Miracle-dz/UniFAR-FTUs huggingface dataset:
The role of image processing in measuring fractal dimension

The characterization of irregular objects with fractal methods often leads to the estimation of the slope of a function plotted against a scale parameter. The slope is usually obtained with a linear regression with upper and lower boundaries that sets the acceptable range of fractal dimension value. This pattern is similar even when the variables are changed. In the present work, we developed a computer application to measure fractal dimension, with emphasis on medical images. The system has the ability to process the images involving the Red, Green, Blue (RGS) and the Hue, Saturation, (luminosity) Value (HSV) before any analysis of the image(s) is carried out. The results of the present work suggest a boundary (which determines how much image processing should be done in order to achieve relevant fractal dimension values) can be identified by systematically changing the parameter.
Effects of fish and krill oil on gene expression in peripheral blood mononuclear cells and circulating markers of inflammation: a randomised controlled trial

Marine n-3 (omega-3) fatty acids alter gene expression by regulating the activity of transcription factors. Krill oil is a source of marine n-3 fatty acids that has been shown to modulate gene expression in animal studies; however, the effect in humans is not known. Hence, we aimed to compare the effect of intake of krill oil, lean and fatty fish with a similar content of n-3 fatty acids, and high-oleic sunflower oil (HOSO) with added astaxanthin on the expression of genes involved in glucose and lipid metabolism and inflammation in peripheral blood mononuclear cells (PBMC) as well as circulating inflammatory markers. In an 8-week trial, healthy men and women aged 18–70 years with fasting TAG of 1·3–4·0 mmol/l were randomised to receive krill oil capsules (n 12), HOSO capsules (n 12) or lean and fatty fish (n 12). The weekly intakes of marine n-3 fatty acids from the interventions were 4654, 0 and 4103 mg, respectively. The mRNA expression of four genes, PPAR γ coactivator 1A (PPARGC1A), steaoryl-CoA desaturase (SCD), ATP binding cassette A1 (ABCA1) and cluster of differentiation 40 (CD40), were differently altered by the interventions. Furthermore, within-group analyses revealed that krill oil down-regulated the mRNA expression of thirteen genes, including genes involved in glucose and cholesterol metabolism and β-oxidation. Fish altered the mRNA expression of four genes and HOSO down-regulated sixteen genes, including several inflammation-related genes. There were no differences between the groups in circulating inflammatory markers after the intervention. In conclusion, the intake of krill oil and HOSO with added astaxanthin alter the PBMC mRNA expression of more genes than the intake of fish.
Looping‐out mechanism for resolution of replicative stress at telomeres

Repetitive DNA is prone to replication fork stalling, which can lead to genome instability. Here, we find that replication fork stalling at telomeres leads to the formation of t‐circle‐tails, a new extrachromosomal structure that consists of circular telomeric DNA with a single‐stranded tail. Structurally, the t‐circle‐tail resembles cyclized leading or lagging replication intermediates that are excised from the genome by topoisomerase II‐mediated cleavage. We also show that the DNA damage repair machinery NHEJ is required for the formation of t‐circle‐tails and for the resolution of stalled replication forks, suggesting that NHEJ, which is normally constitutively suppressed at telomeres, is activated in the context of replication stress. Inhibition of NHEJ or knockout of DNA‐PKcs impairs telomere replication, leading to multiple‐telomere sites (MTS) and telomere shortening. Collectively, our results support a “looping‐out” mechanism, in which the stalled replication fork is cut out and cyclized to form t‐circle‐tails, and broken DNA is religated. The telomere loss induced by replication stress may serve as a new factor that drives replicative senescence and cell aging.
Association between fruit and vegetable consumption and oral cancer: a meta-analysis of observational studies.

