Barbed versus traditional suture for enterotomy closure after laparoscopic right colectomy with intracorporeal mechanical anastomosis: a case–control study

Our aim was to establish the safety and efficacy of barbed suture for enterotomy closure after laparoscopic right colectomy with intracorporeal anastomosis. This study included 47 patients who underwent laparoscopic right hemicolectomy with intracorporeal mechanical anastomosis and barbed suture enterotomy closure (barbed suture closure—BSC) for adenocarcinoma (with the exception of T4 lesions and metastasis), compared with 47 matched patients who underwent laparoscopic right hemicolectomy with intracorporeal mechanical anastomosis and conventional suture enterotomy closure (conventional suture closure—CSC) during the same period. Controls were matched for stage, age, and gender via a statistically generated selection of all laparoscopic right hemicolectomies performed from January 2009 until December 2015. There was no difference between the two groups in terms of age, sex, BMI, ASA, co-morbidity, previous abdominal surgery, cancer site and cancer staging. In terms of operating time (median 120 min for BSC and 127.5 min for CSC), histopathological results, surgical site complications (2.1% for BSC and 8.5% for CSC), hospitalization (median 6 days for BSC and 5 days for CSC), readmission rate (0%), there were no differences between the groups (p > 0.05). No significant differences were noted between the two groups in terms of the postoperative course. Our results support that the use of knotless barbed sutures for enterotomy closure after laparoscopic right colectomy with intracorporeal mechanical anastomosis is safe and reproducible.     

Prevalence and physician awareness of symptoms of urinary bladder dysfunction

PURPOSE: To determine awareness of bladder dysfunction and attitudes towards its management among office-based physicians. MATERIALS AND METHODS: A total of 211,648 patients consulting office-based primary care physicians (PCPs), gynaecologists (OBGs) or urologists (UROs) for any reason were given a questionnaire of four questions related to symptoms of bladder dysfunction. The physicians were asked to discuss the answers with their patients and to choose from a list of suspected diagnoses. They were also asked whether medical therapy would be initiated and/or the patient referred to a specialist. RESULTS: Patients (57%) had a least one symptom of bladder dysfunction, with increased frequency being most common (41.9%), and symptoms of stress incontinence (30.6%), urgency (24.3%) and urge incontinence (20.2%) less frequent. However, patients with symptoms of overactive bladder (OAB), mixed incontinence or stress incontinence according to the questionnaire remained undiagnosed by their physician in 57.5, 47.5 and 38.1% of cases, respectively. When a diagnosis was suspected by the physician, it often did not match what would be expected based on the questionnaire, and in half of all cases did not result in medical treatment. CONCLUSIONS: Bladder dysfunction is highly prevalent among patients consulting an office-based physician for any reason, but remains undiagnosed in many cases and untreated despite diagnosis in many others. Since various effective treatment options are available for bladder dysfunction, educational programs for patients and physicians appear necessary to improve the quality of diagnosis and treatment for this wide-spread condition.     

Biochemical diagnosis of Alzheimer disease by measuring the cerebrospinal fluid ratio of phosphorylated tau protein to beta-amyloid peptide42

BACKGROUND: The antemortem diagnosis of Alzheimer disease (AD) requires time-consuming and costly procedures. Therefore, biochemical tests that can direct the physician rapidly to the correct diagnosis are highly desirable. Measurement of single biochemical markers in cerebrospinal fluid (CSF), such as total tau protein and beta-amyloid peptide42 (Abeta42), shows robust alterations that highly correlate with the clinical diagnosis of AD but generally lack sufficient diagnostic accuracy. OBJECTIVE: To study the combination of CSF phosphorylated tau protein (phospho-tau) and Abeta42 as biochemical markers for AD. METHODS: We combined CSF measurements of phospho-tau and Abeta42 in 100 consecutive patients who under-went diagnostic workup for dementia and in 31 healthy control subjects. RESULTS: We found that the calculated ratio of phospho-tau to Abeta42 was significantly increased in patients with AD and provided high diagnostic accuracy in distinguishing patients with AD from healthy control subjects (sensitivity, 86%; specificity, 97%), subjects with non-AD dementias (sensitivity, 80%; specificity, 73%), and subjects with other neurological disorders (sensitivity, 80%; specificity, 89%). CONCLUSION: The diagnostic usefulness of the CSF ratio of phospho-tau to Abeta42 is superior to either measure alone and can be recommended as an aid to evaluating individuals suspected of having dementia.     

