PubMed Health⌕ Search

Biomedical subjects

F Bosch

Publications and source records attributed to F Bosch.

At least 145 records · Page 8Linked to original sources
PubMed1992

Lithium inhibits hepatic gluconeogenesis and phosphoenolpyruvate carboxykinase gene expression.

Incubation of isolated hepatocytes from fasted rats with 20 mM LiCl for 1 h decreased glucose production from lactate, pyruvate, and alanine. In addition, phosphoenolpyruvate carboxykinase (PEPCK) gene expression in FTO-2B rat hepatoma cells was inhibited by treatment with LiCl. Lithium was also able to counteract the increased PEPCK mRNA levels caused by both Bt2cAMP and dexamethasone, in a concentration-dependent manner. A chimeric gene containing the PEPCK promoter (-550 to +73) linked to the amino-3-glycosyl phosphotransferase (neo) structural gene was transduced into FTO-2B cells using a Moloney murine leukemia virus-based retrovirus. In these infected cells, 20 mM LiCl decreased both the concentration of neo mRNA transcribed from the PEPCK-neo chimeric gene and mRNA from the endogenous PEPCK gene. Lithium also inhibited the stimulatory effect of Bt2cAMP and dexamethasone on both genes. The stability of neo mRNA was not altered by lithium, since in cells infected with retrovirus containing only the neo gene transcribed via the retroviral 5'-LTR and treated with 20 mM LiCl, no change in neo mRNA levels was observed. The intraperitoneal administration of LiCl to rats caused a decrease in hepatic PEPCK mRNA, indicating that lithium could also modify gene expression in vivo. The effects of lithium were not due to an increase in the concentration of insulin in the blood but were correlated with an increase in hepatic glycogen and fructose 2,6-bisphosphate levels. These results indicate that lithium ions, at concentrations normally used therapeutically for depression in humans, can inhibit glucose synthesis in the liver by a mechanism which can selectively modify the expression of hepatic phosphoenolpyruvate carboxykinase.

Animals↗
PubMed1992

Meta-analysis of efficacy of zinc acexamate in peptic ulcer.

Zinc acexamate (ZAC) is a new drug for the treatment of peptic ulcer. The present study was performed in order to evaluate the clinical efficacy of ZAC in peptic ulcer, using a meta-analysis of all randomized clinical trials performed with this drug. Eighteen studies were reviewed, but only 13 were considered in the final analysis. The total number of patients was 757. Control groups included placebo or H2 receptor antagonist drugs. Healing rate, assessed by endoscopy, was selected as the criterion for evaluating drug efficacy. The meta-analysis was performed using a modified version of the Mantel-Haenszel method. ZAC proved to be better than placebo in the treatment of peptic ulcer (pooled odds ratio: POR = 5.55; 95% confidence interval: 95% CI = 2.20-14.04) and not different from H2 receptor antagonist drugs when compared in patients with gastric (POR = 1.14; 95% CI = 0.47-2.72), duodenal (POR = 0.97; 95% CI = 0.13-7.33) or both ulcer types (POR = 1.10; 95% CI = 0.74-1.64). The present results show that ZAC is an effective drug for the treatment of peptic ulcer.

Adult↗
PubMed1992

Polycythaemia vera following non-Hodgkin's lymphoma.

A patient with non-Hodgkin's lymphoma (NHL) who developed polycythaemia vera (PV) is reported. Diffuse large-cell NHL was diagnosed and he was subsequently treated with combination chemotherapy including high dose cyclophosphamide and procarbazine. Four and a half years after chemotherapy splenomegaly developed, coincidently with the appearance of high Hb values, RBC and platelet counts. The screening tests for PV were consistent with this diagnosis, while the search for lymphoma activity was negative. To the best of our knowledge, the present case represents the first well-documented instance of PV following NHL.

Humans↗
PubMed1992

[Granulocyte alkaline phosphatase activity in the chronic phase and blastic crisis of chronic myeloid leukemia. Sequential study of 43 patients].

