I hope you've all having a good holiday! I sure am. My sisters and I and my nephew came to San Antonio for the holidays. We will be here till January 3rd. So glad we came. The weather has not been so great but it is supposed to warm up this week. I don't get back to work till the 9th so at least I will have a few days to relax in Chicago.
I have been a good girl this year so I decided to treat myself to some running shoes. I already own a pair of Pure Cadence which I love so I bought Green Silence and Ravenna.
I LOVE the colors of the Green Silence. I also love that they're so lightweight (about 6.4 oz).
The Ravenna feels so comfortable!
I cannot wait to run in these shoes. So did you get something for yourself for the holidays?


text:
This article is about a fictional character from a story. Faust is also the name of a German krautrock band, Faust (band), and the name of a character in the Guilty Gear fighting game series, Faust (Guilty Gear).
Faust is the protagonist of a popular German tale that has been used as the basis for many different fictional works. The story concerns the fate of a learned gentleman named Faust, who in his quest for forbidden or advanced knowledge of material things, summons the Devil (represented by Mephistopheles), offering to sell him his soul if the Devil will serve him for a period of time.
An anonymous German author wrote the prose volume (chapbook) Historia von D. Iohan Fausten in 1587, which was translated by P. F. Gent[leman] in 1592 as The Historie of the damnable life, and deserved death of Doctor Iohn Faustus. This work was the basis for Christopher Marlowe's Doctor Faustus (pub. c. 1600) which in turn inspired the later Faust by Johann Wolfgang von Goethe, which may be considered the more definitive classical work.
1 Historical origins
2 Works which retell or allude to the Faust tale
2.2 Opera
2.4 Poetry
2.5 Prose fiction
2.6 Movies
2.7 Musicals
2.8 Anime and manga
2.9 Comic books
2.10 Nonfiction
2.11 Pen name
Historical origins
The tale has some possible basis in a Dr. Johann Georg Faust (approximately 1480-1540), who was born in the village of Knittlingen, W�rttemberg, and granted a B.A. in divinity from Heidelberg University in 1509. This identity is not definite, and it may simply be that the name of "Faust" bears attached any number of legendary tales about a charlatan alchemist (some claim "astrologer and necromancer"), whose pride, vanity, and vile hucksterism would inevitably lead to his doom. "Faust's" poor reputation became historical when while in prison, in exchange for wine he "offered to show a chaplain how to remove hair from his face without a razor; the chaplain provided the wine and Faustus provided the chaplain with a salve of arsenic, which removed not only the hair but the flesh." (Barnett) Another very possible inspiration for Marlowe's Doctor Faustus is John Dee (1527-1609), who practised forms of alchemy and science and developed Enochian magic.
Marlowe's Doctor Faustus appears to have been based almost entirely on the P.F. Gent translation, with an additional borrowing from Acts and Monuments by John Foxe, in the exchanges between Pope Adrian and a rival pope.
The story of Theophilus of Adana, a saint who made a deal with the devil, predates the Faust legend and is a likely partial inspiration.
Works which retell or allude to the Faust tale
Anonymous - Historia von D. Iohan Fausten (1587)
Christopher Marlowe's The Tragical History of Doctor Faustus (1604~1610)
Dorothy L. Sayers's The Devil to Pay
Johann Wolfgang von Goethe's Faust, Part One
Johann Wolfgang von Goethe's Faust, Part Two
Gertrude Stein's's Doctor Faustus Lights the Lights
Michel Carre's Faust et Marguerite
Mark Ravenhill's Faust is Dead
Arrigo Boito's Mefistofele (1868)
Havergal Brian's Faust
Ferruccio Busoni's Doktor Faust (1916-25)
D'Herv�'s Le Petit Faust
Charles Gounod's Faust (1859)
Sergei Prokofiev's opera based on Bryusov's The Fiery Angel
Ludwig Spohr's Faust
Heinrich Zoellner's Faust`
Alfred Schnittke's Historia von D. Johann Fausten
The third movement of Charles-Valentin Alkan's Grande Sonate (published 1848)
Hector Berlioz's The Damnation of Faust (1845-46) (sometimes performed in staged opera versions)
Ludwig van Beethoven's Opus 75 no 3 (1809) Song - Aus Goethes Faust: "Es war einmal ein K�nig"
Charles Gounod's Ballet music from his opera Faust (1859). The ballet occurs as an interlude in the Fourth Act during the Walpurgis Night scene familiar from Goethe's Faust Part 1. The ballet or ballet music is often performed independent of the opera.
Franz Liszt's A Faust Symphony (1854-57)
Gustav Mahler's Symphony No. 8 (1906-07)
Modest Mussorgsky: "Mephistopheles' song of the flea", is just that: a version of the song that Mephistopheles sings in the tavern scene of Goethe's Faust, pt. 1.
Alfred Schnittke's cantata Faust (1982-83)
Franz Schubert's Gretchen am Spinnrade (1814)
Robert Schumann's Scenes from Goethe's Faust (completed 1853)
Richard Wagner's Faust overture (1840, originally intended as the first movement of a Faust symphony)
Art Zoyd's song "Faust"
Avantgarde/progressive black metal band Arcturus's album, La Masquerade Infernale (1997) alludes to the tale and is dedicated to the "Faustian spirit."
Melodic power metal band Kamelot's albums, Epica (2003) and The Black Halo (2005) are loosely based on Faust.
Brian DePalma's Phantom of the Paradise (both the plot of the movie and a musical incorporated into the movie, titled "Foster", are based on the legend of Faust).
Heinrich Heine's "Der Doktor Faust"
Carol Ann Duffy's "Mrs Faust"
Prose fiction
Mikhail Bulgakov's The Master and Margarita
Adelbert von Chamisso's Peter Schlemihl's Remarkable Story (Peter Schlemihls wundersame Geschichte, 1814)
Tom Holt's Faust Among Equals
Alfred Jarry's Faustroll
Thomas Mann's Doktor Faustus
Charles Maturin's Melmoth the Wanderer
Terry Pratchett's Faust Eric
Michael Swanwick's Jack Faust
Ivan Turgenev's Faust
Douglass Wallop's The Year the Yankees Lost the Pennant
Zoran Živković's Time-gifts
Valery Bryusov's The Fiery Angel: the tavern scene from Goethe's Faust, Part 1, is spliced into the rest of Bryusov's storyline.
Ed Kleiman's "North End Faust"
Joseph Conrad's "Heart of Darkness"
F. W. Murnau's Faust (1926)
The Band Wagon
Peter Cook and Dudley Moores Bedazzled (1967), remade in 2000.
Brian De Palma's Phantom of the Paradise (1974)
Jan Svankmajer's Faust (1994 film) (1994)
I Was A Teenage Faust
�lex Oll�'s Fausto 5.0
Istv�n Szab�'s Mephisto (1981 film)
Stephen King's Needful Things (1993)
Randy Newman's Faust
Damn Yankees
Shaman King (A character in Shaman King, Faust VIII, is a descendant of Dr. Faust)
Guilty Gear X (A character in the manga-fighting-video-game Guilty Gear X, also in Guilty Gear XX )
Saber Marionette (The antagonistic ruler of the kingdom of Gartlant in Saber Marionette J)
The comic book Faust was published in the 80s and 90s by artist Tim Vigil and writer David Quinn. The book follows a story template similar to the opera Faust, but is an updated version. Rebel Studios, and independent label originally published it, but it was later picked up by Avatar Press and a subsequent sequel series was created. Both are extremely sexual and violent series.
