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111.
Michael M. Shenouda Shady ElGhazaly Harb Sameh A. A. Mikhail Sherif M. Mokhtar Ayman M. A. Osman Arsany T. S. Wassef Nayer N. H. Rizkallah Nader M. Milad Shady E. Anis Tamer Mohamed Nabil Nader Sh. Zaki Antoine Halepian 《Obesity surgery》2018,28(2):389-395
Introduction
Laparoscopic single anastomosis gastric bypass (SAGB) is increasingly performed for morbidly obese patients.Aim of Work
This pilot study aims primarily at evaluating the incidence of bile gastritis after SAGB. The occurrence of reflux oesophagitis and reflux symptoms were also assessed.Patients and Methods
This study included 20 patients having no reflux symptoms. All patients underwent a SAGB as a primary bariatric procedure by a single surgeon. Patients included consented to have an upper GI endoscopy done at 6 months postoperatively. Gastric aspirate was sent for bilirubin level assessment. Gastric and esophageal biopsies were submitted for histopathology and campylobacter-like organism (CLO) test.Results
In our study, the rate of bile gastritis was 30%. In 18 patients, the level of bilirubin in gastric aspirate seems to be related to the degree of mucosal inflammation. The remaining two patients had microscopic moderate to severe gastritis with normal aspirate bilirubin level. Two patients with bilirubin level in aspirate more than 20 mg/dl had severe oesophagitis, gastritis with erosions, and metaplasia. Relationship between bilirubin level and histopathological findings of gastric biopsy examination was statistically significant with a P value of 0.001.Conclusion
The incidence of bile gastritis in this cohort is higher than reported in the literature, and this may be worrying. The correlation between endoscopic findings and patients’ symptoms is poor. Bilirubin level and pH in aspirate might be useful tools to confirm alkaline reflux. Its level might help to choose candidates for revision surgery after SAGB. This needs further validation with larger sample size.112.
113.
Kunal Chaudhary Gautam Phadke Ravi Nistala Charles E. Weidmeyer Samy I. McFarlane Adam Whaley-Connell 《Current diabetes reports》2010,10(1):37-42
Currently used measures to assess kidney function and injury are largely inadequate. Markers such as serum creatinine, formulas
to estimate glomerular filtration rate, cystatin C, and proteinuria largely identify an underlying disease process that is
well established. Thus, there has been a recent effort to identify new biomarkers that reflect kidney function, early injury,
and/or repair that ultimately can relate to progression or regression of damage. Several biomarkers emerged recently that
are able to detect kidney damage earlier than is currently possible with traditional biomarkers such as serum creatinine and
proteinuria. Identification of urine biomarkers has proven to be beneficial in recent years because of ease of handling, stability,
and the ability to standardize the various markers to creatinine or other peptides generally already present in the urine.
Recent markers such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and podocin have
garnered a lot of attention. The emergence of these and other biomarkers is largely because of the evolution of novel genomic
and proteomic applications in investigations of acute kidney injury and chronic kidney disease. In this article, we focus
on the applications of these biomarkers in disease. 相似文献
114.
Kelleher JP Centorrino F Huxley NA Bates JA Drake JK Egli S Baldessarini RJ 《European neuropsychopharmacology》2012,22(6):415-418
The preferential dopamine D(3)-agonist pramipexole (4.25±0.38 mg/day) or placebo were added for up to 12 weeks to ongoing antipsychotic treatment for 24 adult patients with DSM-IV schizophrenia or schizoaffective disorder. Pramipexole was generally well-tolerated (82% trial-completion), and yielded greater decreases in PANSS-total scores (drug/placebo=2.1; p=0.04), with similar decreases in PANSS positive and negative scores and 6.7-fold greater reduction of serum prolactin concentrations compared to placebo. There were no differences in ratings of mood, cognition or extrapyramidal symptoms, all of which were low at intake. 相似文献
115.
