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Adipose tissue morphology predicts improved insulin sensitivity following moderate or pronounced weight loss.

https://arctichealth.org/en/permalink/ahliterature272781
Source
Int J Obes (Lond). 2015 Jun;39(6):893-8
Publication Type
Article
Date
Jun-2015
Author
D. Eriksson-Hogling
D P Andersson
J. Bäckdahl
J. Hoffstedt
S. Rössner
A. Thorell
E. Arner
P. Arner
M. Rydén
Source
Int J Obes (Lond). 2015 Jun;39(6):893-8
Date
Jun-2015
Language
English
Publication Type
Article
Keywords
Adipocytes - metabolism - pathology
Adipose Tissue, White - metabolism - pathology
Adult
Bariatric Surgery
Blood Glucose - metabolism
Body mass index
Cell Enlargement
Cohort Studies
Diabetes Mellitus, Type 2 - etiology - metabolism - prevention & control
Diet, Reducing
Female
Humans
Inflammation - etiology - metabolism
Male
Obesity - complications - metabolism - pathology - surgery
Randomized Controlled Trials as Topic
Sweden
Weight Loss
Abstract
Cross-sectional studies show that white adipose tissue hypertrophy (few, large adipocytes), in contrast to hyperplasia (many, small adipocytes), associates with insulin resistance and increased risk of developing type 2 diabetes. We investigated if baseline adipose cellularity could predict improvements in insulin sensitivity following weight loss.
Plasma samples and subcutaneous abdominal adipose biopsies were examined in 100 overweight or obese individuals before and 10 weeks after a hypocaloric diet (7±3% weight loss) and in 61 obese subjects before and 2 years after gastric by-pass surgery (33±9% weight loss). The degree of adipose tissue hypertrophy or hyperplasia (termed the morphology value) in each individual was calculated on the basis of the relationship between fat cell volume and total fat mass. Insulin sensitivity was determined by homeostasis model assessment-estimated insulin resistance (HOMAIR).
In both cohorts at baseline, subjects with hypertrophy displayed significantly higher fasting plasma insulin and HOMAIR values than subjects with hyperplasia (P
PubMed ID
25666530 View in PubMed
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The epidemiology and pathogenesis of neoplasia in the small intestine.

https://arctichealth.org/en/permalink/ahliterature153834
Source
Ann Epidemiol. 2009 Jan;19(1):58-69
Publication Type
Article
Date
Jan-2009
Author
David Schottenfeld
Jennifer L Beebe-Dimmer
Fawn D Vigneau
Author Affiliation
Department of Epidemiology, University of Michigan, Ann Arbor, Michigan, USA.
Source
Ann Epidemiol. 2009 Jan;19(1):58-69
Date
Jan-2009
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - epidemiology - etiology
Adenoma - epidemiology - etiology
Colorectal Neoplasms - epidemiology - etiology
Cytokines - physiology
Gastrointestinal Stromal Tumors - epidemiology - etiology
Humans
Incidence
Inflammation - etiology - metabolism
Intestinal Mucosa - metabolism - microbiology - pathology
Intestinal Neoplasms - epidemiology - etiology
Intestine, Small - metabolism - microbiology - pathology
Lymphoma, Non-Hodgkin - epidemiology - etiology
Neuroendocrine Tumors - epidemiology - etiology
Prevalence
Risk factors
United States - epidemiology
Abstract
The mucosa of the small intestine encompasses about 90% of the luminal surface area of the digestive system, but only 2% of the total annual gastrointestinal cancer incidence in the United States.
The remarkable contrast in age-standardized cancer incidence between the small and large intestine has been reviewed with respect to the cell type patterns, demographic features, and molecular characteristics of neoplasms.
Particularly noteworthy is the predominance of adenocarcinoma in the colon, which exceeds 98% of the total incidence by cell type, in contrast to that of 30% to 40% in the small intestine, resulting in an age-standardized ratio of rates exceeding 50-fold. The prevalence of adenomas and carcinomas is most prominent in the duodenum and proximal jejunum. The positive correlation in global incidence rates of small and large intestinal neoplasms and the reciprocal increases in risk of second primary adenocarcinomas suggest that there are common environmental risk factors. The pathophysiology of Crohn inflammatory bowel disease and the elevated risk of adenocarcinoma demonstrate the significance of the impaired integrity of the mucosal barrier and of aberrant immune responses to luminal indigenous and potentially pathogenic microorganisms.
In advancing a putative mechanism for the contrasting mucosal susceptibilities of the small and large intestine, substantial differences are underscored in the diverse taxonomy, concentration and metabolic activity of anaerobic organisms, rate of intestinal transit, changing pH, and the enterohepatic recycling and metabolism of bile acids. Experimental and epidemiologic studies are cited that suggest that the changing microecology, particularly in the colon, is associated with enhanced metabolic activation of ingested and endogenously formed procarcinogenic substrates.
Notes
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PubMed ID
19064190 View in PubMed
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Hypothesis: iron chelation plays a vital role in neutrophilic inflammation.

