Update in imaging tests used for the localization of parathyroid pathology.

Preoperative localization of parathyroid pathology, generally a parathyroid adenoma, can be difficult in some cases due to the anatomical variants that these glands present. The objective of this review is to analyse the different imaging techniques used for preoperative localization of parathyroid pathology (scintigraphy, ultrasound, CT, MRI and PET). There is great variability between the different tests for the preoperative localization of parathyroid pathology. The importance of knowing the different diagnostic options lies in the need to choose the most suitable test at each moment and for each patient for an adequate management of primary hyperparathyroidism (PHP) with surgical criteria.

No evidence of cellular alterations by MilliTesla-level static and 50 Hz magnetic fields on S. cerevisiae.

In an attempt to determine whether magnetic field (MF) exposures might induce cellular alterations, S. cerevisiae yeast cells were exposed to static or sinusoidal 50 Hz homogeneous MF (0.35 mT, 1.4 mT, and 2.45 mT) for 1 h and 72 h. Unsynchronized cells grown exponentially while exposed to MF, containing cells in all stages of the mitotic cell cycle. MF was generated by a pair of Helmholtz coils (40 cm in diameter, coaxial, separated by 20 cm). Survival, cell cycle distribution, colony forming ability, and mutation frequency were assayed. No differences in the above-mentioned parameters were observed in MF exposed samples in relation to unexposed controls, suggesting that homogeneous MF at these intensities do not produce appreciable cellular alterations in this organism under typical in vitro growth conditions.

No effect of 50 Hz 2.45 mT magnetic field on the potency of cisplatin, mitomycin C, and methotrexate in S. cerevisiae.

Drug resistance is an obstacle for chemotherapy success. Because of this, this work aims to improve the cell killing effect of antineoplastic drugs by magnetic field (MF) co-exposure. S. cerevisiae cells were exposed to 2.45 mT, sinusoidal 50 Hz MF, during 48 h, and the drugs cisplatin (cisPt), mitomycin C (MMC), or methotrexate (MTX); 100 and 1,000 microg/ml. Survival was assayed by the drop test. The results showed that MF exposures do not induce alterations in the potency of cisPt, MMC, and MTX on these cells in relation to untreated controls. In addition, a strong correlation between temperature and potency of cisPt was found, which contribute to the establishment of the importance of an exhaustive control of temperature in experiments carried out with temperature sensitive antineoplastic agents in co-exposure with MF; avoiding differences between MF-exposed samples and unexposed controls and contributing to the performance of experiments under well-defined and controlled conditions.

Static and 50 Hz magnetic fields of 0.35 and 2.45 mT have no effect on the growth of Saccharomyces cerevisiae.

The present work reports the growth effects induced by static and sinusoidal 50 Hz magnetic fields (MF) on the haploid yeast strain Saccharomyces cerevisiae WS8105-1C. Magnetic fields were generated by a pair of Helmholtz coils (40 cm in diameter) with 154 turns of copper wire in each and separated 20 cm. The experiments were performed at 0.35 and 2.45 mT, and yeasts were exposed to MF during 24 and 72 h in the homogeneous field area. Growth was monitored by measuring the optical density at 600 nm. The data presented in the current report indicate that static and sinusoidal 50 Hz MF (0.35 and 2.45 mT) do not induce alterations in the growth of S. cerevisiae.

Methotrexate cytotoxicity on MCF-7 breast cancer cells is not altered by exposure to 25 Hz, 1.5 mT magnetic field and iron (III) chloride hexahydrate.

