Does Level of Sedation Impact Detection of Advanced Neoplasia?

Background and Aims  

Two of the foremost issues in screening colonoscopy involve delivering quality and maximizing adenoma detection rates (ADR). Little is known about the impact of deep sedation on ADR. This study aims to compare the detection of advanced lesions during screening colonoscopy performed with moderate conscious sedation (MCS) versus deep sedation (DS).     

Biochemical/metabolic changes associated with hepatocellular carcinoma development in mice

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related mortality after lung and stomach cancers. This work was undertaken to investigate some of the biochemical mediators/pathways associated with or implicated in the pathogenesis of HCC. Male albino mice were classified into two groups: normal control group and HCC group. Early stage HCC was induced by injection of diethylnitrosamine (DEN) i.p. 200 mg/kg as a single dose, and after 2 weeks, the mice were given i.p. injection of thioacetamide (TAA) 100 mg/kg twice per week for 4 weeks. Mice were left for further 2 weeks without any treatment, after which, mice were sacrificed; blood and liver samples were collected. Serum was used for determination of activities of glucose-6-phosphate dehydrogenase (G6PDH) and aldolase as well as levels of insulin-like growth factor-1 (IGF-1) and epithelial cadherin (E-cadherin). One portion of the liver was used for histopathological examination and immunohistochemical staining of the tumor suppressor p53 protein. Another portion of the liver was used for determination of citrate synthase activity. Induction of HCC in mice resulted in significant increase in G6PDH and aldolase activities, and E-cadherin level, but significant decrease in IGF-1. HCC mice group showed moderate expression of p53 protein. These results suggest that the molecular pathogenesis of HCC in mice involves reduction of serum level of IGF-1 and increased serum level of E-cadherin accompanied by dysregulation of p53 protein expression. HCC was also associated with reprogrammed metabolic profile shifted toward increased glycolysis and lipogenesis.     

Physical and hormonal profile of male sexual development in epilepsy

PURPOSE: This study was designed to investigate the effect of epilepsy and antiepileptic drugs (AEDs) on both the physical and hormonal aspects of the sexual development of male patients with epilepsy. METHODS: One hundred thirty male subjects with epilepsy, their age ranging between 8 and 18 years (mean, 14 +/- 2.9 years), entered the study; all were taking AEDs. Anthropometric measurements [height, weight, and body mass index (BMI)], testicular volume, penile length, and pubarche were assessed in the studied groups, as well as measurement of the levels of testosterone (T), free testosterone (FT), estradiol (E2), lutenizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin (PRL), and the results were compared with those of a control group. RESULTS: In this study, male patients older than 16 years were significantly shorter than their matched controls. The mean values of testicular volume and penile length were significantly lower in the patients in the different age subgroups, and the pubic hair staging (pubarche) was delayed in the patients older than 16 years. The mean values of total testosterone, estradiol, LH, and FSH serum levels were significantly higher, whereas the mean values of free testosterone, total-T/E2, total. T/LH, and FT/E2 ratios were lower in the patient subgroups compared with their age-matched controls. There were no significant changes in the mean basal PRL serum levels in the patients compared with the controls. The present study demonstrated a reduction in the testicular volume and penile length, significantly lower mean values of free testosterone and total-T/E2, and a higher mean value of E2 in the patients receiving polytherapy in the age subgroup older than 16 years compared with those on monotherapy; however, there was no demonstrable effect of seizure control or the duration of illness in any of the studied parameters. CONCLUSIONS: There is a delay in the sexual development of male patients with epilepsy in the different age subgroups, with endocrine changes in the form of increase in the total testosterone, but the free testosterone is lower, and an increase in estradiol, with lower T/LH levels. Patients receiving polytherapy, especially those older than 16 years, were more likely to have delayed gonadarch and disturbances in their hormonal profile.     

Neurokinin A level in hypoxic–ischemic encephalopathy

Background: The present study was performed to investigate the effect of neonatal hypoxic–ischemic encephalopathy (HIE) on the neurotransmitter neurokinin A (NKA) and determine its relation to the severity of neonatal hypoxia. Methods: Eighteen neonates suffering from HIE were compared to 10 clinically healthy full‐term neonates acting as the control group. Maternal history of each neonate was collected, then deliveries were attended, resuscitation details including the Apgar score and thorough clinical examination of the neonates were performed. Routine laboratory work‐up was done for the enrolled neonates, including complete blood count and C‐reactive protein as well as estimation of NKA by enzyme‐linked immunosorbent assay in the cord blood and after clinical stabilization. Results: NKA was significantly lower in HIE patients compared to the controls at delivery with improvement in the follow‐up sample. Additionally, the maximum decrease was detected in the neonates who suffered severe hypoxia compared to those who suffered mild hypoxia. Significant positive correlations were demonstrated between NKA at birth and Apgar scores at the 10th and 15th min. Regression showed that stage of HIE was the strongest determinant factor for the level of NKA at birth. Conclusion: NKA levels are decreased in HIE and this is more profound in the severe degrees of hypoxia compared to the mild ones. This emphasizes its role in pathogenesis of HIE and further proves that an imbalance in the central neuropeptide system results from HIE in the neonatal period.     

Lower cancer incidence in Amsterdam-I criteria families without mismatch repair deficiency: familial colorectal cancer type X

Context  Approximately 60% of families that meet the Amsterdam-I criteria (AC-I) for hereditary nonpolyposis colorectal cancer (HNPCC) have a hereditary abnormality in a DNA mismatch repair (MMR) gene. Cancer incidence in AC-I families with MMR gene mutations is reported to be very high, but cancer incidence for individuals in AC-I families with no evidence of an MMR defect is unknown. Objective  To determine if cancer risks in AC-I families with no apparent deficiency in DNA MMR are different from cancer risks in AC-I families with DNA MMR abnormalities. Design, Setting, and Participants  Identification (1997-2001) of 161 AC-I pedigrees from multiple population- and clinic-based sources in North America and Germany, with families grouped into those with (group A) or without (group B) MMR deficiency by tumor testing. A total of 3422 relatives were included in the analyses. Main Outcome Measures  Cancer incidence in groups A and B (excluding the 3 affected members used to define each pedigree as AC-I) and computed age- and sex-adjusted standardized incidence ratios (SIRs) using Surveillance, Epidemiology, and End Results data. Results  Group A families from both population- and clinic-based series showed increased incidence of the HNPCC-related cancers. Group B families showed increased incidence only for colorectal cancer (SIR, 2.3; 95% confidence interval, 1.7-3.0) and to a lesser extent than group A (SIR, 6.1; 95% confidence interval, 5.2-7.2) (P<.001). Conclusions  Families who fulfill AC-I criteria but who have no evidence of a DNA MMR defect do not share the same cancer incidence as families with HNPCC-Lynch syndrome (ie, hereditary MMR deficiency). Relatives in such families have a lower incidence of colorectal cancer than those in families with HNPCC-Lynch syndrome, and incidence may not be increased for other cancers. These families should not be described or counseled as having HNPCC-Lynch syndrome. To facilitate distinguishing these entities, the designation of "familial colorectal cancer type X" is suggested to describe this type of familial aggregation of colorectal cancer.