Felix Faust is a magical supervillain in the universe of DC Comics. He appeared first in 1962 as an adversary of the Justice League of America.
Bertrand Russell's essay "A Free Man's Worship"
Pen name
"Minister Faust" is a pen name for Canadian writer, broadcaster and activist Malcolm Azania; as Minister Faust, he wrote the science fiction novel and social satire The Coyote Kings of the Space-Age Bachelor Pad.
Walpurgis Night
The Brocken a.k.a. Blocksberg
Brocken specter
Doctor Faustus by Christopher Marlowe, Edited and with and introduction by Sylvan Barnett (1969, Signet Classics)
Template:Wikiquote
Devilish Deeds in Staufen (http://www.internationalliving.com/postcards.cfm?pcard=2379)
Pacts with the Devil: Faust and Precursors (http://www.usao.edu/~facshaferi/FAUST.HTML)
E-texts:
Template:Gutenberg
At Projekt Gutenberg-DE:
Goethe's Faust, part 1 (http://gutenberg.spiegel.de/goethe/faust1/faust_to.htm)
Goethe's Faust, part 2 (http://gutenberg.spiegel.de/goethe/faust2/faust2.htm)
Heine's Der Doktor Faust (http://gutenberg.spiegel.de/heine/fstheine/fstheine.htm)
Marlowe's Dr. Faustus (http://www.perseus.tufts.edu/Texts/faustus.html)
Jan Svankmajer's Faust (http://www.illumin.co.uk/svank/films/faust/faust.html)
Faust is also the German word for fist, although the name "Faust" may be related to Italian "Fausto" rather than the German word.
da:Faust de:Johann Faust es:Fausto fr:Faust he:פאוסט lb:Faust nl:Faust ja:ファウスト pl:Faust (motyw w sztuce)
Retrieved from "http://academickids.com/encyclopedia/index.php/Faust"
Categories: Fictional characters | Alchemy
This page was last modified 12:16, 17 Jun 2005.

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text:
Microvascular complications burden (nephropathy, retinopathy and peripheral polyneuropathy) affects risk of major vascular events and all-cause mortality in type 1 diabetes: a 10-year follow-up study
Monia Garofolo1,
Elisa Gualdani2,
Rosa Giannarelli1,
Michele Aragona1,
Fabrizio Campi1,
Daniela Lucchesi1,
Giuseppe Daniele1,
Roberto Miccoli1,
Paolo Francesconi2,
Stefano Del Prato ORCID: orcid.org/0000-0002-5388-02701 &
Giuseppe Penno1
Microvascular complications (MC) have been claimed to increase the risk for cardiovascular disease in diabetic subjects. However, the effect of MC burden on the risk of major vascular outcomes and all-cause mortality in type 1 diabetes is still poorly explored. We evaluated the relationship between microvascular complications burden and incidence of major cardiovascular events and all-cause mortality in subjects with type 1 diabetes.
We recruited 774 participants with type 1 diabetes in a single-center observational study over a follow-up of 10.8 ± 2.5 years. Hazard ratios (HR) for cardiovascular outcomes and all-cause death associated with microvascular complications were determined by unadjusted and adjusted Cox regression analysis.
Out of 774 individuals, 54.9% had no-MC, 32.3% 1 MC, 9.7% 2 MC and 3.1% 3 MC. A total of 54 deaths (7.0%) occurred. Death rate increased from no-MC 2.1% (Ref) to 1 MC 7.2% (HR 3.54 [95% CI 1.59–7.87]), 2 MC 14.7% (HR 6.41 [95% CI 2.65–15.49]) and 3 MC 66.7% (HR 41.73 [95% CI 18.42–94.57], p < 0.0001). After adjustments, HRs were: 1 MC 2.05 (95% CI 0.88–4.76), 2 MC 1.98 (95% CI 0.75–5.21), 3 MC 7.02 (95% CI 2.44–20.20, p = 0.002). Forty-nine subjects (6.7%) had at least one cardiovascular event, and cumulative incidence went from no-MC 2.2% (Ref) to 1 MC 5.0%; (HR 2.27 [95% CI 0.96–5.38]), 2 MC 26.8% (HR 12.88 [95% CI 5.82–28.50]) and 3 MC 40.9% (HR 29.34 [95% CI 11.59–74.25], p < 0.0001). Upon adjustments, HRs were: 1 MC 1.59 (95% CI 0.65–3.88), 2 MC 4.33 (95% CI 1.75–10.74), 3 MC 9.31 (95% CI 3.18–27.25, p < 0.0001). Thirty-five individuals (4.8%) had at least one coronary event, which cumulative incidence increased with MC burden (p < 0.0001).
In type 1 diabetes, microvascular complications burden increases in an independent dose-dependent manner the risk of major cardiovascular outcomes and all-cause mortality. The presence and number of microvascular complications should be considered in stratifying overall cardiovascular risk in type 1 diabetes.
In spite of recent reports suggesting reduction of mortality rate among subjects with type 1 diabetes [1], mortality still remains higher compared to the general population [1] as recently reported in North America [2, 3], Europe [4,5,6] and Australia [7]. Petrie et al. reported that Swedish individuals with type 1 diabetes have a life expectancy (LE) gap at age 20 of about 10–12 years compared with the general population [6]. Consistently, Huo et al. show that, at birth, Australian subjects with type 1 diabetes have an estimated LE loss of 12.2 years compared with those without diabetes [7].
This excess risk persists even if all cardiovascular (CV) risk factors are properly controlled [8]. In particular it has been calculated that the risk of all-cause as well as cardiovascular death in type 1 diabetic subjects with good glycaemic control remains twice as much the risks in the general population [9].
These findings highlight the need to improve risk stratification among type 1 diabetic subjects in the attempt to identify those with very high risk. To this purpose, risk prediction models based on easily accessible patient's clinical characteristics have been proposed [10, 11].
Epidemiological studies suggest that the presence of microvascular complications can increase the risk of CV disease and overall mortality in type 1 diabetes [12, 13]. In the Joslin 50-year Medalist Study and in the Finnish Diabetic Nephropathy Study (FinnDiane) the coexistence of proliferative diabetic retinopathy (PDR) and stage ≥ 3b diabetic kidney disease (DKD) was associated with higher prevalence of CV disease in patients with long-standing type 1 diabetes [14]. Nonetheless, till recently [15], cross-sectional [14, 16] and prospective data [17] assessing the impact of cumulative microvascular disease burden on CV disease and overall mortality in type 1 diabetes have been scanty.
Therefore, we have investigated to which extent the cumulative burden of retinopathy, nephropathy, and peripheral neuropathy is associated with the incidence of all-cause mortality, major CV disease and coronary heart disease (CHD) irrespective of conventional CV risk factors in individuals with type 1 diabetes. Our hypothesis is that the increasing microvascular complication burden, i.e. the number of microvascular complications, can increase the risk of all-cause mortality and incidence of CV events, being the highest in those with complications in all three microvascular beds.
