Effect of intravenous fluid therapy on postoperative vomiting in children undergoing tonsillectomy.

BACKGROUND: Postoperative vomiting (POV) is one of the most frequent complications of tonsillectomy in children. The aim of this study was to evaluate the antiemetic effect of super-hydration with lactated Ringer's solution in children undergoing elective otorhinolaryngological surgery. METHODS: One hundred ASA I-II children, aged 1-12 yr, undergoing elective tonsillectomy, with or without adenoidectomy, under general anaesthesia were studied. Induction and maintenance of anaesthesia were standardized with fentanyl, mivacurium, and sevoflurane in N(2)O/O(2). Subjects were assigned to one of the two groups: 10 ml kg(-1) h(-1) lactated Ringer's solution or 30 ml kg(-1) h(-1) lactated Ringer's solution. A multivariable logistic regression was used for assessing the effects of super-hydration on POV (defined as the presence of retching, vomiting, or both). A value of P<0.05 was considered statistically significant. RESULTS: During the first 24 h postoperative, the incidence of POV decreased from 82% to 62% (relative reduction of 24%, P=0.026). In the adjusted logistic regression model, subjects in the 10 ml kg(-1) h(-1) group had an odds ratio of POV that was 2.92 (95% confidence interval: 1.14, 7.51) for POV compared with subjects in the 30 ml kg(-1) h(-1) group. CONCLUSIONS: Intraoperative administration of 30 ml kg(-1) h(-1) lactated Ringer's solution significantly reduced the incidence of POV during the first 24 h postoperative. Our results support the use of super-hydration during tonsillectomy, as an alternative way to decrease the risk of POV in children.

Long-term cardiovascular outcome after elective abdominal aortic aneurysm open repair.

BACKGROUND: We analyzed the incidence of late cardiovascular events and mortality after elective infra-/juxtarenal abdominal aortic aneurysm open repair (AAA-OR). METHODS: We included patients who survived AAA-OR in our center in 1988-2006. We registered late cardiac, cerebrovascular, and peripheral vascular events, as well as all-cause and cardiovascular mortality. We calculated patient survival and freedom from cardiovascular events (Kaplan-Meier) and evaluated risk factors (multivariate analysis). RESULTS: We studied 297 patients: 292 (98.3%) men, aged 67 +/- 7 (44-83) years, 143 (48.1%) bifurcated grafts. In a mean follow-up of 78.7 +/- 52.9 months, we registered 203 cardiovascular events in 123 (41.4%) patients, at a rate of 0.16 cardiovascular events/patient-year. Eleven (3.7%) patients suffered graft-related complications. Freedom from cardiovascular events was 94.2%, 67.2%, 45.7%, and 27.6% at 1, 5, 10, and 15 years, respectively. Survival was 96.6%, 74.7%, 50.7%, and 31.5%, respectively. The main cause of death was cardiovascular disease (n = 54, 18.2%), followed by cancer (n = 43, 14.5%). Only four (1.3%) deaths were graft-related. Coronary artery disease and chronic renal failure were predictive of cardiovascular mortality (p = 0.033 and 0.006). CONCLUSION: Although long-term survival is similar to that in the general population, successful AAA-OR patients remain at increased risk of cardiovascular events throughout their lifetime. Graft-related complications are rare, confirming the durability of the procedure.

Search for serum biomarkers associated with abdominal aortic aneurysm growth--a pilot study.

INTRODUCTION: Serological biomarkers could reflect asymptomatic infrarenal aortic aneurysm (AAA) activity and guide patient management. REPORT: Serum concentrations of C-reactive protein (CRP), alpha 1-antitrypsin and lipoprotein(a) were measured in blood samples from 35 AAA patients and 35 controls and correlated with the aortic diameter and AAA growth in the previous 12 months. We found a positive correlation between CRP and AAA diameter (r=0.46; p=0.007) and alpha 1-antitrypsin and AAA growth (r=0.55; p=0.004). CONCLUSIONS: Alpha 1-antitrypsin may be a promising biomarker of AAA growth.

Regulation of yeast H(+)-ATPase by protein kinases belonging to a family dedicated to activation of plasma membrane transporters.

The regulation of electrical membrane potential is a fundamental property of living cells. This biophysical parameter determines nutrient uptake, intracellular potassium and turgor, uptake of toxic cations, and stress responses. In fungi and plants, an important determinant of membrane potential is the electrogenic proton-pumping ATPase, but the systems that modulate its activity remain largely unknown. We have characterized two genes from Saccharomyces cerevisiae, PTK2 and HRK1 (YOR267c), that encode protein kinases implicated in activation of the yeast plasma membrane H(+)-ATPase (Pma1) in response to glucose metabolism. These kinases mediate, directly or indirectly, an increase in affinity of Pma1 for ATP, which probably involves Ser-899 phosphorylation. Ptk2 has the strongest effect on Pma1, and ptk2 mutants exhibit a pleiotropic phenotype of tolerance to toxic cations, including sodium, lithium, manganese, tetramethylammonium, hygromycin B, and norspermidine. A plausible interpretation is that ptk2 mutants have a decreased membrane potential and that diverse cation transporters are voltage dependent. Accordingly, ptk2 mutants exhibited reduced uptake of lithium and methylammonium. Ptk2 and Hrk1 belong to a subgroup of yeast protein kinases dedicated to the regulation of plasma membrane transporters, which include Npr1 (regulator of Gap1 and Tat2 amino acid transporters) and Hal4 and Hal5 (regulators of Trk1 and Trk2 potassium transporters).