PURPOSE: To evaluate in a sequential fashion the activity of the leukocyte alkaline phosphatase (LAP) in the chronic phase and the blastic crisis of chronic myelogenous leukaemia (CML). MATERIAL AND METHODS: This study is comprised of 43 patients diagnosed of CML according to standard criteria. The initial LAP scores were compared with those recorded in the blastic crisis, using cytochemical methods. The statistical analysis was performed with Student's test and chi-square. RESULTS: The LAP activity at diagnosis was low in 40 of the 43 cases (93%), the score being 0 in 20 instances. In the blastic crisis low scores were found in 27 patients (63%), while LAP activity appeared normal or increased in 16 others (37%). When the LAP scores of the two phases of the disease were compared the differences were found statistically significant (p less than 0.0001 and p less than 0.0007, respectively). CONCLUSIONS: These results confirm that the onset of the blastic crisis of CML is often accompanied by an increase of the LAP activity, although this last persists low in the majority of the patients.

Adolescent↗
PubMed1992

[Chronic myeloid leukemia beginning as thrombocythemia. Analysis of 5 cases].

The clinico-haematological and evolutive features of five patients with Ph'-positive chronic myelogenous leukaemia (CML) whose initial profile suggested the diagnosis of essential thrombocythaemia (ET) were analysed. The patients were women with severe thrombocytosis (greater than or equal to 1000 x 10(9)/L) and moderate leucocytosis (less than 25 x 10(9)/L), and only two of them had splenomegaly. Increased basophil count in peripheral blood was present in all cases, and peripheral myelocytosis was seen in three. The molecular analysis showed rearrangement of the BCR gene in the three patients on which it was performed. Increasing leucocyte count was seen in the three patients with extended follow-up, this reaching values in accordance with CML. Finally, the three patients who died suffered a blastic crisis. The analysis of this series, along with others reported in the literature, suggests that such cases correspond to atypical forms of CML rather than actual TE patients.

Adult↗
PubMed1991

Hormonal control of interacting promoters introduced into cells by retroviruses.

The interaction of promoters contained in a Moloney murine leukemia virus (MoMLV)-based retroviral vector was studied after infection of FTO-2B rat hepatoma and NIH 3T3 mouse fibroblast cells. Segments of the phosphoenolpyruvate carboxykinase (PEPCK) promoter-regulatory region, which are known from previous studies to confer responsiveness to hormones, were linked to the structural genes for bovine growth hormone, amino-3'-glycosyl phosphotransferase (neo), and herpes-virus thymidine kinase and inserted into a MoMLV-based retroviral vector. In vectors in which PEPCK was the only internal promoter, it was the major site of gene transcription. This dominant effect was independent of the orientation of the PEPCK promoter relative to the 5' long terminal repeat of the provirus and was noted with as little as -174 base pairs of the 5'-flanking sequence. NIH 3T3 cells, which do not express the endogenous PEPCK gene, transcribed the transduced PEPCK-chimeric genes at the same high levels as was observed in hepatoma cells. When two promoters were present in the provirus, the expression of chimeric structural genes depended on the relative position and orientation of these genes as well as the type of cell infected by the retrovirus. Differential responses of proviral promoters in infected cells were also observed in the presence of hormones. Dibutyryl cyclic AMP increased the expression of genes linked to the PEPCK promoter in FTO-2B and NIH 3T3 cells, whereas glucocorticoids stimulated transcription from both the PEPCK promoter and the long terminal repeat in FTO-2B cells. The effect of these hormones on transcription of proviral promoters depended on their position relative to the 5' long terminal repeat. In contrast, insulin uniformly inhibited transcription from the PEPCK promoter in a position-independent manner but only in hepatoma cells and not in fibroblasts. In clonally isolated FTO-2B cells infected with a retrovirus, the site of proviral integration was also a major factor determining the expression and hormonal regulation from the internal promoters. The data suggest that the hormonal regulation of the expression of genes contained in retroviral vectors depends on the type and position of the regulatory elements present in the provirus and the lineage of the infected cell.