BACKGROUND Oral cancer ranks as the seventh most common form of cancer worldwide. Recent reports have examined the effect of fruit and vegetable intake on the risk of oral cancer, but results are controversial. OBJECTIVE A meta-analysis was performed to arrive at quantitative conclusions about the contribution of fruit and vegetable intakes to the occurrence of oral cancer. DESIGN A comprehensive, systematic bibliographic search of medical literature published up to September 2005 was conducted to identify relevant studies. Separate meta-analyses were conducted for fruit and vegetable consumption. The effect of portion or daily intake of fruit or vegetables on the risk of oral cancer was calculated. A multivariate meta-regression analysis was performed to explore heterogeneity. This multivariate meta-regression analysis examined the effect of quality score, the type of cancers included, citrus fruit and green vegetable consumption, and the time interval for dietary recall of the studies on the role of fruit or vegetable consumption in the risk of oral cancer. The presence of publication bias was assessed with a funnel plot for asymmetry. RESULTS Sixteen studies (15 case-control studies and 1 cohort study) met the inclusion criteria and were included in the meta-analysis. The combined adjusted odds ratio (OR) estimates showed that each portion of fruit consumed per day significantly reduced the risk of oral cancer by 49% (OR: 0.51; 95% CI: 0.40, 0.65). For vegetable consumption, the meta-analysis showed a significant reduction in the overall risk of oral cancer of 50% (OR: 0.50; 95% CI: 0.38, 0.65). The multivariate meta-regression showed that the lower risk of oral cancer associated with fruit consumption was significantly influenced by the type of fruit consumed and by the time interval of dietary recall. CONCLUSION The consumption of fruit and vegetables is associated with a reduced risk of oral cancer.
A tracer investigation of obligatory oxidative amino acid losses in healthy, young adults.

BACKGROUND Estimation of the minimum requirement for indispensable amino acids (IAAs) has been attempted by assuming that obligatory oxidative losses (OOLs) of IAAs can be approximated from nitrogen losses and that the efficiency of utilization of IAAs at requirement intakes is approximately 70%. OBJECTIVE We wished to determine the rates of OOLs in healthy adults, using L-[1-(13)C]leucine and L-[1-(13)C, methyl-(2)H(3)]methio-nine as tracers, after adjustment to a protein-free diet and how these rates compare with those when either sulfur amino acids (SAAs: methionine and cyst(e)ine) or leucine were removed from an otherwise adequate diet. DESIGN Eleven subjects were randomly assigned to a 5-d protein-free diet or a 5-d diet providing adequate nitrogen and amino acids except for the SAAs or leucine. A 24-h constant intravenous infusion of [(15)N, (15)N]urea and L-[1-(13)C]leucine (Leu group; n = 5) or L-[1-(13)C, methyl-(2)H(3)]methionine (Met group; n = 6 ) began at 1800 on day 5 and rates of amino acid oxidation were determined. RESULTS Mean (+/-SD) oxidation rates (mg kg(-)(1) d(-)(1)) of methionine and leucine were 6.4 +/- 1.4 and 24.7 +/- 3.6, respectively, with the protein-free diet; rates were significantly lower (3.9 +/- 2.2 and 7. 2 +/- 3.4, respectively) after the SAA- and leucine-free diets. Urea production was significantly lower (P < 0.01) with the protein-free than with the SAA- or leucine-free diet. CONCLUSIONS Isotopically determined OOLs for methionine and leucine are consistent with losses predicted from nitrogen excretion, and consistent with our previous measurements of cysteine oxidation as an index of total SAA losses. The data further support our earlier conclusions regarding methionine sparing by cysteine and tentative recommended SAA requirements in adults.
Electrical physiological evidence for high-and low-affinity vagal CCK-A receptors

Li, Ying, Jinxia Zhu, and Chung Owyang. Electrical physiological evidence for highand low-affinity CCK-A receptors. Am. J. Physiol. 277 (Gastrointest. Liver Physiol. 40): G469–G477, 1999. —We have demonstrated that under physiological conditions CCK acts through vagal high-affinity CCK-A receptors to mediate pancreatic secretion. In this study, we evaluated the vagal afferent response to endogenous CCK in rats and defined the CCK-receptor affinity states and the vagal-receptive field responsive to CCK stimulation using electrophysiological studies. Experiments were performed on anesthetized rats prepared with bile-pancreatic fistula. Plasma CCK levels were elevated by diverting bilepancreatic juice (BPJ). The single-unit discharge of sensory neurons supplying the gastrointestinal tract was recorded from the nodose ganglia. All units studied were either silent or they had a very low resting discharge frequency. Thirtytwo single units were studied extensively; seven were shown to be stimulated by diversion of BPJ (2.6 6 2 impulses/min at basal to 40 6 12 impulses/min after diversion). Acute subdiaphragmatic vagotomy or perivagal capsaicin treatment abolished the response. The CCK-A-receptor antagonist CR-1409, but not the CCK-B antagonist L-365260, blocked the vagal response to endogenous CCK stimulation. Infusion of the low-affinity CCK-receptor antagonist CCK-JMV-180 completely blocked the vagal afferent response to the diversion of BPJ in three of seven rats tested but had no effect on the response in the remaining four. In a separate study, we demonstrated that gastric, celiac, or hepatic branch vagotomy abolished the response in different subgroups of neurons. In conclusion, under physiological conditions, CCK acts on both highand low-affinity CCK-A receptors present on distinct vagal afferent fibers. The vagal CCK-receptor field includes the regions innervated by the gastric, celiac, and hepatic vagal branches. This study provides electrophysiological evidence that vagal CCK receptors are present on the vagal gastric, celiac, and hepatic branches and may occur in highand low-affinity states.
Perioperative use of selective serotonin reuptake inhibitors and risks for adverse outcomes of surgery.