The cell wall integrity/remodeling MAPK cascade is involved in glucose activation of the yeast plasma membrane H(+)-ATPase.

Glucose triggers transcriptional and post-transcriptional mechanisms that increase the amount and the activity of Saccharomyces cerevisiae plasma membrane H(+)-ATPase. In a previous study, we found that a mutation in the Rsp5 ubiquitin-protein ligase enzyme affected the post-transcriptional activation of the enzyme by glucose. Mutations at the RSP5 locus alter the glucose-triggered K(m) decrease. In a genetic screening for multicopy suppressors of the rsp5 mutation, we identified the WSC2/YNL283c gene. Deletion of the WSC2 gene disturbs ATPase activation by glucose, abolishing the K(m) decrease that occurs during this process. Wsc2 is a component of the PKC1-MPK1 mitogen-activated protein kinase (MAPK) signaling pathway that controls the cell wall integrity. Deletion of the MPK1/SLT2 gene disturbs the glucose-triggered K(m) decrease in ATPase.

Head morphogenesis genes of the Bacillus subtilis bacteriophage SPP1.

We have identified and characterized the phage cistrons required for assembly of SPP1 heads. A DNA fragment containing most of the head morphogenesis genes was cloned and sequenced. The 3'-end of a previously identified gene (gene 6) and eight complete open reading frames (7 to 15) were predicted. We have assigned genes 7, 8, 9, 11, 12, 13, 14 and 15 to these orfs by correlating genetic and immunological data with DNA and protein sequence information. G7P was identified as a minor structural component of proheads and heads, G11P as the scaffold protein, G12P and G15P as head minor proteins and G13P as the coat protein. Characterization of intermediates in head assembly, which accumulate during infection with mutants deficient in DNA packaging or in morphogenetic genes, allowed the definition of the head assembly pathway. No proteolytic processing of any of the head components was detected. Removal of G11P by mutation leads to the accumulation of prohead-related structures and aberrant particles which are similar to the assemblies formed by purified G13P in the absence of other phage-encoded proteins. The native molecular masses of G11P and G13P are about 350 kDa and larger than 5000 kDa, respectively (predicted molecular masses 23.4 kDa and 35.3 kDa, respectively). G13P, upon denaturation and renaturation, assembles from protomers into some prohead-related structures. The organization of the DNA packaging and head genes of SPP1 resembles the organization of genes in the analogous regions of phage lambda and P22.

Characterization of an allele-nonspecific intragenic suppressor in the yeast plasma membrane H+-ATPase gene (Pma1).

We have analyzed the ability of A165V, V169I/D170N, and P536L mutations to suppress pma1 dominant lethal alleles and found that the P536L mutation is able to suppress the dominant lethality of the pma1-R271T, -D378N, -D378E, and -K474R mutant alleles. Genetic and biochemical analyses of site-directed mutants at Pro-536 suggest that this amino acid may not be essential for function but is important for biogenesis of the ATPase. Proteins encoded by dominant lethal pma1 alleles are retained in the endoplasmic reticulum, thus interfering with transport of wild-type Pma1. Immunofluorescence studies of yeast conditionally expressing revertant alleles show that the mutant enzymes are correctly located at the plasma membrane and do not disturb targeting of the wild-type enzyme. We propose that changes in Pro-536 may influence the folding of the protein encoded by a dominant negative allele so that it is no longer recognized and retained as a misfolded protein by the endoplasmic reticulum.

Glucose activation of the yeast plasma membrane H+-ATPase requires the ubiquitin-proteasome proteolytic pathway.

Glucose triggers transcriptional and post-transcriptional mechanisms that increase the level and activity of Saccharomyces cerevisiae plasma membrane H+-ATPase. We have studied the post-transcriptional activation of the enzyme by glucose and have found that Rsp5, a ubiquitin-protein ligase enzyme, Ubc4, a ubiquitin-conjugating enzyme, and the 26S proteasome complex are implicated in this activation. These results suggest that ATPase activation by glucose requires the ubiquitin-proteasome proteolytic pathway. This is supported by the fact that over-expression of the ubiquitin-specific protease Ubp2, which cleaves ubiquitin from its branched conjugates, inhibits this activation. We propose that glucose triggers degradation of an inhibitory protein resulting in enzyme activation.

Yeast gene YOR137c is involved in the activation of the yeast plasma membrane H+-ATPase by glucose.