This is an observational, cross-sectional, single-centre study with baseline CV risk stratification and prospective assessment of all-cause mortality and major vascular outcomes in a cohort of individuals with type 1 diabetes. The research design and study population have been previously described [18]. All subjects (n = 843) attending the Diabetes Outpatient Clinic of the Azienda Ospedaliero-Universitaria Pisana from January 1, 2001 to December 31, 2009 for their usual screening for diabetic complications were considered eligible. Type 1 diabetes was diagnosed on the basis of age at diagnosis < 36 years, immediate requirement of insulin therapy and unbroken need for insulin therapy for the first year after diagnosis [19]. Pregnant women, participants of not-white ethnicity, those with diabetes duration < 1 year, those on dialysis or with renal transplantation, and three individuals for whom valid information on vital status could not be retrieved were excluded. Finally, a total of 774 individuals (52.6% men; age 40.2 ± 11.7 years; duration of diabetes 19.4 ± 12.2 years, mean ± SD) entered the study. The Ethics Committee of the University of Pisa approved the study protocol, consent procedures, and data analysis plan.
Information about onset and duration of diabetes (DD), smoking habits, insulin therapy, and blood pressure- and lipid-lowering therapies were collected for all subjects along with body mass index (BMI), waist-to-hip ratio (WHR), and resting blood pressure (BP). Hypertension was defined as systolic BP > 140 mmHg and/or diastolic BP > 80 mmHg and/or use of antihypertensive medications.
Serum creatinine, glycated haemoglobin (HbA1c), total- and HDL-cholesterol, triacylglycerol, alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), uric acid and fibrinogen were determined in all subjects at the time of first screening for diabetic complications.
Albumin-to-creatinine ratio (ACR) was determined in at least three first-voided urine samples obtained with at least 1-month interval in the year preceding the recruitment. Urine samples (n = 175, 6.7%) with abnormal sediment (nitrites or ≥ 250 leucocytes/ml) were discarded. All other samples were assayed for albumin (BNII; Dade Behring Diagnostic, Marburg, Germany; intra- and inter-assay variation < 2.0% and < 3.5%, respectively) and creatinine (modified Jaffé reaction) on the same morning of collection.
HbA1c was measured by high-performance liquid chromatography using DCCT-aligned methods [20]; triacylglycerol, total- and HDL-cholesterol were determined by colorimetric enzymatic methods, and LDL-cholesterol was calculated by the Friedewald formula [21]. Standard clinical laboratory methods have been employed for the measurement of serum creatinine, ALT, AST, GGT, uric acid and fibrinogen.
Assessment of diabetes complications
Diabetic kidney disease was established based on the geometric mean of three ACR values, and estimated glomerular filtration rate (eGFR) was calculated by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation [22]. DKD was diagnosed on the basis of ACR > 3.4 mg/mmol [23] and/or eGFR < 60 mL/min/1.73 m2 [24].
The presence and severity of diabetic retinopathy (DR) was assessed by retinal photography using a wide-angle (45°) midriatic camera. Photos of disc-macula-temporal and disc-nasal regions were taken [25] and the eye with worse retinal condition including previous photocoagulation or surgical treatment, was used for retinopathy staging: absent, mild, moderate or severe non-proliferative, proliferative diabetic retinopathy, or maculopathy, according to the Global Diabetic Retinopathy Project Group criteria [26]. For further analysis, individuals with non-proliferative retinopathy of mild or moderate degree were classified as non-advanced diabetic retinopathy, whereas those with severe non-proliferative, proliferative, maculopathy, or blindness were grouped into the advanced, sight-threatening diabetic retinopathy category.
Diabetic peripheral neuropathy was defined on the presence of symptoms and signs assessed by the Michigan Neuropathy Screening Instrument questionnaire designed to identify symptoms of muscle weakness and sensory dysfunction [19, 27], by the examination of the feet for neuropathic ulcerations, by reduced or absent knee and ankle reflexes, and/or by measurement of vibration perception threshold using a biothesiometer applied bilaterally at the medial malleolus and the tip of the big toe [19, 27]. The mean of three readings at 10 s intervals on each site was calculated and interpreted according to age-specific reference values [28].
Presence of previous CV disease was ascertained on the basis of medical history of any major acute CV events, i.e. myocardial infarction, stroke, ischemic foot ulcer or gangrene, amputation and coronary, carotid, and/or lower limb revascularization. A 12 lead resting ECG was recorded and coded according to the Minnesota Code [29]. Peripheral vascular disease was defined on a positive history of ischemic ulceration, gangrene, amputation or lower limb revascularization, or diagnosed on the presence of reduced or absent femoral and/or foot pulses and reduced ankle/brachial pressure ratio (< 0.9).
Calculation of the EURODIAB PCS risk score
The EURODIAB Prospective Complications Study (PCS) risk score was calculated as proposed by Soedamah-Muthu et al. [10]. The score calculates risk for major outcomes (CHD, stroke, end stage renal disease, amputation, blindness) and all-cause death in type 1 diabetes on the basis of age, HbA1c, WHR, ACR, and HDL levels allowing risk stratification as low (LS, ≤ 15), intermediate (IS, 16 to 19) and high score (HS, ≥ 20).
Assessment of outcomes
The primary outcome was the time to all-cause mortality. Follow-up data for each patients were verified up to December 31, 2017. Vital status was available for all participants and was verified over a mean follow-up of 10.8 ± 2.5 years (median 10.2, IQR 9.2–12.3) by interrogation of the Italian Health Card Database (http://sistemats1.sanita.finanze.it/wps/portal/). The secondary outcomes were the time to first major CV event (i.e. occurrence of first event of myocardial infarction, coronary revascularization, stroke, carotid revascularization, and ulcer, gangrene, amputation and peripheral revascularization) and the time to first coronary event (i.e. occurrence of first event of myocardial infarction or coronary revascularization). Data for major CV and coronary events were available for 736 participants (95.1%), and were obtained, upon data anonymization (in compliance with current privacy legislation), in collaboration with ARS Toscana (Regional Health Agency of the Tuscany Region) through hospital discharge registers. ICD-9-CM codes (International Classification of Diseases, 9th Edition, Clinical Modification) was used to detect major CV and coronary artery events (Additional file 1: Table S1). All events (for primary and secondary outcomes) occurring between date of enrollment and end of follow-up or death were considered as incident.
Data are expressed as median (interquartile range, IQR) and/or mean ± SD for continuous variables, and number of cases and percentage for categorical variables. Continuous variables were compared by the Student's t-test or one-way ANOVA (Welch robust test for equality of means when appropriate based on the Levene statistic) for normally distributed variables. Wilcoxon Sum-of-Ranks (Mann–Whitney) U test or Kruskal–Wallis tests were used for variables with skewed distribution. Pearson χ2 or the Fisher exact tests were applied to categories. The Spearman's rank-order correlation was run to measure strength and direction of associations between two variables measured on ordinal scale. For post hoc comparisons, Scheffe's test or Tamhane's test, Mann–Whitney U test and χ2 test were used for normally distributed, not-normally distributed, and categorical variables, respectively.