IMPORTANCE Single-site studies have described an association between use of selective serotonin reuptake inhibitors (SSRIs) and adverse outcomes of surgery. Multicenter studies including a broad range of surgical procedures that explore rare outcomes, such as bleeding and mortality, and that account for indications for administration of SSRIs are needed. OBJECTIVE To determine whether perioperative use of SSRIs is associated with adverse outcomes of surgery in a national sample of patients. DESIGN Retrospective study of patients 18 years or older who underwent major surgery from January 1, 2006, through December 31, 2008, at 375 US hospitals. We used multivariable hierarchical models to estimate associations between SSRI use and our outcomes. Pharmacy data were used to determine whether a patient received an SSRI in the perioperative period. SETTING Three hundred seventy-five US hospitals. PARTICIPANTS Five hundred thirty thousand four hundred sixteen patients 18 years or older. EXPOSURE Perioperative use of SSRIs. MAIN OUTCOMES AND MEASURES In-hospital mortality, length of stay, readmission at 30 days, bleeding events, transfusions, and incidence of ventricular arrhythmias. RESULTS Patients receiving SSRIs were more likely to have obesity, chronic pulmonary disease, or hypothyroidism (P < .001 for each) and more likely to have depression (41.0% vs 6.2%, P < .001). After adjustment, patients receiving SSRIs had higher odds of in-hospital mortality (adjusted odds ratio, 1.20 [95% CI, 1.07-1.36]), bleeding (1.09 [1.04-1.15]), and readmission at 30 days (1.22 [1.18-1.26]). Similar results were observed in propensity-matched analyses, although the risk of inpatient mortality was attenuated among patients with depression. Sensitivity analyses suggest that, to invalidate our results, an unmeasured covariate would have to have higher prevalence and be more strongly associated with mortality than any covariate included in our models. CONCLUSIONS AND RELEVANCE Receiving SSRIs in the perioperative period is associated with a higher risk for adverse events. Determining whether patient factors or SSRIs themselves are responsible for elevated risks requires prospective study.
Use of a triaxial accelerometer to validate reported food intakes.

BACKGROUND An easy and cheap method for validating reported energy intake (EI) is needed. OBJECTIVE Reported EI was compared with calculated energy expenditure (EE(calc)) and with energy expenditure measured by the doubly labeled water method (EE(DLW)). DESIGN EE was calculated on the basis of basal metabolic rate (BMR) measured with the ventilated-hood technique and physical activity (PA) measured with a triaxial accelerometer (EE(VH+PA)) and on the basis of BMR estimated by using World Health Organization equations and PA (EE(WHO+PA)): EE(calc) = -1.259 + 1.55 x BMR + 0.076 x counts/min (r(2) = 0.90, P = 0.0001). Subjects [n = 12 men and 12 women aged 60 +/- 3 y; body mass index (in kg/m(2)): 26 +/- 4] reported their food intakes for 7 d and EE(DLW), EE(VH+PA), and EE(WHO+PA) were assessed over the same 7 d. RESULTS Reported EI (9.0 +/- 2.1 MJ/d) was lower (P: < 0.0001) than were EE(DLW) (11.3 +/- 2.3 MJ/d), EE(VH+PA) (10.8 +/- 1.7 MJ/d), and EE(WHO+PA) (10.8 +/- 1.8 MJ/d). Underreporting was 19.4 +/- 14.0%, 16.7 +/- 13.6%, and 16.4 +/- 15.5% on the basis of EE(DLW), EE(VH+PA), and EE(WHO+PA), respectively. The difference of 2.7 +/- 8.0% between EE(DLW) and EE(VH+PA) was not related to the average of both percentages and was not significantly different from zero. The percentage of underreporting calculated with EE(WHO+PA) was not significantly different from that calculated with EE(DLW). CONCLUSIONS The use of a combination of BMR (measured or estimated) and PA is a good method for validating reported EI. There was no significant difference between the percentage of underreporting calculated with EE(VH+PA), EE(WHO+PA), or EE(DLW).
Transcriptome analysis for UVB‐induced phototoxicity in mouse retina