Animals↗
PubMed1991

[Self-medication with analgesics. A study on odontalgia].

BACKGROUND: Odontalgia is a painful condition which is frequently associated to self-medication with analgesics. The purpose of the present study was to evaluate the main characteristics of self-medication on these patients. METHODS: A total of 226 patients who requested medical care for odontalgic problems at ambulatory level were evaluated. A case from was completed for each patient, considering diagnostic syndrome, pain characteristics and self-medication. RESULTS: Pain was present in 59% of the patients with a mean duration of near 20 days. Its intensity was mainly from moderate to severe, but one third of the patients referred very severe or excruciating pain. Near seventy percent of all patients with pain complaints were self-medicating with analgesics, 55% of them with one drug, 36% with two and 8% with three. A clear trend to use more drugs when pain intensity was higher was observed. The most frequently used drugs were paracetamol (39%), acetilsalicylic acid (24%) and metamizol (17%). The majority of patients selected themselves the drug and only a small number were advised by pharmacist or non health professionals. CONCLUSIONS: The present study shows a high frequency of self-medication in patients with odontalgia suggesting that this type of pain might be useful as a model to study self-medication with analgesic drugs.

Adolescent↗
PubMed1991

Prostaglandins E2 and F2 alpha increase fructose 2,6-bisphosphate levels in isolated hepatocytes.

In hepatocytes isolated from fed rats, prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) increased, in a time- and dose-dependent manner, fructose 2,6-bisphosphate [Fru(2,6)P2] levels and stimulated the glycolytic flux. The rise in Fru(2,6)P2 was related to an increase in glucose 6-phosphate levels which resulted from the stimulation of glycogenolysis. In cells obtained from 24 h-starved rats, no effects of either PGE2 or PGF2 alpha could be observed. In addition, when the stimulation of glycogenolysis was abolished by incubation of fed-rat hepatocytes in a Ca2(+)-depleted medium, Fru(2,6)P2 levels did not increase. Furthermore, no effects of PGs on 6-phosphofructo-2-kinase activity could be observed. These results indicate that PGE2 and PGF2 alpha show similar actions to Ca2(+)-dependent hormones on hepatic glucose metabolism.

Animals↗
PubMed1991

Activation by vanadate of glycolysis in hepatocytes from diabetic rats.

In hepatocytes from starved streptozocin-induced diabetic rats, vanadate increases the glycolytic flux because it raises the levels of fructose-2,6-bisphosphate (Fru-2,6-P2), the main regulatory metabolite of this pathway. This effect of vanadate on Fru-2,6-P2 levels is time and dose dependent, and it remains in cells incubated in a calcium-depleted medium. Vanadate is also able to counteract the decrease on Fru-2,6-P2 levels produced by glucagon, colforsin, or exogenous cAMP. However, vanadate does not modify 6-phosphofructo-2-kinase and pyruvate kinase activities, but it does counteract the inactivation of these enzymes induced by glucagon. Likewise, Fru-2,6-P2ase activity is also not affected by vanadate. In addition, vanadate is able to increase the production of both lactate and CO2 in hepatocytes from streptozocin-induced diabetic rats incubated in the presence of glucose in the medium. Vanadate behaves as a glycolytic effector in these cells, and this effect may be related to its ability to normalize blood glucose levels in diabetic animals.

Animals↗
PubMed1991

[Causes of death in chronic myeloid leukemia. Analysis of 109 patients].