Crude mortality rates and incidence of outcomes were described as events per 1000 person-years (PYs), with 95% exact Poisson Confidence Intervals (CI). Time to all-cause death or to each first outcome was plotted according to the MC groups as Kaplan–Meier (K–M) curves, and comparison was made using the log rank test. Univariate and multivariate Cox proportional hazard models were used to identify the effect of key covariates such as sex and age (model 1), or sex, age and cardiovascular risk factors (model 2), and sex, cardiovascular risk factors and the EURODIAB PCS risk score (model 3). Results are expressed as Hazard Ratio (HR) and 95% CI. Analyses have been performed in the whole cohort as well as in subjects free of CV disease at baseline (CVD−). A two-sided p value ≤ 0.05 was considered statistically significant.
A post hoc power calculation has been performed to evaluate the statistical power of our sample size for the primary outcome, i.e. all-cause mortality. Compared to the reference group (subject without MC), our groups of subjects with 1, 2 and 3 MC have a post hoc power of 87.5%, 97% and 100%, respectively, to detect the observed differences in mortality rate with an alpha error level of 5%.
All statistical analyses were performed using SPSS package 25.0 version (IBM SPSS, Chicago, IL).
We recruited 774 individuals with type 1 diabetes who have been followed up to a mean of 10.8 ± 2.5 years equivalent to 8387 PYs follow-up. At screening, 425 participants (54.9%) had no-MC, 250 (32.3%) had 1 MC, 75 (9.7%) 2 MC, and 24 (3.1%) 3 MC (Additional file 1: Figure S1). Distribution was unchanged (n = 418, 57.0%; n = 236, 32.2%; n = 62, 8.5% and n = 17, 2.3%, respectively; p = 0.620) upon exclusion of 41 subjects (5.3%) with prior CV events (CVD+).
Table 1 and Additional file 1: Table S2 show the baseline characteristics of the whole cohort. Overall the presence and severity of MC were associated with age, diabetes duration, BMI and WHR, HbA1c, systolic and diastolic BP, prevalence of hypertension, and rates of treatment with BP-lowering agents and renin-angiotensin system (RAS) blockers. On the contrary, there was no difference in gender distribution, smoking history, HDL-cholesterol, and triacylglycerol. Total- and LDL-cholesterol tended to be lower in individuals with 3 MC, most likely because of more common use of lipid-lowering therapy. MC burden was also associated with increasing levels of non-conventional risk factors such as uric acid and fibrinogen, lower eGFR and higher ACR (p < 0.0001 for all). Finally, the rate of previous CV events and prevalence of high-risk EURODIAB PCS score (≥ 20) also increased with MC (p < 0.0001 for both).
Table 1 Baseline characteristics of the study cohort, both overall and according to microvascular complications burden
Microvascular complications and all-cause mortality in the whole cohort
During study follow-up 54 individuals (7.0%; 6.44 × 1000 PYs) died. Mortality increased with MC (p < 0.0001) going from 2.1% in subjects with no-MC (n = 9; 1.92 × 1000 PYs; Ref), to 7.2% in those with 1 MC (n = 18; 6.76 × 1000 PYs; HR 3.54 [95% CI 1.59–7.87]), 14.7% in those with 2 MC (n = 11; 12.93 × 1000 PYs; HR 6.41 [95% CI 2.65–15.49]), and 66.7% in individuals with 3 MC (n = 16; 79.77 × 1000 PYs; HR 41.73 [95% CI 18.42–94.57]; Fig. 1a). After adjustment for confounders (Fig. 2, Models 1 to 3), the HRs for primary outcome remained significant with the risk being the highest in those with 3 MC. In particular, in Model 3, HRs for death went from 2.05 in 1 MC (95% CI 0.88–4.76), to 1.98 (95% CI 0.75–5.21) in 2 MC, and 7.02 (95% CI 2.44–20.20, p = 0.002) in 3 MC, with independent effects for active smoking, triacylglycerol, uric acid and intermediate- (HR 3.08 [95% CI 1.25–7.56]) and high-risk EURODIAB PCS score (HR 8.59 [95% CI 3.40–21.71], p < 0.0001).
Kaplan–Meier curves for all-cause death and cumulative incidences of major vascular and coronary events by MC. no-MC: dotted green line, 1 MC: dashed blue line, 2 MC: dashdotted violet line, 3 MC: solid red line. Percentages of events and Cox proportional unadjusted HRs (95% CI) are shown for each MC group. a Survival from all-cause death: K–M Logrank 187.35, p < 0.0001. Pairwise over strata logrank statistic provides the following results: 1 MC vs. no-MC, logrank 10.96 (p = 0.0009); 2 MC vs. no-MC, logrank 22.77 (p < 0.0001); furthermore, 3 MC vs. no-MC, logrank 223.18, vs. 1 MC, logrank 78.94 and vs. 2 MC, logrank 30.62 (p < 0.0001, for all). b Cumulative incidence of major vascular events: K–M Logrank 127.61, p < 0.0001. Pairwise over strata logrank statistic provides the following results: 1 MC vs. no-MC, logrank 3.71 (p = 0.054); 2 MC vs. no-MC, logrank 67.22 and vs. 1 MC, logrank 28.49 (p < 0.0001, for both); furthermore, 3 MC vs. no-MC, logrank 110.38, vs. 1 MC, logrank 57.81 (p < 0.0001, for both) and vs. 2 MC, logrank 4.15 (p = 0.042). c Cumulative incidence of coronary events: K–M Logrank 81.47, p < 0.0001. Pairwise over strata logrank statistic provides the following results: 2 MC vs. no-MC, logrank 40.60 and vs. 1 MC, logrank 26.17 (p < 0.0001, for both); 3 MC vs. no-MC, logrank 55.23, vs. 1 MC, logrank 44.18 (p < 0.0001, for both)
Adjusted HR for all-cause mortality by MC in the whole cohort. Model 1: adjusted for age and sex. Model 2: adjusted for age, sex, smoking habits, age at diagnosis of diabetes ≤ 18 years (n = 342; 44.2%), diabetes duration, BMI, HbA1c, LDL-cholesterol, HDL-cholesterol, triglycerides, uric acid, fibrinogen, hypertension and prior CV events. Model 3: adjusted for sex, smoking habits, age at diagnosis of diabetes ≤ 18 years, diabetes duration, LDL-cholesterol, triglycerides, uric acid, fibrinogen, hypertension, previous CV events and EURODIAB PCS risk score categories
Microvascular complications and all-cause mortality in subjects free of CV disease at baseline (CVD−)
Death rate increased with MC also in CVD− (n = 733; p < 0.0001). At follow-up 43 subjects (5.9%) died: 2.2% in no-MC (n = 9; 1.95 × 1000 PYs), 6.4% in 1 MC (n = 15; 5.95 × 1000 PYs), 12.9% in 2 MC (n = 8; 11.30 × 1000 PYs), and 64.7% in 3 MC (n = 11; 72.00 × 1000 PYs; Additional file 1: Figure S2). In CVD−, after adjustments (Fig. 3, Models 1 to 3), the effects of MC on all-cause mortality remained significant up to Model 3, where the HR for 3 MC was 5.46 (95% CI 1.67–17.86, p = 0.005) independently of uric acid and the EURODIAB PCS score.