Throughout life, the human eye is continuously exposed to sunlight and artificial lighting. Ambient light exposure can lead to visual impairment and transient or permanent blindness. To mimic benign light stress conditions, Mus musculus eyes were exposed to low‐energy UVB radiation, ensuring no severe morphological changes in the retinal structure post‐exposure. We performed RNA‐seq analysis to reveal the early transcriptional changes and key molecular pathways involved before the activation of the canonical cell death pathway. RNA‐seq analysis identified 537 genes that were differentially modulated, out of which 126 were clearly up regulated (>2‐fold, P < .01) and 51 were significantly down regulated (<2‐fold, P < .01) in response to UVB irradiation in the mouse retina. Gene ontology analysis revealed that UVB exposure affected pathways for cellular stress and signaling (eg, Creb3, Ddrgk1, Grin1, Map7, Uqcc2, Uqcrb), regulation of chromatin and gene expression (eg, Chd5, Jarid2, Kat6a, Smarcc2, Sumo1, Zfp84), transcription factors (eg, Asxl2, Atf7, Per1, Phox2a, Rxra), RNA processing, and neuronal genes (eg, B4gal2, Drd1, Grm5, Rnf40, Rnps1, Usp39, Wbp4). The differentially expressed genes from the RNA‐seq analysis were validated by quantitative PCR. Both analyses yielded similar gene expression patterns. The genes and pathways identified here improve the understanding of early transcriptional responses to UVB irradiation. They may also help in elucidating the genes responsible for the inherent susceptibility of humans to UVB‐induced retinal diseases.
Breakfast glycemic index affects subsequent daily energy intake in free-living healthy children.

BACKGROUND Experimental studies have reported that the effect of a meal's glycemic index (GI) on subsequent energy intake depends on the timing of the subsequent meal. OBJECTIVE We examined whether the timing of the next meal after breakfast modifies the effect of the breakfast GI (GI(br)) on subsequent daytime energy intake of healthy free-living children. DESIGN Analyses included 381 participants of the DOrtmund Nutritional and Anthropometrical Longitudinally Designed (DONALD) Study who had provided weighed dietary records at ages 2, 4-5, and 7 y. RESULTS At all ages, among children who consumed their next meal in the early postprandial phase (after 3-4 h), children with a lower GI(br) consumed more calories throughout the remainder of the day than did children with a higher GI(br), independent of major dietary confounders. For the age groups 2, 4-5, and 7 y, energy intakes in tertiles 1 and 3 were 785 kcal (95% CI: 743-830 kcal) and 717 kcal (678-758 kcal), P for trend = 0.2; 993 kcal (941-1047 kcal) and 949 kcal (900-1000 kcal), P for trend = 0.05; 1255 (1171-1344) and 1166 (1090-1247 kcal), P for trend = 0.03, respectively. Conversely, among children consuming their next meal in the late postprandial phase (>3-4 h), subsequent daytime energy intake was not associated with GI(br). CONCLUSION This study confirms differential early and late postprandial effects of the GI(br) on subsequent daytime energy intake for free-living children at different ages. Interestingly, the apparent short-term satiating effect of a higher GI(br), in particular, persisted throughout the day, if a second breakfast was consumed midmorning.
Choline supplemented as phosphatidylcholine decreases fasting and postmethionine-loading plasma homocysteine concentrations in healthy men.