Colony-Stimulating Factor-1 Promotes Kidney Growth and Repair via Alteration of Macrophage Responses
Maliha A. Alikhan Christina V. Jones Timothy M. Williams Anthony G. Beckhouse Anne L. Fletcher Michelle M. Kett Samy Sakkal Chrishan S. Samuel Robert G. Ramsay James A. Deane Christine A. Wells Melissa H. Little David A. Hume Sharon D. Ricardo 《The American journal of pathology》2011,179(3):1243-1256
Colony-stimulating factor (CSF)-1 controls the survival, proliferation, and differentiation of macrophages, which are recognized as scavengers and agents of the innate and the acquired immune systems. Because of their plasticity, macrophages are endowed with many other essential roles during development and tissue homeostasis. We present evidence that CSF-1 plays an important trophic role in postnatal organ growth and kidney repair. Notably, the injection of CSF-1 postnatally enhanced kidney weight and volume and was associated with increased numbers of tissue macrophages. Moreover, CSF-1 promotes postnatal renal repair in mice after ischemia-reperfusion injury by recruiting and influencing macrophages toward a reparative state. CSF-1 treatment rapidly accelerated renal repair with tubular epithelial cell replacement, attenuation of interstitial fibrosis, and functional recovery. Analysis of macrophages from CSF-1-treated kidneys showed increased expression of insulin-like growth factor-1 and anti-inflammatory genes that are known CSF-1 targets. Taken together, these data suggest that CSF-1 is important in kidney growth and the promotion of endogenous repair and resolution of inflammatory injury.Macrophages are versatile cells that have been long recognized as immune effectors where their recruitment to sites of injury is a fundamental feature of inflammation. Although their role in host defense has been well documented, macrophages and their precursors are also important during embryogenesis, normal tissue maintenance, and postnatal organ repair.1,2 Almost all developing organs contain a population of resident monocytes that infiltrate very early during organogenesis and persist throughout adult life.3–6 In addition to their phagocytic capabilities during tissue remodeling-associated apoptosis,5,7 fetal macrophages have many trophic effects that promote tissue and organ growth.6,8,9Colony-stimulating factor (CSF)-1 controls the differentiation, proliferation, and survival of macrophages by binding to a high-affinity cell-surface tyrosine kinase receptor (CSF-1R), encoded by the c-fms proto-oncogene that is expressed on macrophages and their progenitors.6 CSF-1 is critical for both adult and embryonic macrophage development. This is manifested by multiple organ growth deficiencies observed in osteopetrotic (Csf1op/Csf1op) mice that have a spontaneous mutation in the csf-1 gene. These mice show growth restriction and developmental abnormalities of the bones, brain, and reproductive and endocrine organs,10–13 a phenotype that can be rescued by injection of exogenous CSF-1 or insertion of a csf-1 transgene.14–16In adult organs, there is considerable heterogeneity of monocytes and macrophages with distinct subsets defined by phenotype, function, and the differential expression of cell surface markers.17–19 Subpopulations of macrophages directly contribute to wound healing and tissue repair, supporting the concept that some macrophage phenotypes can promote organ regeneration after a pro-inflammatory state of injury.20 The concept of macrophage polarization states has emerged; the M1 “classically activated” pro-inflammatory cell type apparently opposed by an M2 “alternatively activated” immune regulatory macrophage.18 In general, these two states are thought to be analogous to the opposing T helper 1 and T helper 2 immune responses, although in both cases this model is probably too simplistic. Functionally, it is more likely that distinct subpopulations of macrophages may exist in the same tissue and play critical roles in both the injury and recovery phases of inflammatory scarring.20Our previous study provided evidence that the addition of CSF-1 to a developing murine kidney promotes a growth and differentiation response that is accompanied by increased numbers of macrophages.3 Furthermore, with the use of expression profiling we demonstrated that fetal kidney, lung, and brain macrophages share a characteristic gene expression profile that includes the production of factors important in the suppression of inflammation and the promotion of proliferation.3 Embryonic macrophages appear to play a positive trophic role that may have parallel reparative functions in many adult tissues undergoing repair and cellular replacement.1,20 A number of studies have suggested that infiltrating macrophages along with the trophic factors they release participate in tissue repair of the kidney,20–22 brain,23 skin,24,25 lung,26 liver,27 heart,28 gastrointestinal tract,29,30 and skeletal muscle.31,32 Indeed, the pleiotrophic roles for CSF-1 in reproduction, development of multiple organ systems, and maternal-fetal interactions during pregnancy by macrophage-mediated processes have also been well defined.2,33,34To determine the physiological relevance of CSF-1 as a component of the mammalian growth regulatory axis, CSF-1 was administered to neonatal mice. We report that CSF-1 administration to newborn mice increased body weight and kidney weight and volume and was associated with increased numbers of macrophages. Our results also establish that CSF-1 injection into mice after ischemia-reperfusion (IR) injury promoted endogenous repair with characteristic rapid re-epithelialization of the damaged tubular epithelium, leading to functional recovery. Flow cytometric and gene expression analyses were used to delineate the macrophage profile present in the kidneys during the early and resolution phase of IR injury with and without CSF-1 therapy. We thus provide evidence that CSF-1 recruits macrophages to the reparative site and influences their phenotype, partly through an insulin-like growth factor (IGF)-1 signaling response. Therefore, macrophages under the stimulus of CSF-1 in an acute setting of renal disease markedly accelerate renal cell replacement and tissue remodeling while attenuating downstream interstitial extracellular matrix accumulation. 相似文献
116.
