The effect on the middle-ear cavity of an absorbable gelatine sponge alone and with corticosteroids

The objectives of this study were to establish whether there is an obvious difference between intact mucosa and abraded mucosa of the middle-ear cavity in respect to the potential side effects from the application of absorbable gelatine sponge (Gelfoam) and to investigate if Gelfoam combined with corticosteroid ointment (cortimycine, sterile 1% hydrocortisone acetate) can reduce the occurrence of these effects. Twenty Albino rats were used in the study. These animals were divided into four groups, with ten ears in each group. In group A, the middle-ear mucosa was kept intact, and Gelfoam was inserted into the middle-ear cavity. In group B, the middle-ear mucosa was abraded, and Gelfoam was inserted. In group C, Gelfoam with corticosteroid was implanted over the intact mucosa, and in group D, the mucosa was abraded prior to the insertion of Gelfoam with corticosteroid. The changes were evaluated 8 weeks postoperatively. In group A, there was a minimal increase in fibroblastic activity, vascular proliferation with mild to moderate fibrosis and all but two tympanic membranes were perfectly normal. However, in group B, we encountered a significant increase in fibroblastic activity, vascular proliferation and fibrosis, and we observed that all tympanic membranes were moderately to severely thickened. These histopathologic changes related to Gelfoam were noted to be decreased in group C and especially in group D. As previously reported in the literature, Gelfoam was found to promote the formation of connective tissue in the middle-ear cavity regardless of the status of the mucosa. The unwanted effects of this material may be decreased if it is combined with corticosteroids in the middle-ear cavity.     

Is regional tonometry a reliable index of tissue oxygenation? A comparative study with conventional global monitoring

This study was carried out on 30 critically ill patients admitted to the ICU of Farwania Hospital (Kuwait). All patients had clinical evidence of organ dysfunction or impending multiple organ failure. The severity of their pathology on admission was assessed according to the APACHE II score. The study of each patient began after inserting the pulmonary artery catheter. The prospectively defined end-point of the study was the removal of the pulmonary artery catheter (72 hours) or death of the patient with the catheter in situ. The aim of the study was to determine the sensitivity and specificity of the intra-gastric mucosal pH (pHi) and other derived data in assessing the adequacy of tissue oxygenation, guiding therapy and prediction outcome. The results showed that pHi, pHa-Hi and PaCO2-PO2regional (reg) gradients were the most sensitive indices of tissue oxygenation and predictors of outcome. The mortality rate increased when pHi, PaCO2-PCO2reg and pHa-pHi gradients were < 7.3, > 10 mm Hg and < 0.2 respectively. The derived variables obtained by invasive monitoring like base deficit (BD), lactate concentration in mixed venous blood (Lmv) and oxygn uptake index (O2 UI) were valuable adjunct indices of tissue oxygenation. The risk ofmortality increased whten the BD was > -5.5 +/- 1.2 meq.L-1, Lmv was > 4.5 +/- 1.2 mmol.L-1, and O2UI was < 100 +/- 6 ml.min-1.m-2. We recommend the use of gastric tonometry in routine ICU clinical practice.     

Distribution of protein kinase Mzeta and the complete protein kinase C isoform family in rat brain

Protein kinase C (PKC) is a multigene family of at least ten isoforms, nine of which are expressed in brain (alpha, betaI, betaII, gamma, delta, straightepsilon, eta, zeta, iota/lambda). Our previous studies have shown that many of these PKCs participate in synaptic plasticity in the CA1 region of the hippocampus. Multiple isoforms are transiently activated in the induction phase of long-term potentiation (LTP). In contrast, a single species, zeta, is persistently activated during the maintenance phase of LTP through the formation of an independent, constitutively active catalytic domain, protein kinase Mzeta (PKMzeta). In this study, we used immunoblot and immunocytochemical techniques with isoform-specific antisera to examine the distribution of the complete family of PKC isozymes and PKMzeta in rat brain. Each form of PKC showed a widespread distribution in the brain with a distinct regional pattern of high and low levels of expression. PKMzeta, the predominant form of PKM in brain, had high levels in hippocampus, frontal and occipital cortex, striatum, and hypothalamus. In the hippocampus, each isoform was expressed in a characteristic pattern, with zeta prominent in the CA1 stratum radiatum. These results suggest that the compartmentalization of PKC isoforms in neurons may contribute to their function, with the location of PKMzeta prominent in areas notable for long-term synaptic plasticity.     

Mutation Spectrum of Familial Adenomatous Polyposis Patients in Turkish Population: Identification of 3 Novel APC Mutations

BackgroundFamilial adenomatous polyposis (OMIM #175100) and MUTYH-associated polyposis (OMIM #608456) are rare cancer-prone disorders characterized by hundreds of adenomatous polyps in the colon and rectum, which have a high probability of malignant transformation. Attenuated familial adenomatous polyposis is a variant of familial adenomatous polyposis, which is a term used for the condition in which patients have less than 100 colorectal polyps. Germline heterozygous Adenomatous polyposis coli (APC) and biallelic MUTYH (mutY DNA glycosylase) pathogenic variations are responsible for familial adenomatous polyposis and MUTYH-associated polyposis respectively. The aim of this study is to discuss the clinical manifestations of patients having pathogenic APC and MUTYH variations.MethodsWe included 27 probands who have more than 10 colonic polyps in this study. After evaluation of their clinical and family histories, the probands were screened for APC and MUTYH variations via next generation sequencing. The family members of the probands carrying pathogenic variations were screened via Sanger sequencing. ResultsAmong 27 probands, pathogenic APC and MUTYH variations were detected in 3 and 6 probands respectively. In the APC gene, 3 novel truncating variations (p.Leu360*, p.Leu1489Phefs*23, and p.Leu912*) were detected in 3 unrelated probands. In the MUTYH gene, only 2 distinct pathogenic variations were detected (p.Pro295Leu and p.Glu480del) in the homozygous or compound heterozygous state.ConclusionIn this study, molecular etiology was clarified in 9 familial polyposis patients. The p.Pro295Leu and p.Glu480del variations seem to be common in the Turkish population and may be considered as a first-step genetic test in Turkish familial polyposis patients showing autosomal recessive inheritance. However more studies are needed to reveal the exact frequency of these variations.