The action of electromagnetic fields (EMF) on different pathways related to cell physiology, proliferation, toxicity of chemicals, gene expression, etc., are currently being investigated although the results are still not conclusive and even conflicting. In laboratory and animal studies, EMF has been found to produce a great variety of effects such as: increase in ornithine decarboxylase activity in breast, increase in beta-galactosidase gene expression and oncogene transcription after exposure to 50/60 Hz. Animal studies have shown that the use of EMF can enhance drug delivery across biological barriers (rat abdominal skin), using benzoic acid as the drug candidate. It has been reported by different authors that pulsed EMF (PEMF) can produce alterations in antineoplastic drugs potency. In the present study, we investigated the effects of PEMF on methotrexate cytotoxicity in MCF-7 breast cancer cells and the effects with simultaneous exposure to FeCl3. The data presented in the current report indicate that PEMF (25 Hz, 1.5 mT) do not induce modulation of the action of methotrexate (with and without iron-III) in MCF-7 cells when they are exposed to PEMF for 2 h/day during 3 days.

25 Hz electromagnetic field exposure has no effect on cell cycle distribution and apoptosis in U-937 and HCA-2/1cch cells.

It is reported that exposure to 50 Hz extremely low-frequency electromagnetic field (ELF-EMF) can produce apoptosis and small variations in cell cycle distribution on different cell lines. In order to study the effect of ELF-EMF on tumoral cells in vitro, two cell lines (U-937, from a histiocytic lymphoma, and HCA-2/1cch, from a human colon adenocarcinoma) were exposed to 25 Hz, 1.5 mT, for 2 h and 45 min. Cell cycle distribution, apoptosis (spontaneous and dexamethasone-induced) and cell growth were evaluated. Neither significant alteration in cell cycle phases nor induction of apoptosis was observed. Nevertheless, the relative cell number was found to decrease to 55.84+/-7.35% (p <0.05, Student's t-test) for HCA-2/1cch cells after exposure to EMF in the presence of dexamethasone. The presence of dexamethasone during the EMF exposure could probably produce a decrease in the cell growth of this cell line.

P-glycoprotein, glutathione and glutathione S-transferase increase in a colon carcinoma cell line by colchicine.

The acquisition of resistance to anticancer agents used in chemotherapy is the main cause of treatment failure in malignant disorders, provoking tumours to become resistant during treatment, although they initially respond to it. The main multidrug resistance (MDR) mechanism in tumour cells is the expression of P-gly-coprotein (P-gly), that acts as an ATP-dependent active efflux pump of chemotherapeutic agents. Furthermore, an increased detoxification of compounds mediated by high levels of glutathione (GSH) and glutathione S-transferase (GST), has been found in resistant cells. We developed a study aiming to evaluate the evolution of the main drug resistance markers in tumour cells: P-gly, GSH and GST, during the acquisition of resistance to colchicine, for the purpose of studying the adaptation process and its contribution to the MDR phenomenon. A human colon adenocarcinoma cell line was exposed to colchicine during 82 days, being P-gly, GSH levels and GST activity evaluated by flow cytometry, spectrofluorimetry and spectrophotometry, during exposure time. P-gly and GSH levels increased gradually during the exposure to colchicine, reaching 2.35 and 3.21 fold each. On day 82, GST activity increased 1.84 fold at the end of the exposure period. Moreover, an increment in drug cross-resistance was obtained that ranges from 2.62 to 5.22 fold for colchicine, vinblastine, vincristine and mitomycin C. The increments obtained in P-gly, GSH and GST could probably contribute to the MDR phenomenon in this human colon adenocarcinoma cell line.

Multidrug resistance increment in a human colon carcinoma cell line by colchicine.

The most important mechanism in drug resistance is the multidrug resistance (MDR) phenomenon. It is possible to select MDR cells by in vitro exposure to cytotoxic agents. The resistance is due to the hyperexpression of the P-glycoprotein (P-Gp) that take drugs out from the cells. In this study, a colchicine resistant subline (HCA-2/1cch) was selected from a human colon adenocarcinoma after a short period of drug exposure, as an in vitro model of drug resistance selection. These cells showed cross-resistance to other drugs, which were not present in the medium during selection. The relative resistance was 3.32 for colchicine, 3.15 for vinblastine, 2.62 for vincristine and 5.22 for mitomycin C. P-glycoprotein levels were assayed by flow cytometry. It was found that a significant increase of 2.35 and 1.59 had occurred in the peak and mean channel of fluorescence, respectively, indicating an increment of P-glycoprotein expression in relation to the parental line. Moreover, verapamil (10 microg/ml) produced a partial reversion of multidrug resistance. The sensitisation rates were 7.41 for colchicine, 1.25 for vinblastine, 2.36 for vincristine and 1.17 for mitomycin C. The data obtained suggest that colchicine exposure period (10 weeks) and dose (0.5 microg/ml) assayed were sufficient to produce an increment in multidrug resistance. This resistance could be due to higher level of P-Gp expression.