Adjusted HR for all-cause mortality by MC in CVD−. Model 1: adjusted for age and sex. Model 2: adjusted for age, sex, smoking habits, age at diagnosis of diabetes ≤ 18 years (n = 324; 44.2%), diabetes duration, BMI, HbA1c, LDL-cholesterol, HDL-cholesterol, triglycerides, uric acid, fibrinogen, hypertension and prior CV events. Model 3: adjusted for sex, smoking habits, age at diagnosis of diabetes ≤ 18 years, diabetes duration, LDL-cholesterol, triglycerides, uric acid, fibrinogen, hypertension, previous CV events and EURODIAB PCS risk score categories
Microvascular complications and incidence of major cardiovascular and coronary events in the whole cohort
Major CV events occurred in 49 out of 736 subjects (6.7%; 6.42 × 1000 PYs) during a mean follow-up of 10.4 ± 2.9 years. Incidence of major CV events increased with MC (p < 0.0001): no-MC 2.2% (n = 9; 2.09 × 1000 PYs; Ref), 1 MC 5.0% (n = 12; 4.79 × 1000 PYs; HR 2.27 [95% CI 0.96–5.38]), 2 MC 26.8% (n = 19; 27.56 × 1000 PYs; HR 12.88 [95% CI 5.82–28.50]), 3 MC 40.9% (n = 9; 63.82 × 1000 PYs; HR 29.34 [95% CI 11.59–74.25]; Fig. 1b). In adjusted Cox regression analysis (Fig. 4a, Models 1 to 3), the risk for major CV events, compared to no-MC, increased in subjects with 2 MC and more so in those with 3 MC. In particular, in Model 3, HRs were: 1 MC 1.59 (95% CI 0.65–3.88), 2 MC 4.33 (95% CI 1.75–10.74), 3 MC 9.31 (95% CI 3.18–27.25, p < 0.0001) with independent effects for fibrinogen, hypertension, and prior CV events.
Adjusted HR for major vascular (a) and coronary events (b) by MC in the whole cohort. Model 1: adjusted for age and sex. Model 2: adjusted for age, sex, smoking habits, age at diagnosis of diabetes ≤ 18 years (n = 322, 43.8%), diabetes duration, BMI, HbA1c, LDL-cholesterol, HDL-cholesterol, triglycerides, uric acid, fibrinogen, hypertension and prior CV events. Model 3: adjusted for sex, smoking habits, age at diagnosis of diabetes ≤ 18 years, diabetes duration, LDL-cholesterol, triglycerides, uric acid, fibrinogen, hypertension, previous CV events and EURODIAB PCS risk score categories
Coronary events occurred in 35 out of 736 subjects (4.8%; 4.54 × 1000 PYs) during a mean follow-up of 10.5 ± 2.7 years with incidence increasing with MC (p < 0.0001): no-MC 2.2% (n = 9; 2.09 × 1000 PYs; Ref), 1 MC 2.5% (n = 6; 2.37 × 1000 PYs; HR 1.12 [95% CI 0.40–3.15]), 2 MC 19.7% (n = 14; 19.62 × 1000 PYs; HR 9.12 [95% CI 3.94–21.10]), 3 MC 27.3% (n = 6; 39.13 × 1000 PYs; HR 18.35 [95% CI 6.51–51.76]; Fig. 1c). In the adjusted Cox regression analysis (Fig. 4b, Models 1 to 3), the risk for coronary events, compared to no-MC, increased in subjects with 2 MC and to a greater extent in those with 3 MC. In particular, in Model 3, HRs were: 1 MC 0.66 (95% CI 0.23–1.95), 2 MC 2.39 (95% CI 0.85–6.69), 3 MC 5.26 (95% CI 1.55–17.85, p = 0.005) with independent effects for uric acid, EURODIAB PCS score and prior CV events.
Microvascular complications and incidence of major cardiovascular and coronary events in CVD−
Among CVD− (n = 697), incidence of major CV events (n = 32, 4.6%) increased with MC (p < 0.0001): 2.0% in no-MC (n = 8; 1.88 × 1000 PYs), 3.9% in 1 MC (n = 9; 3.77 × 1000 PYs), 18.6% in 2 MC (n = 11; 18.50 × 1000 PYs), and 26.7% in 3 MC (n = 4; 32.50 × 1000 PYs; Additional file 1: Figure S3). The effect, though attenuated, remained significant after multiple adjustments up to Model 3, where the HR for 3 MC resulted 8.88 (95% CI 2.44–32.34, p = 0.001; Fig. 5a, Model 1 to 3), with independent effect for hypertension.
Adjusted HR for major vascular (a) and coronary events (b) by MC in CVD−. Model 1: adjusted for age and sex. Model 2: adjusted for age, sex, smoking habits, age at diagnosis of diabetes ≤ 18 years (n = 305, 43.8%), diabetes duration, BMI, HbA1c, LDL-cholesterol, HDL-cholesterol, triglycerides, uric acid, fibrinogen, hypertension and prior CV events. Model 3: adjusted for sex, smoking habits, age at diagnosis of diabetes ≤ 18 years, diabetes duration, LDL-cholesterol, triglycerides, uric acid, fibrinogen, hypertension, previous CV events and EURODIAB PCS risk score categories
Consistently, incidence of coronary events (n = 23, 3.3%) increased with MC (p < 0.0001): 2.0% in no-MC (n = 8; 1.88 × 1000 PYs), 1.8% in 1 MC (n = 4; 1.66 × 1000 PYs), 13.6% in 2 MC (n = 8; 13.24 × 1000 PYs), and 20.0% in 3 MC (n = 3; 23.47 × 1000 PYs; Additional file 1: Figure S4). Once again, the effect remained significant even after multiple adjustments (Fig. 5b, Model 1 to 3).
Retinopathy, mortality and other outcomes
Diabetic retinopathy was the most frequent MC (n = 322; 41.6%); 82 individuals had nephropathy (10.6%) and 68 neuropathy (8.8%). The prevalence of advanced retinopathy increased from individuals with 1 to those with 3 MC (p < 0.0001; Additional file 1: Figure S1).
Mortality was 2.7% (n = 12; 2.41 × 1000 PYs; Ref) in 452 subjects without DR (DR−) and increased to 13.0% (n = 42; 12.36 × 1000 PYs, HR 5.18 [95% CI 2.72–9.83]) in the remaining 322 DR+ individuals (p < 0.0001; Additional file 1: Figure S5A). Adjustment for nephropathy and neuropathy did not reduce the risk for mortality associated with DR+ (HR 2.71 [95% CI 1.35–5.43]; p = 0.005) nor it did adjustment for other potential confounders (Additional file 1: Table S3, Models 1 to 3). In Model 3, death HRs were 2.07 (95% CI 1.02–4.19; p = 0.044) for DR+, and 3.02 (95% CI 1.24–7.36) and 9.65 (95% CI 4.02–23.16), respectively, for intermediate- and high-risk EURODIAB PCS score (p < 0.0001), with an independent role for nephropathy, smoking, and uric acid. Mortality occurred in 9.4% among subjects with non-advanced DR (n = 19 out of 202; 8.91 × 1000 PYs; HR 3.74 [95% CI 1.81–7.70]) versus 19.2% in those with advanced DR (n = 23 out of 120; 18.16 × 1000 PYs; HR 7.60 [95% CI 3.78–15.28]; p < 0.0001; Additional file 1: Figure S5B). HRs remained significant with no difference between non-advanced and advanced DR (2.71 [95% CI 1.30–5.69] and 2.69 [95% CI 1.20–6.05]; p = 0.008 and p = 0.017, respectively) after adjustment for nephropathy and neuropathy. Mortality HRs remained significant for non-advanced DR after adjustment for confounders, with an independent effects for active smoking, uric acid, and EURODIAB PCS score (data not shown).