Omri S Behar-Cohen F de Kozak Y Sennlaub F Verissimo LM Jonet L Savoldelli M Omri B Crisanti P 《The American journal of pathology》2011,179(2):942-953
Diabetic retinopathy is associated with ocular inflammation, leading to retinal barrier breakdown, macular edema, and visual cell loss. We investigated the molecular mechanisms involved in microglia/macrophages trafficking in the retina and the role of protein kinase Cζ (PKCζ) in this process. Goto Kakizaki (GK) rats, a model for spontaneous type 2 diabetes were studied until 12 months of hyperglycemia. Up to 5 months, sparse microglia/macrophages were detected in the subretinal space, together with numerous pores in retinal pigment epithelial (RPE) cells, allowing inflammatory cell traffic between the retina and choroid. Intercellular adhesion molecule-1 (ICAM-1), caveolin-1 (CAV-1), and PKCζ were identified at the pore border. At 12 months of hyperglycemia, the significant reduction of pores density in RPE cell layer was associated with microglia/macrophages accumulation in the subretinal space together with vacuolization of RPE cells and disorganization of photoreceptors outer segments. The intraocular injection of a PKCζ inhibitor at 12 months reduced iNOS expression in microglia/macrophages and inhibited their migration through the retina, preventing their subretinal accumulation. We show here that a physiological transcellular pathway takes place through RPE cells and contributes to microglia/macrophages retinal trafficking. Chronic hyperglycemia causes alteration of this pathway and subsequent subretinal accumulation of activated microglia/macrophages. 相似文献
117.
Shakirin G Braess H Fiedler F Kunath D Laube K Parodi K Priegnitz M Enghardt W 《Physics in medicine and biology》2011,56(5):1281-1298
An independent assessment of the dose delivery in ion therapy can be performed using positron emission tomography (PET). For that a distribution of positron emitters which appear as the result of interaction between ions of the therapeutic beam and the irradiated tissue is measured during or after the irradiation. Three concepts for PET monitoring implemented in various therapy facilities are considered in this paper. The in-beam PET concept relies on the PET measurement performed simultaneously to the irradiation by means of a PET scanner which is completely integrated into the irradiation site. The in-room PET concept allows measurement immediately after irradiation by a standalone PET scanner which is installed very close to the irradiation site. In the off-line PET scenario the measurement is performed by means of a standalone PET/CT scanner 10-30 min after the irradiation. These three concepts were evaluated according to image quality criteria, integration costs, and their influence onto the workflow of radiotherapy. In-beam PET showed the best performance. However, the integration costs were estimated as very high for this modality. Moreover, the performance of in-beam PET depends heavily on type and duty cycle of the accelerator. The in-room PET is proposed for planned therapy facilities as a good compromise between the quality of measured data and integration efforts. For facilities which are close to the nuclear medicine departments off-line PET can be suggested under several circumstances. 相似文献
118.
119.
120.
Am��lie Bonnefond Martine Vaxillaire Yann Labrune C��cile Lecoeur Jean-Claude Ch��vre Nabila Bouatia-Naji St��phane Cauchi Beverley Balkau Michel Marre Jean Tichet Jean-Pierre Riveline Samy Hadjadj Yves Gallois S��bastien Czernichow Serge Hercberg Marika Kaakinen Susanne Wiesner Guillaume Charpentier Claire L��vy-Marchal Paul Elliott Marjo-Riitta Jarvelin Fritz Horber Christian Dina Oluf Pedersen Robert Sladek David Meyre Philippe Froguel 《Diabetes》2009,58(11):2687-2697