BACKGROUND A high homocysteine concentration is a potential risk factor for cardiovascular disease that can be reduced through betaine supplementation. Choline is the precursor for betaine, but the effects of choline supplementation on plasma total homocysteine (tHcy) concentrations in healthy humans are unknown. OBJECTIVE The objective was to investigate whether supplementation with phosphatidylcholine, the form in which choline occurs in foods, reduces fasting and postmethionine-loading concentrations of plasma tHcy in healthy men with mildly elevated plasma tHcy concentrations. DESIGN In a crossover study, 26 men ingested approximately 2.6 g choline/d (as phosphatidylcholine) or a placebo oil mixture for 2 wk in random order. Fatty acid composition and fat content were similar for both treatments. A methionine-loading test was performed on the first and last days of each supplementation period. RESULTS Phosphatidylcholine supplementation for 2 wk decreased mean fasting plasma tHcy by 18% (-3.0 micromol/L; 95% CI: -3.9, -2.1 micromol/L). On the first day of supplementation, a single dose of phosphatidylcholine containing 1.5 g choline reduced the postmethionine-loading increase in tHcy by 15% (-4.8 micromol/L; 95% CI: -6.8, -2.8 micromol/L). Phosphatidylcholine supplementation for 2 wk reduced the postmethionine-loading increase in tHcy by 29% (-9.2 micromol/L; 95% CI: -11.3, -7.2 micromol/L). All changes were relative to placebo. CONCLUSIONS A high daily dose of choline, supplemented as phosphatidylcholine, lowers fasting as well as postmethionine-loading plasma tHcy concentrations in healthy men with mildly elevated tHcy concentrations. If high homocysteine concentrations indeed cause cardiovascular disease, choline intake may reduce cardiovascular disease risk in humans.
Hyperthermia enhances cytomegalovirus regulation of HIV-1 and TNF-α gene expression.

The immediate-early (IE) genes of human cytomegalovirus (CMV) can be expressed in monocytic cells and are known to regulate viral and cellular genes. Reactivation of human immunodeficiency virus (HIV-1) may be stimulated by a variety of factors including other viruses and inflammatory cytokines. These studies examine the role of hyperthermia and CMV in the regulation of HIV-1 and tumor necrosis factor (TNF)-α. THP-1 cells were transfected with the CMV IE genes. HIV-1 and TNF-α transcription were assessed with chloramphenicol acetyltransferase promoter constructs. Hyperthermia sufficient to stimulate production of heat shock proteins was used to stimulate the cells. Hyperthermia significantly enhances the effect of CMV IE gene products on the expression of HIV-1 and TNF-α. The increases in HIV-1 transcription appear to be in part due to increases in TNF-α. Heat shock proteins induced by hyperthermia may play an important role in the viral regulation of monocytic function by CMV.
Methodologic considerations in the measurement of glycemic index: glycemic response to rye bread, oatmeal porridge, and mashed potato.

BACKGROUND Methodologic choices affect measures of the glycemic index (GI). The effects on GI values of blood sampling site, reference food type, and the number of repeat tests have been insufficiently determined. OBJECTIVE The objective was to study the effect of methodologic choices on GI values. Comparisons were made between venous and capillary blood sampling and between glucose and white bread as the reference food. The number of tests needed for the reference food was assessed. Rye bread, oatmeal porridge, and instant mashed potato were used as the test foods. DESIGN Twelve healthy volunteers were served each test food once and both reference foods 3 times at 1-wk intervals in a random order after they had fasted overnight. Capillary and venous blood samples were drawn at intervals for 3 h after each study meal. RESULTS GIs and their CVs based on capillary samples were lower than those based on venous samples. Two tests of glucose solution as the reference provided stable capillary GIs for the test foods. The capillary GIs did not differ significantly when white bread was used as the reference 1, 2, or 3 times, but the variation was lower when tests were performed 2 and 3 times. Capillary GIs with white bread as the reference were 1.3 times as high as those with glucose as the reference. The capillary GIs of rye bread, oatmeal porridge, and mashed potato were 77, 74, and 80, respectively, with glucose as the reference. CONCLUSIONS Capillary blood sampling should be used in the measurement of GI, and reference tests with glucose or white bread should be performed at least twice.
The rat Pkd2 protein assumes distinct subcellular distributions in different organs.

Mutations in the PKD2 gene account for ∼15% of all cases of autosomal-dominant polycystic kidney disease. In the present study the cellular distribution of the Pkd2 protein was investigated by immunohistochemistry in different rat organs. Although the Pkd2 protein showed a widespread expression, a strikingly different distribution of the protein was observed between individual organs. Whereas in renal distal tubules and in striated ducts of salivary glands a basal-to-basolateral distribution of Pkd2 was found, a punctate cytoplasmic location was detected in the adrenal gland, ovary, cornea, and smooth muscle cells of blood vessels. Interestingly, in the adrenal gland and ovary, the rat Pkd2 protein was more heavily N-glycosylated than in the kidney and salivary gland. These results suggest that Pkd2 accomplishes its functions by interacting with proteins located in different cellular compartments. The extrarenal expression pattern of the Pkd2 protein hints at other candidate sites of disease manifestations in patients carrying PKD2 mutations.