The cause of death was revised in 109 cases of Ph'-positive chronic myelogenous leukaemia (CML) who died in a 15-year period. The median survival of the series, which included eight patients with initial criteria of blastic crisis, was 33.7 months (ranging between 2 and 192). Eight patients (7.3%) died during the chronic phase of the disease, 7 (6.4%) in the accelerated phase, and 94 (86.3%) in the blastic crisis. The cause of death in the chronic phase was frequently unrelated to CML (a second malignancy, cirrhosis of the liver, suicide, in four cases as opposed to infection, haemorrhage of hyperuricaemic renal failure in four others), but this was not so in the deaths occurred in the accelerated phase or blastic crisis. Thus, most of the deaths appearing in the accelerated phase were due to infection or haemorrhage, whereas in the blastic crisis they were mainly due to infection (54 of the 94 cases), followed by haemorrhage and leucostasis. All in all, these three complications were responsible for 94% of the deaths occurring in that evolutive phase of CML.

Adolescent↗
PubMed1990

Hepatic gene transfer in animals using retroviruses containing the promoter from the gene for phosphoenolpyruvate carboxykinase.

Two methods are described for directing the expression of genes to the livers of animals using retroviral vectors containing the predominantly liver-specific promoter from the gene for phosphoenolpyruvate carboxykinase (PEPCK)-linked to the structural gene for either amino 3'-glycosyl phosphotransferase (neo) or bovine growth hormone (bGH). Replication-incompetent retrovirus was used to infect the livers of fetal rats by intraperitoneal injection of animals in utero or to infect adult rats by direct injection into the portal vein after partial hepatectomy. The proviruses were integrated into the hepatic DNA, and the chimeric genes were expressed from the PEPCK promoter for as long as 8 months after infection. The expression of the PEPCK-bGH gene was regulated by diet and hormones in a manner similar to the regulation of the endogenous PEPCK gene in the liver. The potential of this method for targeting genes to the liver is discussed.

Animals↗
PubMed1990

Vanadate inhibits expression of the gene for phosphoenolpyruvate carboxykinase (GTP) in rat hepatoma cells.

Vanadate, at concentrations between 0.5 and 2 mM, rapidly decreased the basal level of P-enolpyruvate carboxykinase (GTP) (EC 4.1.1.32) mRNA and blocked the dibutyryl cyclic AMP (Bt2cAMP)-induced increase in enzyme mRNA in both FTO-2B and H4IIE rat hepatoma cells. The concentration of vanadate necessary to inhibit the expression of this gene was similar to that required for the vanadate-mediated activation of the insulin receptor tyrosine kinase. To determine whether vanadate could inhibit PEPCK gene transcription, a series of chimeric genes containing several deletions in the P-enolypyruvate carboxykinase promoter between -550 and -68 was linked to the structural genes for either amino-3-glycosyl phosphotransferase (neo) or chloramphenicol acetyltransferase and introduced into hepatoma cells using three methods: (a) infection with a Moloney murine leukemia virus-based retrovirus, (b) transfection and stable selection for neo expression, or (c) transient expression of chloroamphenicol acetyltransferase. In FTO-2B hepatoma cells infected with retrovirus, vanadate rapidly (within 1 h) inhibited transcription of the PEPCK-neo gene and blocked induction of gene expression caused by the addition of either Bt2cAMP or dexamethasone to the cells. Vanadate was not a general transcription inhibitor since, it like insulin, stimulated the expression of the c-fos gene. Also, the inhibitory effect of vanadate was rapidly reversible in FTO-2B cells since PEPCK gene expression could be stimulated by Bt2cAMP and dexamethasone after removal of vanadate. A series of 5' deletions in the P-enolpyruvate carboxykinase promoter (-550 to +73) was ligated to the structural gene for neo and stably transfected into hepatoma cells. Sequences responsive to vanadate were detected between -109 and -68. This result was confirmed using H4IIE hepatoma cells transiently expressing the PEPCK-CAT gene. The most likely target for vanadate in that region of the P-enolpyruvate carboxykinase promoter is cAMP regulatory element 1 which maps from -91 to -84. A comparison of the inhibitory effects of insulin and vanadate in this system indicated a major difference in the site of action of these two compounds on PEPCK gene transcription.

