Anal incontinence after vaginal delivery or cesarean section.

INTRODUCTION: Uncertainties remain as to whether cesarean section is protective for short and long term development of anal incontinence. Our aim was to explore whether women who had only delivered vaginally were at greater risk of anal incontinence compared to nulliparous women and women who had undergone caesarean sections only. MATERIAL AND METHODS: Background information, medical history and data on anal incontinence (defined as fecal or flatus incontinence weekly or more) reported by women participating in a large population-based health survey in Norway (HUNT 3) during the period October 2006-June 2008, was collected and linked to data from the Medical Birth Registry of Norway. Anal incontinence prevalence was calculated and multivariable logistic regression analyses were applied. RESULTS: Mean age amongst the 12.567 women was 49.9 years. Age and educational level were similar in women with caesarean sections only and those with vaginal delivery and obstetric anal sphincter injuries (OASIS). Nulliparas and women with vaginal delivery and no OASIS were older and had higher educational achievements. One in four women with OASIS reported anal incontinence compared to one in six amongst the other women(p<.001). Age, educational level, diarrhea, constipation, birthweight and OASIS increased the risk of anal incontinence in all women. Parity was associated with anal incontinence in parous women only. No differences were found for fecal urgency. CONCLUSIONS: Women with vaginal deliveries complicated by OASIS were at increased risk of anal incontinence. However, no increased risk of anal incontinence was found in nulliparous women or women with cesarean sections only or vaginal deliveries not complicated by OASIS

Risk assessment of the biocontrol product Nemaslug 2.0 with the active organisms Phasmarhabditis californica (strain P19D) and Moraxella osloensis

publishedVersio

The addition of locust bean gum but not water delayed the gastric emptying rate of a nutrient semisolid meal in healthy subjects

BACKGROUND: Most of the previous studies regarding the effects of gel-forming fibres have considered the gastric emptying of liquid or solid meals after the addition of pectin or guar gum. The influence of locust bean gum, on gastric emptying of nutrient semisolid meals in humans has been less well studied, despite its common occurrence in foods. Using a standardised ultrasound method, this study was aimed at investigating if the gastric emptying in healthy subjects could be influenced by adding locust been gum, a widely used thickening agent, or water directly into a nutrient semisolid test meal. METHODS: The viscosity of a basic test meal (300 g rice pudding, 330 kcal) was increased by adding Nestargel (6 g, 2.4 kcal), containing viscous dietary fibres (96.5%) provided as seed flour of locust bean gum, and decreased by adding 100 ml of water. Gastric emptying of these three test meals were evaluated in fifteen healthy non-smoking volunteers, using ultrasound measurements of the gastric antral area to estimate the gastric emptying rate (GER). RESULTS: The median value of GER with the basic test meal (rice pudding) was estimated at 63 %, (range 47 to 84 %), (the first quartile = 61 %, the third quartile = 69 %). Increasing the viscosity of the rice pudding by adding Nestargel, resulted in significantly lower gastric emptying rates (p < 0.01), median GER 54 %, (range 7 to 71 %), (the first quartile = 48 %, the third quartile = 60 %). When the viscosity of the rice pudding was decreased (basic test meal added with water), the difference in median GER 65 %, (range 38 to 79 %), (the first quartile = 56 %, the third quartile = 71 %) was not significantly different (p = 0.28) compared to the GER of the basic test meal. CONCLUSIONS: We conclude that the addition of locust bean gum to a nutrient semisolid meal has a major impact on gastric emptying by delaying the emptying rate, but that the addition of water to this test meal has no influence on gastric emptying in healthy subjects

Loss of function mutations in GEMIN5 cause a neurodevelopmental disorder.

GEMIN5, an RNA-binding protein is essential for assembly of the survival motor neuron (SMN) protein complex and facilitates the formation of small nuclear ribonucleoproteins (snRNPs), the building blocks of spliceosomes. Here, we have identified 30 affected individuals from 22 unrelated families presenting with developmental delay, hypotonia, and cerebellar ataxia harboring biallelic variants in the GEMIN5 gene. Mutations in GEMIN5 perturb the subcellular distribution, stability, and expression of GEMIN5 protein and its interacting partners in patient iPSC-derived neurons, suggesting a potential loss-of-function mechanism. GEMIN5 mutations result in disruption of snRNP complex assembly formation in patient iPSC neurons. Furthermore, knock down of rigor mortis, the fly homolog of human GEMIN5, leads to developmental defects, motor dysfunction, and a reduced lifespan. Interestingly, we observed that GEMIN5 variants disrupt a distinct set of transcripts and pathways as compared to SMA patient neurons, suggesting different molecular pathomechanisms. These findings collectively provide evidence that pathogenic variants in GEMIN5 perturb physiological functions and result in a neurodevelopmental delay and ataxia syndrome