Growth modification of human colon adenocarcinoma cells exposed to a low-frequency electromagnetic field.

The influence of variable low-intensity, low-frequency electromagnetic fields on culture cells is investigated. Human colon adenocarcinoma cells were exposed to a rectangular and variable magnetic field (1 and 25 Hz; 1.5 mT peak). Cultures were exposed to a dose for 15 and 360 minutes, and after 24 hours incubation, cell viability was measured with neutral red stain. The group treated for 15 minutes showed a statistically significant increase in cell growth with 1 Hz (p < 0.002) and 25 Hz (p < 0.003). In contrast, a significant decrease in cell growth was found in those cultures treated with 1 Hz for 360 minutes (p < 0.02). The effects reported could be influenced by the magnetic field frequency and the exposure time.

[P-glycoprotein, a membrane pump that represents a barrier to chemotherapy in cancer patients]. / La glicoproteína-P una bomba de membrana que representa una barrera a la quimioterapia de los pacientes con cáncer.

Multidrug resistance (MDR) in oncology is considered to be the main cause of chemotherapy failure in the treatment of patients with cancer. The resistance mechanism consists in decrease intracellular drug accumulation by P-glycoprotein (Gp-P) overexpression. This protein acts as a drug-extracting pump that needs energy in the process. The efflux takes place by mean of a pore in the cell membrane that consist in twelve segments. The activity of this pump is regulated by protein kinase C and shows homology with other transport systems. The analysis of the presence of Gp-P and the characterization of MDR phenotype in biopsy material could be important in the overcome of the resistance to cancer chemotherapy.

[Multidrug resistance (MDR) in oncology]. / Multirresistencia a drogas (MDR) en oncología.

Multidrug resistance or mdr is a frequent phenomenon for which tumor cells can develop, in only one step, cross-resistance to a different anticancer drugs such as antibiotics, vinca alkaloids and podophylotoxins. This is due to an extrusion of drugs out of the cells, since it is interrelated with the decrease of the intracellular concentration of the drug, compared to sensitive cells. This phenomeno of multidrug resistance (mdr) is considered one of the principal causes of failure in quimiotherapic treatment of cancer, and is associated in many cases to an hyperexpression of mdr-I gene, that codifies for a high molecular weight glycoprotein (p-170) (170-180 Kdaltons), also called p-glycoprotein (pgp). Locadet it in the cellular membrane extracts, like a pump, the quimiotherapic drugs with consumption of ATP. In humans, there are two principal genes that codify for pgp: mdr-I and mdr2/3; being the most important the mdr-I gene. The structure of p-glycoprotein consists in two symmetrical halves anchored in the cellular membrane that includes three extracellular dominances each one, and on intracellular portion with the ATP binding site. Also, has got an for extracellular carbohydrates chain. It is specially important to find drugs that reverse the multidrug resistance. Chemicals such as verapamil, nifedine, quinidine and calmodulin inhibitors are joined to pgp inhibiting it. A Cyclosporine and its non-immunosuppressors derivateds such as SDZ 280-125 and SDZ PSC 833 reverse mdr. At present it is being advancing in clinical trials, but the results are not satisfactory. Most useful chemicals are verapamil, better R-verapamil and A-cyclosporine or its non-immunosuppressors derivates. Futures possibilities are grateful. From diagnostic point of view the mains are: 1. Detection of mdr-I gene. 2. Recognition of the presence of mRNA for pgp. 3. Detection of pgp by flow cytometry or western blot. 4. Immunohistochemistry with monoclonal antibodies to pgp. 5. Rhodamine 123 to study mdr phenotype. 6. Multidrug resistance modulators in vitro. 7. pgp in vivo as a tumor marker. From therapeutic point of view: 1. To assay mdr modulators with higher power and better tolerated. 2. Reversing of mdr with in vivo MoAbs and/or immunotoxins. 3. Gene therapy. 4. New chemicals that joined to tubulin do not be extrused by pgp. 5. Drugs joined to liposomes. 6. Interpheron to increase the efficacy of MoAbs in mdr reversion. 7. Photodynamic therapy. Other possibilities can be the use of MoAbs in diagnostic (immunodetection) by PET and SPECT: and the MoAbs joined to drugs and radioisotopes.