Cumulative incidence of major CV events was 2.1% (n = 9; 1.97 × 1000 PYs; Ref) among 426 DR− and 12.9% (n = 40; 13.05 × 1000 PYs; HR 6.59 [95% CI 3.20–13.59]) in 310 DR+ (p < 0.0001; Additional file 1: Figure S6A). In this case too, the risk remained significantly higher after adjustment for nephropathy and neuropathy, and several other confounders (Additional file 1: Table S4, Models 1 to 3). In Model 3, HRs for CV events were 2.76 (95% CI 1.25–6.07; p = 0.012) for DR+, and 2.31 (95% CI 0.98–5.41) and 3.71 (95% CI 1.47–9.37) for intermediate- and high-risk EURODIAB PCS score, respectively (p = 0.021), with an independent role for nephropathy and prior CV events. Moreover, the event rate was lower for non-advanced as compared to advanced DR (p < 0.0001; Additional file 1: Figure S6B), even after adjustment for the other MC and confounders (data not shown). A similar trend was observed as far incidence of coronary events (Additional file 1: Figures S7A, B), although in Model 2 and 3 DR did not enter as a covariate of coronary events, while independent roles were played by nephropathy, prior CV disease, uric acid and EURODIAB score (Additional file 1: Table S5, Models 1 to 3).
For each outcome, in all regression models no interaction (p ≥ 0.368 for all, data not shown) has been observed between nephropathy or neuropathy with the presence of retinopathy even if, as anticipated by the low number of individuals with nephropathy or neuropathy free from retinopathy, confidence intervals should, in many cases, interpreted with caution.
We found that in a cohort of 774 subjects with type 1 diabetes, over a more than 10 year follow-up the presence of microvascular disease at study entry was an independent determinant of all-cause mortality and cardiovascular events. Moreover, we found that number and severity of microvascular complications were associated with an increase in the rate of all-cause death, first major cardiovascular and first coronary event. The presence of one or more MC was also associated with worse profile of conventional and non conventional CV risk factors, including a contemporary specific vascular risk score. Yet, even accounting for these variables, MC remained an independent predictor of major outcomes, including all-cause mortality and CV events. These observations were fully confirmed in the 733 individuals free of established CV disease at baseline. Finally, retinopathy, the most frequent MC in our cohort, conferred by itself a higher risk of mortality and CV outcomes irrespective of CV risk profile and of the effect of nephropathy and neuropathy.
The pathophysiologic processes leading to CV disease in type 1 diabetes are complex and largely unidentified. Microvascular beds are the sites where the earliest consequences of inflammatory processes occur, leading to endothelial and smooth muscle cell dysfunction, and altered structure and composition of the extracellular matrix. These modifications are recognized as risk factors for the development of atherosclerotic disease in large arteries as well [30]. Also, a rule in diabetic vascular complications has been suggested for advanced glycation end-products assessed by skin autofluorescence [31, 32], HDL dysfunction [33], and altered regulation of extracellular matrix remodeling [34], both in type 1 and type 2 diabetes. Among microvascular beds, the eye and the kidney are vulnerable target end-organs where functional and structural microvascular alterations anticipate and predict incident CV events [30].
In line with all this, recent cross-sectional studies reported an association between microvascular complications, mainly diabetic retinopathy, and subclinical atherosclerosis in subjects with type 1 diabetes. In a cohort of subjects with type 1 diabetes without previous CV disease or DKD, Carbonell et al. found an independent association between PDR and higher atherosclerotic burden in the carotid arteries [35]. Furthermore, in subjects with long-lasting diabetes (≥ 50 years) Lovshin et al. found that retinopathy and large-nerve fiber neuropathy were associated with presence of higher coronary artery calcification volume score [36].
These observations suggest that involvement of microvascular beds may reflect underlying, as jet unidentified, pathways linked to vascular disease.
An association between microvascular complications and risk of CV disease has been recently reported in type 2 diabetes. A cohort of 49,027 individuals with type 2 diabetes and no history of CV disease at baseline was studied by Brownrigg et al. over a median follow-up of 5.5 years [37]. In this study, the investigators found a dose-dependent relationship between the number of microvascular complications, the overall risk of experiencing a CV event, as well as risk of other endpoints such as all-cause mortality, CV death and hospitalization for heart failure. The same study found that isolated retinopathy, peripheral neuropathy or nephropathy, independent of conventional risk factors, conferred risk of CV events similar to the one associated with blood pressure, HbA1c and LDL-cholesterol. Furthermore, no deviation from linearity was found in subgroups stratified by varying degrees of risk factors control [37].
On the contrary, robust data assessing the effects of microvascular complications on all-cause mortality and CV risk are still lacking in type 1 diabetes [38]. Previous reports have shown an increase in CV risk and mortality in subjects with type 1 diabetes with diabetic kidney disease [9, 12, 39,40,41,42] and peripheral [43] or autonomic neuropathy [43,44,45]. A recent report from FinnDiane showed that in subjects with long-standing type 1 diabetes severe DR, even without DKD, increases the risk of CV disease, in particular for peripheral artery disease, independently of common CV risk factors [46].
We now provide evidence that incidence of all-cause death increases in individuals with type 1 diabetes with one (6.76/1000 PYs), two (12.93/1000 PYs) or three (79.77/1000 PYs) as compared to subjects free of microvessel damage (1.92/1000 PYs). Adjustment for potential confounders attenuated HR for primary outcome across all three groups, but the microvascular burden remained an independent predictor in particular for those individuals with 3 MC. This was also true among those subjects without prior CV events even after correction for the EURODIAB PCS score, a powerful integrated predictor of major outcomes including all-cause mortality. The association is similar, if not stronger, between cumulative burden of MC and major vascular events. Unadjusted rates were 2.09, 4.79, 27.56, and 63.82/1000 PYs for individuals with no-MC and for those with one, two, or three MC, respectively. Again HRs for major vascular outcomes were attenuated across the three groups after adjustment for confounders. A similar pattern was observed for coronary events.
The attenuation of the HRs for each outcome after multiple adjustments confirms the role of conventional CV risk factors. Yet, the persistence of the predictive effect of MC, even after full adjustment (i.e. Model 3), supports the negative impact of existing microvascular complications, which exert an effect similar to the one of active smoking on all-cause mortality (Fig. 2) [47]. Also, the coexistence of two microvascular complications is a stronger predictor for major CV events than hypertension (Fig. 4a) and three MC are associated with coronary events to a greater extent than the EURODIAB PCS score (Fig. 4b).