https://arctichealth.org/en/permalink/ahliterature208800
Source
Biometals. 1997 Apr;10(2):135-42
Publication Type
Article
Date
Apr-1997
Author
A J Ghio
C A Piantadosi
A L Crumbliss
Author Affiliation
National Health and Environmental Effects Research Laboratory, EPA, Research Triangle Park, NC, USA.
Source
Biometals. 1997 Apr;10(2):135-42
Date
Apr-1997
Language
English
Publication Type
Article
Keywords
Animals
Fibrosis - etiology - metabolism
Free Radicals - adverse effects
Humans
Inflammation - etiology - metabolism - pathology
Iron - metabolism
Iron Chelating Agents - pharmacology
Lactoferrin - metabolism
NADH, NADPH Oxidoreductases - metabolism
Neoplasms - etiology - metabolism
Neutrophils - drug effects - enzymology - pathology
Oxidation-Reduction
Phagocytes - cytology - drug effects - metabolism
Abstract
Neutrophil influx into tissues occurs in many diverse diseases and can be associated with both beneficial and injurious effects. We hypothesize that the stimulus for certain neutrophilic inflammatory responses can be reduced to a series of competing reactions for iron, with either a labile or reactive coordination site available, between host chelators and chelators not indigenous to that specific living system. The iron focuses the transport of host phagocytic cells through a metal catalyzed generation of oxidant sensitive mediators including cytokines and eicosanoids. Many of these products are chemotactic for neutrophils. We also postulate that the iron increases the activity of the phagocyte associated NADPH oxidoreductase in the neutrophil. The function of this enzyme is likely to be the generation of superoxide in the host's attempt to chemically reduce and dislodge the iron from its chelate complex. After the reoxidation of Fe2+ in an aerobic environment, Fe3+ will be coordinated by host lactoferrin released by the neutrophil. When complexed by this glycoprotein, the metal does not readily undergo oxidation/reduction and is safely transported to the macrophages of the reticuloendothelial system where it is stored in ferritin. Finally, we propose that the neutrophil will attempt to destroy the chelator not indigenous to the host by releasing granular contents other than lactoferrin. Inability to eliminate the chelator allows this sequence to repeat itself, which can lead to tissue injury. Such persistence of a metal chelate in the host may be associated with biomineralization, fibrosis, and cancer.
PubMed ID
9210296 View in PubMed
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Inflammatory response in the rabbit after phacoemulsification and intraocular lens implantation using a 5.2 or 11.0 mm incision.

https://arctichealth.org/en/permalink/ahliterature51043
Source
J Cataract Refract Surg. 1997 Jan-Feb;23(1):126-31
Publication Type
Article
Author
C G Laurell
C. Zetterström
B. Lundgren
L. Törngren
K. Andersson
Author Affiliation
S:t Erik's Eye Hospital, Stockholm, Sweden.
Source
J Cataract Refract Surg. 1997 Jan-Feb;23(1):126-31
Language
English
Publication Type
Article
Keywords
Animals
Aqueous Humor - cytology - metabolism
Comparative Study
Dinoprostone - metabolism
Eye Diseases - etiology - metabolism - pathology
Inflammation - etiology - metabolism - pathology
Lenses, Intraocular - adverse effects
Leukocyte Count
Methylmethacrylates
Phacoemulsification - adverse effects - methods
Postoperative Complications
Rabbits
Radioimmunoassay
Random Allocation
Research Support, Non-U.S. Gov't
Sutures
Abstract
PURPOSE: To study the effect of two incision sizes, 5.2 and 11.0 mm, on the inflammatory response in rabbit eyes after lens extraction with phacoemulsification. SETTING: S:t Erik's Eye Hospital, Stockholm, and Pharmacia, Uppsala, Sweden. METHODS: Bilateral endocapsular phacoemulsification was performed on 32 rabbits. The wound was enlarged to 5.2 mm, and a poly(methyl methacrylate) intraocular lens (IOL) was implanted in the capsular bag. In each rabbit, one eye was selected at random and the wound in that eye enlarged to 11.0 mm. In both eyes the wound was sutured with a 9-0 polypropylene continuous suture. The number of white blood cells (WBCs) and prostaglandin E2 (PGE2) in the aqueous humor were measured at days 1, 3, 7, and 28 postoperatively. Corneal thickness was also measured by pachymetry. RESULTS: The number of WBCs at day 3 and the PGE2 levels at days 1, 3, and 7 were significantly higher in eyes with 11.0 mm incisions than in eyes with 5.2 mm incisions. One week after surgery, the corneas in the eyes with 11.0 mm incisions were significantly thicker than in those with 5.2 mm incisions. CONCLUSION: The results indicate that incision size is an important factor in the inflammatory response following phacoemulsification and IOL implantation in the rabbit eye.
PubMed ID
9100120 View in PubMed
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