Iron(III) chloride hexahydrate does not enhance methotrexate cytotoxicity on Saccharomyces cerevisiae.

Methotrexate is a potent inhibitor of dihydropholate reductase that has been used as effective antineoplastic treatment due to its capacity to inhibit cell growth. In a previous work published in Bioelectrochemistry 2003;60:81-86, we reported a statistically significant increment of 40.1 and 29.4% in methotrexate potency when MCF-7 breast cancer cells were exposed simultaneously to iron(III) chloride hexahydrate (FeCl(3).6H(2)O) and methotrexate. The aim of this study was to investigate whether iron(III) could produce, on a Saccharomyces cerevisiae wild-type strain, alterations on methotrexate potency by the drop test survival assay and proliferation studies measured after 24 and 96 h of exposure. The data presented in the current report indicate that FeCl(3).6H(2)O (1, 10, 100 and 500 microg/ml) does not induce modulation of the action of methotrexate (10, 100 and 500 microg/ml) in S. cerevisiae yeast cells when they are exposed simultaneously for 24 and 96 h.

He-Ne laser has no effect on cell cycle phases of human colon adenocarcinoma cells.

The aim of this study is to investigate the effect of He-Ne continuous laser (12.6 mW, 632.8 nm), at low energy densities, on cell cycle synchronization of monolayer growing human colon adenocarcinoma cell line. The doubling time of cell culture was used as optimum time to verify laser effect. The monolayer cultures were exposed to single doses of different energy densities (0.042 J cm-2 to 1.68 J cm-2). The nuclear DNA content has been studied by flow cytometry to obtain the cell percentage in each cell cycle phase. Results show no effect of He-Ne laser irradiation on cell cycle short time synchronization under the previously mentioned conditions and cell type. Higher energy densities and multiple irradiations should be investigated.

Influence of 1 and 25 Hz, 1.5 mT magnetic fields on antitumor drug potency in a human adenocarcinoma cell line.

The resistance of tumor cells to antineoplastic agents is a major obstacle during cancer chemotherapy. Many authors have observed that some exposure protocols to pulsed electromagnetic fields (PEMF) can alter the efficacy of anticancer drugs; nevertheless, the observations are not clear. We have evaluated whether a group of PEMF pulses (1.5 mT peak, repeated at 1 and 25 Hz) produces alterations of drug potency on a multidrug resistant human colon adenocarcinoma (HCA) cell line, HCA-2/1(cch). The experiments were performed including (a) exposures to drug and PEMF exposure for 1 h at the same time, (b) drug exposure for 1 h, and then exposure to PEMF for the next 2 days (2 h/day). Drugs used were vincristine (VCR), mitomycin C (MMC), and cisplatin. Cell viability was measured by the neutral red stain cytotoxicity test. The results obtained were: (a) The 1 Hz PEMF increased VCR cytotoxicity (P < 0.01), exhibiting 6.1% of survival at 47.5 microg/ml, the highest dose for which sham exposed groups showed a 19.8% of survival. For MMC at 47.5 microg/ml, the % of survival changed significantly from 19.2% in sham exposed groups to 5.3% using 25 Hz (P < 0.001). Cisplatin showed a significant reduction in the % of survival (44.2-39.1%, P < 0.05) at 25 Hz and 47.5 microg/ml, and (b) Minor significant alterations were observed after nonsimultaneous exposure of cells to PEMF and drug. The data indicate that PEMF can induce modulation of cytostatic agents in HCA-2/1(cch), with an increased effect when PEMF was applied at the same time as the drug. The type of drug, dose, frequency, and duration of PEMF exposure could influence this modulation.