We found no independent association of baseline HbA1c with mortality, major vascular outcomes or coronary events. Besides the much debated effect of glycaemic control on these outcomes, the present finding should be interpreted with caution as a single baseline HbA1c value is unlikely to capture and predict cumulative exposure to hyperglycemia. Also, one could argue that glycaemic control is well incorporated in the degree of the microvascular bed involvement given the well known relationship between glucose control and development of microvessel damage.
Due to the size of our study population, we could not analyze data according to individual effect of retinopathy, nephropathy or peripheral neuropathy. However, we found that retinopathy, the most common microvascular complication in our cohort, conferred per se an increased risk for all-cause mortality and vascular outcomes, an association that remained valid after adjustment for concomitant nephropathy and peripheral neuropathy as well as adjustment for other confounders.
This particular finding is at variance with the results very recently published by Bjerg et al. [15]. In a larger population of 3828 subjects with type 1 diabetes over a 26,665 PYs follow-up they found that neuropathy and diabetic kidney disease were strong and independent risk factors of mortality with no evidence for an association with retinopathy. Furthermore, on the contrary of the present study, authors found no evidence that multiple complications could increase the risk conferred by each complication separately [15]. A number of reasons could account for these discrepancies, including difference in population size. Since diabetic retinopathy was by far the most common microvascular condition in a smaller population with a longer follow-up, this may have greater chance to show a significant association. Nonetheless, the relative role of microvascular complications on mortality and cardiovascular risk in type 1 diabetes may require more attention. Systematic reviews have recently examined the associations between diabetic retinopathy and common macrovascular complications [48, 49]. The analysis by Pearce et al. included both type 1 and type 2 diabetes and showed that DR was consistently associated with other complications of diabetes. In keeping with our own results, the meta-analysis also reported an association between severity of DR and CV risk. In particular, DR was a strong predictor of stroke, major CV events and peripheral artery disease [48]. In the meta-analysis by Guo et al. DR was associated with increased risk of CV disease (relative risk 2.42 [95% CI 1.77–3.31]); this risk was stronger in type 1 diabetes (relative risk 3.59 [95% CI 1.79–7.20]) [49]. A recent report from FinnDiane found that severe DR, even in the absence of concomitant DKD, increases cardiovascular risk, in particular the risk of peripheral artery disease, independently of common CV risk factors [46]. Moreover, the Joslin Medalist Study showed that the CV risk was greater in subjects with severe DR on top of DKD than in those with DKD alone [14]. In summary, besides the discrepancy with respect to the specific effect of DR, our study and the one by Bjerg et al. [15] support the concept that microvascular complications can contribute in increasing the risk of all-cause and cardiovascular mortality in subjects with type 1 diabetes.
There are a number of limitations of the present study. First, the number of events (54 deaths and 49 major CV events) was limited suggesting some caution should be used in extrapolating from multivariate analysis and its clinical implications. Second, we have no information on the course of microvascular diseases over time; this precluded us to assess the effects of progression or regression of the microvascular involvement on relevant outcomes. For instance, while progression of diabetic nephropathy confers an increased risk for cardiovascular disease and premature death, it has been recently reported that, in type 1 diabetes, regression of albuminuria reduces the risk of cardiovascular events and all-cause and cardiovascular mortality to the same level as for those who did not progress [50]. A similar limitation of the study is the lack of data on time-varying exposure to glycated haemoglobin levels and conventional cardiovascular risk factors during follow-up. Third, data on autonomic neuropathy were not available at baseline. In the Diabetes Control and Complications Trial/Epidemiology of Diabetes Intervention and Complications (DCCT/EDIC) cohort, individuals with cardiovascular autonomic neuropathy at study closeout had higher long-term risk of CV events [45]. A further limitation of our study is that we could not retrieve reliable data about cause of death, including CV death, from the Regional Registry, somewhat limiting the detail of study results. Finally, the results of this study should be interpreted taking into consideration the characteristics of our cohort, with retinopathy being by far the most frequent microvascular complication. Thus, in addition to the co-existence of microvascular complications, also the severity of retinopathy (as an alternative way to assess the degree of microvascular burden) has been associated with each study outcome.
The study, however, also have some strengths, such as the single-centre nature of the study and the relatively long follow-up. Moreover, registry linkage with individuals' unique personal identification codes provides survival information for virtually all participants and 95% coverage for major vascular events. Of relevance, details on retinopathy classification was available for all individuals allowing meaningful sensitivity analyses for advanced and early stages of the condition.
In summary, our data corroborate initial information and more recent publications [15] that the presence and severity of microvascular complications contribute in an independent manner to increase the risk of all-cause mortality and cardiovascular outcomes in individuals with type 1 diabetes. As the assessment of microvascular disease is an essential component of routine clinical care, these findings show how screening and staging for microvascular complications can offer a convenient and unexpensive tool for improving risk prediction in subjects with type 1 diabetes.
Data collected for this study can be shared and made available upon reasonable request to the corresponding author and subject to an approved proposal and data access agreement.
ACR:
albumin-to-creatinine ratio
alanine aminotransferase
AST:
aspartate aminotransferase
CKD-EPI:
chronic kidney disease epidemiology collaboration equation
diabetes duration
DKD:
diabetic kidney disease
DR:
EURODIAB PCS:
EURODIAB Prospective Complications Study
GGT:
gamma-glutamyltransferase
intermediate score
Kaplan–Meier
LE:
LS:
low score
microvascular complication
PDR:
proliferative diabetic retinopathy
PYs:
person-years
WHR:
waist-to-hip ratio
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Mogensen UM, Jensen T, Køber L, Kelbæk H, Mathiesen AS, Dixen U, et al. Cardiovascular autonomic neuropathy and subclinical cardiovascular disease in normoalbuminuric type 1 diabetic patients. Diabetes. 2012;61(7):1822–30.
Pop-Busui R, Braffett BH, Zinman B, Martin C, White NH, Herman WH, et al. DCCT/EDIC Research Group. cardiovascular autonomic neuropathy and cardiovascular outcomes in the diabetes control and complications trial/epidemiology of diabetes interventions and complications (DCCT/EDIC) study. Diabetes Care. 2017;40(1):94–100.
Pongrac Barlovic D, Harjutsalo V, Gordin D, Kallio M, Forsblom C, King G, et al. FinnDiane Study Group. The association of severe diabetic retinopathy with cardiovascular outcomes in long-standing type 1 diabetes: a longitudinal follow-up. Diabetes Care. 2018;41(12):2487–94.
Feodoroff M, Harjutsalo V, Forsblom C, Groop PH, FinnDiane Study Group. Dose-dependent effect of smoking on risk of coronary heart disease, heart failure and stroke in individuals with type 1 diabetes. Diabetologia. 2018;61(12):2580–9.
Pearce I, Simó R, Lövestam-Adrian M, Wong DT, Evans M. Association between diabetic eye disease and other complications of diabetes: implications for care. A systematic review. Diabetes Obes Metab. 2019;21(3):467–78.
Guo VY, Cao B, Wu X, Lee JJW, Zee BC. Prospective association between diabetic retinopathy and cardiovascular disease-a systematic review and meta-analysis of cohort studies. J Stroke Cerebrovasc Dis. 2016;25(7):1688–95.