Gut bacterial profile in patients newly diagnosed with treatment-na&amp;iuml;ve Crohn&amp;#39;s disease

Petr Ricanek,1,2 Sheba M Lothe,1 Stephan A Frye,1 Andreas Rydning,2 Morten H Vatn,3,4 Tone T&amp;oslash;njum1,51Centre for Molecular Biology and Neuroscience and Department of Microbiology, Oslo University Hospital, Rikshospitalet, Oslo, 2Department of Gastroenterology, Akershus University Hospital, L&amp;oslash;renskog and Faculty Division Akershus University Hospital, University of Oslo, L&amp;oslash;renskog, 3EpiGen Institute, Faculty Division Akershus University Hospital, University of Oslo, L&amp;oslash;renskog, 4Department of Medicine, Oslo University Hospital, Rikshospitalet, Oslo, 5Centre for Molecular Biology and Neuroscience and Department of Microbiology, University of Oslo, Oslo, NorwayObjectives: The aim of this study was to define the composition of the gut bacterial flora in Norwegian patients with early stage Crohn&amp;#39;s disease (CD). Methods: By using a nonselective metagenomics approach, the general bacterial composition in mucosal biopsies from the ileum and the colon of five subjects, four patients with different phenotypes of CD, and one noninflammatory bowel disease control, was characterized. After partial 16S ribosomal RNA (rRNA) gene sequencing, BLAST homology searches for species identification and phylogenetic analysis were performed.Results: An overall biodiversity of 106 different bacterial operational taxonomic units (OTUs) was detected in the cloned libraries. Nearly all OTUs belonged to the phylae Bacteroidetes (42% in CD, 71% in the control) or Firmicutes (42% in CD, 28% in the control), except for some OTUs that belonged to the phylum Proteobacteria (15% in CD, 0% in the control) and a few OTUs that could not be assigned to a phylum (2% in CD, 1% in the control).Conclusion: Based on the high incidence of inflammatory bowel disease (IBD) in Norway, this pilot study represents a relevant determination of the gut microbiota in Norwegian patients compared to previous findings in other countries. The bacterial profile of Norwegian CD patients was found to be similar to that of CD patients in other countries. The findings do not support a particular bacterial composition as a predominant causative factor for the high incidence of IBD that exists in some countries.Keywords: Crohn&amp;#39;s disease, gut microbiota composition, inflammatory bowel disease, IBD, metagenomics, 16S rRNA gene sequence

Homocarnosinosis: A historical update and findings in the SPG11 gene

OBJECTIVES: A family with homocarnosinosis was reported in the literature in 1976. Three affected siblings had spastic paraplegia, retinitis pigmentosa, mental retardation, and cerebrospinal fluid (CSF) homocarnosine concentrations 20 times higher than in controls. Based on the clinical findings and new genetic techniques, we have been able to establish a precise genetic diagnosis. METHOD: The medical records were re-evaluated, and genetic analyses were performed post-mortem in this original family. SNP array-based whole genome homozygosity mapping and Sanger sequencing of the SPG11 gene were performed. Seven additional Norwegian SPG11 patients and their disease-causing variants and clinical findings were evaluated. Homocarnosine levels in CSF were measured in four of these seven patients. RESULTS: A homozygous pathogenic splice-site variant in the SPG11 gene, c.2316 + 1G>A, was found. The clinical findings in the original family correlate with the heterogeneous SPG11 phenotype. The same variant was found in seven other Norwegian SPG11 patients, unrelated to the original family, either as homozygous or compound heterozygous constellation. Normal homocarnosine levels were found in the CSF of all unrelated SPG11 patients. CONCLUSIONS: A re-evaluation of the clinical symptoms and findings in the original family correlates with the SPG11 phenotype. The increased levels of homocarnosine do not seem to be a biomarker for SPG11 in our patients. Homocarnosinosis is still a biochemical aberration with unknown clinical significance

Reduced expression of aquaporins in human intestinal mucosa in early stage inflammatory bowel disease