[Gallstones in children. Report of one case and review of the literature (author's transl)]. / Litiasis biliar en niños. Aportación de un caso y revisión de la literatura

A 12 year old boy is presented with choleithiasis and cholecystitis diagnosed by oral cholecistogram and intravenous cholangiogram and managed surgically with a cholecystectomy. A review of 667 cases of cholelithiasis in children is presented from literature, since the first report of gallstones in 1737, until 1975. It is showed that childhood cholelithiasis is a uncommon disease, occurring in all ages but (commoner) in preadolescent and adolescent girls. Etiologic significance of obesity, family history of cholelithiasis, pregnancy and history of previous abdominal surgery is reported. Haemolytic disease is an underlying etiologic agent in less than 19% of 416 cases reviewed. A high percentage of gallstones were visible on plain films of the abdomen and oral cholecystograms were diagnostic of cholelithiasis or showed changes highly suggestive of gallstones in 86% of cases reviewed. In a child with abdominal pain of unknown etiology, it is imperative to exculade the possibility of gallstones, and plain films of the abdomen and oral cholecystography are the best investigative techniques to do this.

[Mesomelic dwarfism Langer type associated to mixed gonadal dysgenesis, whit cariotipe 46,XY/45 X (author's transl)]. / Nanismo mesomélico tipo Langer asociado a disgenesia gonadal mixtra (Shoval) con cariotipo 46,XY/45 X. A propósito de una observación.

Authors present a case of Langer type mesomelic dwarfism in a six months infant, who presented preferentially a mesomelic affection of the limbs, with a typical shortening and deformity of the ulna, radius, tibia and fibula. Articular alteration of the phalanxes of both hands has not been found described in the literature revised. The inusual association of intersexual condition, which corresponds to a Shoval mixed gonadal dysgenesis, with cariotype 46,XY/45 X seems of great interest.

La glicoproteína-P una bomba de membrana que representa una barrera a la quimioterapia de los pacientes con cáncer / P-glycoprotein, a membrane pump that represents a barrier to chemotherapy in cancer patients

La resistencia oncológica a múltiples agentes antineoplásicos o MDR se considera una de las mayores causas de fallo clínico en el tratamiento quimioterápico de pacientes con cáncer. El mecanismo de resistencia consiste en una disminución en la acumulación intracelular de droga por sobreexpresión de la glicoproteína-P (Gp-P). Esta proteína actúa como una bomba extrusora de drogas, dependiente de energía. El eflujo se realiza a través de un canal que forma en la membrana plasmática, constituido por doce segmentos transmembranales. La actividad de esta bomba extrusora esta regulada por la proteína quinasa C y presenta homología con otros sistemas de transporte. El análisis de la presencia de Gp-P y la caracterización del fenotipo MDR en biopsias tumorales podría tener gran importancia en el abordamiento del problema clínico que representa la resistencia tumoral a la quimioterapia (AU)

Multidrug resistance (MDR) in oncology is considered to be the main cause of chemotherapy failure in the treatment of patients with cancer. The resistance mechanism consists in decrease intracellular drug accumulation by P-glycoprotein (Gp-P) overexpression. This protein acts as a drug-extracting pump that needs energy in the process. The efflux takes place by mean of a pore in the cell membrane that consist in twelve segments. The activity of this pump is regulated by protein kinase C and shows homology with other transport systems. The analysis of the presence of Gp-P and the characterization of MDR phenotype in biopsy material could be important in the overcome of the resistance to cancer chemotherapy (AU)