affects both remote regions and the site of stimulation, and the ability to induce immobility.

Analgesia↗
PubMed1992

Characterization of glutamate efflux from preoptic area synaptosomes.

Treatment of ovariectomized rats in vivo with ovarian steroids has been found to influence the efflux of glutamate and gamma-aminobutyric acid from preoptic area synaptosomes incubated in vitro. Since these studies indicated a possible role of the glutamate carrier in steroid-modulated release of amino acids, the present studies examined the characteristics of efflux of glutamate and of the carrier system for glutamate in synaptosomes of the preoptic area derived from ovariectomized hormone-treated rats. The efflux of [3H]glutamate from preoptic area synaptosomes, was induced by glutamate and by the glutamate carrier agonist, D-aspartate; the putative glutamate carrier antagonist dihydrokainate failed to block this efflux. Dihydrokainate inhibited the uptake of glutamate but it was less effective than D-aspartate. The excitatory amino acid receptor agonists, N-methyl-D-aspartate and kainate were without effect while quisqualate modestly stimulated the efflux of [3H]glutamate. Efflux of [3H]glutamate, induced by glutamate itself or by D-aspartate was not blocked by the excitatory amino acid receptor antagonists, D-2-amino-5-phosphonovaleric acid, 6,7-dinitroquinoxaline-2,3-dione or kynurenate. Glutamate-induced efflux of [3H]glutamate did not require external Ca2+. Glutamate altered neither the basal nor the potassium-induced increases in the intrasynaptosomal concentration of Ca2+ as measured by the fura-2 method. Glutamate-induced efflux of [3H]glutamate was blocked by the putative chloride channel antagonist, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. It is concluded that the glutamate-induced efflux of [3H]glutamate in synaptosomes of the preoptic area is a carrier-mediated process that does not require activation of receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Estradiol plus progesterone promote glutamate-induced release of gamma-aminobutyric acid from preoptic area synaptosomes.

Treatment of ovariectomized rats with both estradiol and progesterone in vivo resulted in a marked enhancement of glutamate-induced release of newly synthesized [3H]gamma-aminobutyric acid (GABA) from synaptosomes of the preoptic area in vitro. With this treatment, as little as 0.01 nM glutamate, in vitro, enhanced release of GABA. In contrast, glutamate, in vitro, did not stimulate release of GABA from synaptosomes, obtained from rats treated with either estradiol or progesterone alone and only large concentrations of glutamate (1.0 and 10 mM) caused a modest release of GABA from synaptosomes from ovariectomized, vehicle-treated rats. Also, treatment with estradiol plus progesterone did not alter glutamate-induced release or exchange of [3H]glutamate. Glutamate-induced release of GABA was calcium-independent and attenuated by the putative chloride channel antagonist, 4,4'-diisothiocyanatostilbene-2,2'-DL-disulfonic acid. Thus, glutamate-induced, steroid-enhanced release of GABA may occur through a chloride-dependent carrier rather than by exocytosis. In addition to enhancement by glutamate, release of GABA was also enhanced by D-aspartate, an agent that is transported by the neuronal glutamate carrier. It is postulated that enhancement of glutamate-induced release of GABA, by estradiol plus progesterone in the preoptic area, represents one process by which these steroids modulate reproductive function in female rats.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