Glucose triggers transcriptional and post-transcriptional mechanisms that increase the level and activity of Saccharomyces cerevisiae plasma membrane H+-ATPase. We have studied the post-transcriptional activation of the enzyme by glucose and have found that the YOR137c gene product is implicated in this activation. Deletion of YOR137c does not affect the level of Pma1 at the plasma membrane, but disturbs the glucose-triggered Vmax increase of the enzyme. We propose that at least two independent mechanisms are involved in glucose activation of the H+-ATPase.

7-[3-(1-piperidinyl)propoxy]chromenones as potential atypical antipsychotics. 2. Pharmacological profile of 7-[3-[4-(6-fluoro-1, 2-benzisoxazol-3-yl)-piperidin-1-yl]propoxy]-3-(hydroxymeth yl)chromen -4-one (abaperidone, FI-8602).

A series of novel 7-[3-(1-piperidinyl)propoxy]chromenones was synthesized and tested as potential antipsychotics in several in vitro and in vivo assays. The compounds possessed good affinity for D2 receptors, together with a greater affinity for 5-HT2 receptors, a profile which has been proposed as a model for atypical antipsychotics. Several agents also displayed a high potency in the climbing mice assay on oral administration, suggesting a potent antipsychotic effect as compared to reference standards. Compound 23 was selected for further pharmacological evaluation. Induction of catalepsy and inhibition of stereotypies weaker than standards, along with a lower increase in serum prolactin levels, were indicative of a potential atypical profile for this compound. From these results, 7-[3-[4-(6-fluoro-1, 2-benzisoxazol-3-yl)piperidin-1-yl]propoxy]-3-(hydroxymethyl )chromen- 4-one (23, abaperidone) has been proposed for clinical evaluation in humans as a potential atypical antipsychotic.

[A case of erythropsia]. / Un caso de eritropsia.

Erythropsia or red vision (from the Greek erythros = red, and opsis = sight) is a temporary distortion of colour vision. This phenomenon is a chromatopsia or impaired vision. It consists of seeing all objects with a uniform reddish tint. This vision symptom usually alarms the patient. It is a Little known process and is usually transient. It may be due to benign processes such as post-operative cataracts and drug toxicity or to be a consequence of more serious processes such as vitreous haemorrhage.

Analysis of expansion patterns in 4-4.9 cm abdominal aortic aneurysms.

Our objective was to analyze the growth pattern of 4-4.9 cm infrarenal abdominal aortic aneurysms (AAAs). We used an observational, longitudinal, prospective study design. We followed 4-4.9 cm AAAs with 6-monthly abdominal computed tomographic (CT) scans (January 1988-August 2004). AAA growth was defined as an increase in aortic diameter > or =2 mm in each surveillance period. We established the aortic expansion pattern in AAA with three or more CT scans as continuous, discontinuous. The latter includes at least one period of nongrowth (<2 mm/6 months). We studied the influence of cardiovascular risk factors (CVRFs), comorbidity, and AAA anatomical characteristics using the chi-squared test, t-test, life tables, and Kaplan-Meier for statistical analysis. We included 195 patients: 183 (93.8%) men, age 71 +/- 8.3 years (50-90). The follow-up period was 50 +/- 36.4 months (6.5-193.7). The growth pattern (n =131) was continuous in 15 (11.5%) and discontinuous in 116 (88.5%) AAA. The mean expansion rate was higher in AAAs with continuous expansion (7.92 +/- 3.74 vs. 2.74 +/- 2.94 mm/year, p < 0.0001). No CVRFs or comorbidity influenced the expansion pattern (p > 0.05). The eccentric thrombus was associated with a greater incidence of continuous growth (p = 0.05), with no influence of aortic calcification (p > 0.1). The expansion of 4-4.9 cm AAA is mostly irregular and unpredictable. We have not found any modifiable risk factors which influence their growth pattern. The eccentric distribution of the thrombus is associated with continuous expansion.

Un caso de eritropsia / A case of erythropsia

La eritropsia o visión roja (del griego erythros=rojo, y opsis=vista) es una alteración en la percepción de los colores de carácter temporal. Este fenómeno es una cromatopsia o visión alterada. Consiste en la aparición de un tinte rojizo, de presentación uniforme que parece colorear todos los objetos. Este síntoma visual suele alarmar al paciente. Se trata de un proceso poco conocido y que suele ser transitorio. Puede deberse a procesos benignos como el post-operatorio de las cataratas y por toxicidad farmacológica ó ser consecuencia de procesos más graves como la hemorragia vítrea (AU)

Erythropsia or red vision (from the Greek erythros=red, and opsis=sight) is a temporary distortion of colour vision. This phenomenon is a chromatopsia or impaired vision. It consists of seeing all objects with a uniform reddish tint. This vision symptom usually alarms the patient. It is a little known process and is usually transient. It may be due to benign processes such as post-operative cataracts and drug toxicity or to be a consequence of more serious processes such as vitreous haemorrhage (AU)