A technique for cast duplication

A simple, effective, and inexpensive method of cast duplication used for models and working casts is described.     

Experimental parkinsonism modulates multiple genes involved in the transduction of dopaminergic signals in the striatum

The irreversible loss of the dopamine-mediated control of striatal function is considered the functional substrate of the motor symptoms of Parkinson's disease. This pathological event causes a complex rearrangement of neuronal activity which involves specific dopamine-regulated cellular functions and, secondarily, several other cellular properties and transmitter systems. In the present study, we applied recently developed cDNA microarray technology to investigate the genetic correlates of the alterations produced by 6-hydroxydopamine-induced dopamine denervation in the nucleus striatum. We found that chronic dopamine denervation caused the modulation of 50 different genes involved in several cellular functions. In particular, products of the genes modulated by this experimental manipulation are involved both in the intracellular transduction of dopamine signal and in the regulation of glutamate transmission in striatal neurons, providing some information on the possible neuronal events which lead to the reorganization of glutamate transmission in the striatum of parkinsonian rats.     

Chromosome mapping of multiple loci affecting the genetic predisposition to rat liver carcinogenesis

Previous studies on (BNxF344)F1 (BFF1) rat model of genetic predisposition to hepatocarcinogenesis led to the identification, in BFF1xF344 backcross progeny, of two hepatocarcinogenesis susceptibility (Hcs) and three resistance (Hcr) loci affecting the progression of neoplastic liver nodules. To evaluate the presence of other hepatocarcinogenesis-related loci in the BFF1 genome, nodule induction by resistant hepatocyte model in 116 male BFF2 rats 32 weeks after initiation with diethylnitrosamine was subjected to quantitative trait loci analysis. The rats were typed with 179 genetic markers, and linkage analysis identified three loci on chromosomes 1, 16, and 6, in significant linkage with nodule mean volume (V), volume fraction, and number, respectively, and two loci on chromosomes 4 and 8 in suggestive linkage with V. These loci were differently positioned with respect to Hcs and Hcr loci mapped previously in backcross rats. On the basis of phenotypic and allele distribution patterns of BFF2 rats, loci on chromosomes 1 and 16 were identified as Hcs3 and Hcs4, and loci on chromosomes 4, 8, and 6 as Hcr4, Hcr5, and Hcr6. Additive interactions occurred between Hcs3 and Hcs4, and Hcr4 and a locus on chromosome 3 with less than suggestive linkage with V. All of the loci were in chromosomal regions syntenic to mouse and/or human chromosomal segments showing allelic gain or loss in hepatocellular carcinomas. These data indicate that inheritance of predisposition to rat liver tumor is characterized by the interplay of several genetic factors and suggest some possible mechanisms of polygenic control of human liver cancer.     

Cell cycle deregulation in liver lesions of rats with and without genetic predisposition to hepatocarcinogenesis

Preneoplastic and neoplastic hepatocytes undergo c-Myc up-regulation and overgrowth in rats genetically susceptible to hepatocarcinogenesis, but not in resistant rats. Because c-Myc regulates the pRb-E2F pathway, we evaluated cell cycle gene expression in neoplastic nodules and hepatocellular carcinomas (HCCs), induced by initiation/selection (IS) protocols 40 and 70 weeks after diethylnitrosamine treatment, in susceptible Fisher 344 (F344) rats, and resistant Wistar and Brown Norway (BN) rats. No interstrain differences in gene expression occurred in normal liver. Overexpression of c-myc, Cyclins D1, E, and A, and E2F1 genes, at messenger RNA (mRNA) and protein levels, rise in Cyclin D1-CDK4, Cyclin E-CDK2, and E2F1-DP1 complexes, and pRb hyperphosphorylation occurred in nodules and HCCs of F344 rats. Expression of Cdk4, Cdk2, p16(INK4A), and p27(KIP1) did not change. In nodules and/or HCCs of Wistar and BN rats, low or no increases in c-myc, Cyclins D1, E, and A, and E2F1 expression, and Cyclin-CDKs complex formation were associated with p16(INK4A) overexpression and pRb hypophosphorylation. In conclusion, these results suggest deregulation of G1 and S phases in liver lesions of susceptible rats and block of G1-S transition in lesions of resistant strains, which explains their low progression capacity.