Animals↗
PubMed1990

Influence of extracellular calcium in the effects of dibekacin and diltiazem on indirectly elicited tetanic responses in the rat phrenic-hemidiaphragm preparation.

1. Dibekacin (70 microM-3 mM) produced a decrease of peak tetanic tension in a concentration-dependent manner and this effect was dependent on extracellular calcium (0.3-2.5 mM Ca2+). Only minimal fade was observed and it was not related with extracellular calcium concentrations. 2. Diltiazem (30-300 microM) decreased peak tetanic tension and produced tetanic fade. Both effects were independent of extracellular calcium, although a significant potentiation was observed at 0.3 mM calcium. 3. It is concluded that tetanic parameters are related differently to extracellular calcium.

Animals↗
PubMed1990

A survey of pain complaints and treatment by general practitioners in the Spanish public health organization.

The therapeutic habits of general practitioners are an important clue when drug therapy is considered, because they are treating the most frequent complaints. When pain problems are considered, it would be valuable to determine the characteristics of the pain consultations and their therapeutic attempts to solve these complaints. The present study was designed to elucidate the characteristics of pain diagnoses and treatment approaches at primary-care level in Spain. A total of 299 patients were evaluated, considering pain location, diagnostic syndrome, previous therapies, and treatments selected by the 13 participating physicians. Limb and back pain were the most frequent pain complaints. A third of the patients had received previous treatment and 36% were self-medicating, mainly with aspirin or paracetamol. Physicians prescribed diclofenac at full doses, but aspirin and paracetamol were used at subtherapeutic dosages. The study showed that (a) rheumatic pain was the most frequent at primary-care level, (b) a high level of self-medication was determined, therefore recommending a careful drug history, and (c) misconceptions about analgesic drugs may partially explain the therapeutic failure in some patients. Educational programs in rheumatic pain and analgesic therapy for general practitioners are strongly recommended.

Adult↗
PubMed1989

Effects of vanadate on protein kinases in rat hepatocytes.

In rat hepatocytes, vanadate modifies neither the intracellular concentration of cyclic AMP nor the --cyclic AMP/+cyclic AMP activity ratio for cyclic AMP-dependent protein kinase. Vanadate can, however, counteract the increase in cyclic AMP and the increase in the --cyclic AMP/+cyclic AMP activity ratio of cyclic AMP-dependent protein kinase induced by glucagon. On the other hand, vanadate treatment of hepatocytes can produce a time- and concentration-dependent increase in cyclic AMP- and Ca2+-independent casein kinase activity. Maximal activation at the optimal time with 5 mM-vanadate was about 70% over control. A clear relationship was observed between the activation of casein kinase and the inactivation of glycogen synthase after vanadate treatment. These results suggest that casein kinase activity may be involved in vanadate actions in rat hepatocytes.

Animals↗
PubMed1989

Oxytocin inactivates and phosphorylates rat hepatocyte glycogen synthase.

Incubation of isolated rat hepatocytes with oxytocin produces a time- and dose-dependent inactivation of glycogen synthase. Such inactivation is associated with an increase in the phosphorylation state of the 88 kDa subunit of the enzyme, as observed after electrophoretic analysis of the 32P-labelled enzyme isolated by immunoprecipitation from cells incubated with [32P]phosphate. CNBr cleavage of the immunoprecipitated glycogen synthase showed that multiple sites were phosphorylated after exposure of the cells to the hormone. The effect of oxytocin on hepatocyte glycogen synthase activity was not observed in the absence of extracellular Ca2+. Inactivation of glycogen synthase by oxytocin was partially abolished in the presence of insulin. These results indicate that the effects of oxytocin on glycogen synthase from rat hepatocytes are similar to those observed for other Ca2+-mediated glycogenolytic hormones, such as vasopressin.

Animals↗