Petr Ricanek,1,2 Lisa K Lunde,3 Stephan A Frye,1 Mari St&oslash;en,1 St&aring;le Nyg&aring;rd,4 Jens P Morth,5,6 Andreas Rydning,2 Morten H Vatn,7,8 Mahmood Amiry-Moghaddam,3 Tone T&oslash;njum,1,9 1Department of Microbiology, Oslo University Hospital, Rikshospitalet, Oslo, 2Department of Gastroenterology, Akershus University Hospital, L&oslash;renskog and Campus Ahus, Institute of Clinical Medicine, University of Oslo, L&oslash;renskog, 3Department of Anatomy, Institute of Basic Medical Sciences, University of Oslo, 4Bioinformatics Core Facility, Institute for Medical Informatics, Oslo University Hospital and University of Oslo, 5Centre for Molecular Medicine, Nordic EMBL Partnership, University of Oslo, 6Institute for Experimental Research, Oslo University Hospital (Ullevaal), Oslo, 7EpiGen Institute, Campus Ahus, Institute of Clinical Medicine, University of Oslo, L&oslash;renskog, 8Section of Gastroenterology, Oslo University Hospital, Rikshospitalet, Oslo, 9Department of Microbiology, University of Oslo, Oslo, Norway Objectives: The aim of this study was to investigate the relationship between aquaporin (AQP) water channel expression and the pathological features of early untreated inflammatory bowel disease (IBD) in humans. Methods: Patients suspected to have IBD on the basis of predefined symptoms, including abdominal pain, diarrhea, and/or blood in stool for more than 10 days, were examined at the local hospital. Colonoscopy with biopsies was performed and blood samples were taken. Patients who did not meet the diagnostic criteria for IBD and who displayed no evidence of infection or other pathology in the gut were included as symptomatic non-IBD controls. AQP1, 3, 4, 5, 7, 8, and 9 messenger RNA (mRNA) levels were quantified in biopsies from the distal ileum and colon by quantitative real-time polymerase chain reaction. Protein expression of selected AQPs was assessed by confocal microscopy. Through multiple alignments of the deduced amino acid sequences, the putative three-dimensional structures of AQP1, 3, 7, and 8 were modeled. Results: AQP1, 3, 7, and 8 mRNAs were detected in all parts of the intestinal mucosa. Notably, AQP1 and AQP3 mRNA levels were reduced in the ileum of patients with Crohn&#39;s disease, and AQP7 and AQP8 mRNA levels were reduced in the ileum and the colon of patients with ulcerative colitis. Immunofluorescence confocal microscopy showed localization of AQP3, 7, and 8 at the mucosal epithelium, whereas the expression of AQP1 was mainly confined to the endothelial cells and erythrocytes. The reduction in the level of AQP3, 7, and 8 mRNA was confirmed by immunofluorescence, which also indicated a reduction of apical immunolabeling for AQP8 in the colonic surface epithelium and crypts of the IBD samples. This could indicate loss of epithelial polarity in IBD, leading to disrupted barrier function. Conclusion: AQPs 1 and 8 and the aquaglyceroporins AQPs 3 and 7 are the AQPs predominantly expressed in the lower intestinal tract of humans. Their expression is significantly reduced in patients with IBD, and they are differentially expressed in specific bowel segments in patients with Crohn&#39;s disease and ulcerative colitis. The data present a link between gut inflammation and water/solute homeostasis, suggesting that AQPs may play a significant role in IBD pathophysiology. Keywords: inflammatory bowel disease, Crohn&#39;s disease, ulcerative colitis, aquaporins, aquaglyceroporin

Epidemiology of traumatic cervical spinal fractures in a general Norwegian population

Background In Western countries, the typical cervical spine fracture (CS-Fx) patient has historically been a young male injured in a road traffic accident. Recent reports and daily clinical practice clearly indicate a change in the typical patient from a young male to an elderly male or female with comorbidities. This study aimed to establish contemporary population-based epidemiological data of traumatic CS-Fx for use in health-care planning and injury prevention. Methods This is a population-based retrospective database study (with prospectively collected data) from the Southeast Norway health region with 3.0 million inhabitants. We included all consecutive cases diagnosed with a CS-Fx between 2015 and 2019. Information regarding demographics, preinjury comorbidities, trauma mechanisms, injury description, treatment, and level of hospital admittance is presented. Results We registered 2153 consecutive cases with CS-Fx during a 5-year period, with an overall crude incidence of CS-Fx of 14.9/100,000 person-years. Age-adjusted incidences using the standard population for Europe and the World was 15.6/100,000 person-years and 10.4/100,000 person-years, respectively. The median patient age was 62 years, 68% were males, 37% had a preinjury severe systemic disease, 16% were under the influence of ethanol, 53% had multiple trauma, and 12% had concomitant cervical spinal cord injury (incomplete in 85% and complete in 15%). The most common trauma mechanisms were falls (57%), followed by bicycle injuries (12%), and four-wheel motorized vehicle accidents (10%). The most common upper CS-Fx was C2 odontoid Fx, while the most common subaxial Fx was facet joint Fx involving cervical level C6/C7. Treatment was external immobilization with a stiff neck collar alone in 65%, open surgical fixation in 26% (giving a 3.7/100,000 person-years surgery rate), and no stabilization in 9%. The overall 90-day mortality was 153/2153 (7.1%). Conclusions This study provides an overview of the extent of the issue and patient complexity necessary for planning the health-care management and injury prevention of CS-Fx. The typical CS-Fx patient was an elderly male or female with significant comorbidities injured in a low-energy trauma. The overall crude incidences of CS-Fx and surgical fixation of CS-Fx in Southeast Norway were 14.9/100,000 person-years and 3.7/100,000 person-years, respectively