Jansson FJ, Forsblom C, Harjutsalo V, Thorn LM, Wadén J, Elonen N, et al. FinnDiane Study Group. Regression of albuminuria and its association with incident cardiovascular outcomes and mortality in type 1 diabetes: the FinnDiane Study. Diabetologia. 2018;61(5):1203–11.
We are indebted to all patients attending the Outpatients Diabetic Clinic and to the staff of the "Renzo Navalesi" Diabetes Centre in Pisa, in particular to the Clinical Lab and the Medical Records Unit.
This work was supported by a grant from the Regione Toscana, Italy, Resolution 1157 (December 19, 2011), ID Number D55E11002680005. The funder had no role in the original study design, data collection, data analysis, data interpretation, writing of the manuscript, or decision to submit the report for publication. All authors had full access to all the data of the study, and the corresponding author had final responsibility for the decision to submit for publication.
Section of Diabetes and Metabolic Disease, Department of Clinical and Experimental Medicine, University of Pisa and Azienda Ospedaliero-Universitaria Pisana, Via Paradisa, 2, 56124, Pisa, Italy
Monia Garofolo, Rosa Giannarelli, Michele Aragona, Fabrizio Campi, Daniela Lucchesi, Giuseppe Daniele, Roberto Miccoli, Stefano Del Prato & Giuseppe Penno
Epidemiology Unit, Regional Health Agency (ARS) of Tuscany, Florence, Italy
Elisa Gualdani & Paolo Francesconi
Monia Garofolo
Elisa Gualdani
Rosa Giannarelli
Michele Aragona
Fabrizio Campi
Daniela Lucchesi
Giuseppe Daniele
Roberto Miccoli
Paolo Francesconi
Stefano Del Prato
Giuseppe Penno
MG, GP and SDP designed the study, drafted the manuscript and approved its final version; MG, GD, RM, GP, and DL contributed to the study design and to analysis and interpretation of data, revised the article's intellectual content and approved its final version; MG, EG, PF, RG, MA and FC acquired data, revised the article's intellectual content and approved its final version. MG, GP and SDP take full responsibility for the integrity of this work as a whole, including the study design, access to data, and the decision to submit and publish the manuscript. All authors read and approved the final manuscript.
Correspondence to Stefano Del Prato.
The local ethics committee approved the study protocol, and the study was carried out in accordance with Declaration of Helsinki. Each participant signed a written informed consent.
MG has received travel grants from AstraZeneca and Novo Nordisk. MA has received speaker/advisory honoraria from Abbott Laboratories. FC has received travel grants from Novo Nordisk. GD reports past participation in advisory boards from AstraZeneca, Eli Lilly and Co and Novartis Pharmaceuticals. SDP reports past participation in advisory boards and/or receiving research grants from Abbott Laboratories, AstraZeneca, Boehringer Ingelheim, Eli Lilly and Co, Merck Sharp & Dohme, Novartis Pharmaceuticals, Novo Nordisk, Sanofi, Servier, and Takeda Pharmaceuticals. GP has received travel grants and speaker/advisory honoraria from AstraZeneca, Boehringer Ingelheim, Eli Lilly and Co, Merck Sharp & Dohme, Mundipharma Pharmaceuticals, Novo Nordisk, and Takeda Pharmaceuticals. All other authors (EG, RG, DL, MR, and PF) declare that they have no competing interests.
International Classification of Diseases (ICD-9) system codes collected during follow-up. Table S2. Baseline clinical characteristics of individuals with retinopathy, nephropathy and neuropathy compared with those with no MC. Table S3. Survival analysis by Cox proportional hazards regression according to presence of any degree of retinopathy at baseline. Table S4. Incidence analysis of major CV events by Cox proportional hazards regression according to presence of any degree of retinopathy at baseline. Table S5. Incidence analysis of coronary events by Cox proportional hazards regression according to presence of any degree of retinopathy at baseline. Figure S1. Distribution of microvascular diseases in the 774 participants with type 1 diabetes. Figure S2. Kaplan–Meier curves showing survival from all-cause death by MC groups in individuals without prior CV events. Figure S3. Kaplan–Meier curves showing cumulative incidence of major vascular events by MC groups in individuals without prior CV events. Figure S4. Kaplan–Meier curves showing cumulative incidence of coronary events in by MC groups in individuals without prior CV events. Figure S5. Kaplan–Meier curves showing survival from all-cause death in participants with retinopathy vs. those without DR. Figure S6. Kaplan–Meier curves showing cumulative incidence of major CV events in participants with retinopathy vs. those without DR. Figure S7. Kaplan–Meier curves showing cumulative incidence of coronary events in participants with retinopathy vs. those without DR.
Garofolo, M., Gualdani, E., Giannarelli, R. et al. Microvascular complications burden (nephropathy, retinopathy and peripheral polyneuropathy) affects risk of major vascular events and all-cause mortality in type 1 diabetes: a 10-year follow-up study. Cardiovasc Diabetol 18, 159 (2019). https://doi.org/10.1186/s12933-019-0961-7
Microvascular complications
Microvascular burden
Peripheral diabetic polyneuropathy


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Program Review: "Investing in Talent" Summit.
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Register for the 5th Annual Massachusetts Jobs and Workforce Summit today! Also, don't forget to submit your nominations for the WSG Champion Awards!
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Join us on April 10th up at the state house for the 2014 Youth Pathways Advocacy Day. Click here to RSVP!


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Hong Kong 'Umbrella' protesters found guilty of public nuisance
Nine pro-democracy activists in Hong Kong have been found guilty of public nuisance charges for their role in a civil disobedience movement that called for free elections in the city.
Among them are three prominent activists, seen as figureheads of Hong Kong's pro-democracy movement.
They could be jailed for up to seven years for their part in the "Umbrella Movement" protests of 2014.
Thousands marched demanding the right for Hong Kong to choose its own leader.
Those convicted include the so-called "Occupy trio" – sociology professor Chan Kin-man, 60, law professor Benny Tai, 54, and Baptist minister Chu Yiu-ming, 75.
They are seen as the founders of the movement that galvanised protesters in their campaign of civil disobedience.
"No matter what happens today… we will persist on and do not give up," Mr Tai told reporters ahead of the verdict.
Mr Tai, Mr Chan and five others were found guilty of two charges of public nuisance, and Mr Chu and one other of just one charge.
A large crowd gathered outside the court on Thursday to support them. It is not yet clear when they will be sentenced.
Like just another day
The nine defendants walked into the court building looking refreshed and in high spirits. All but one said a few words in what might have been their last hours of freedom before their predicted jail term.
Delivering his verdict, Justice Johnny Chan said the defendants had caused a nuisance – by occupying major roads – leading to injuries among civilians. The nine looked calm and not particularly emotional. By lunchtime they had gone, released on bail. Benny Tai, Chan Kin-man and Chu Yiu-ming smiled as they passed me, as if it was just another day.
They are yet to say if they will appeal. The court was adjourned for the day as the lawyers are yet to finish their mitigation submissions. The sentences have yet to be announced.
The broader pro-democracy camp already has bad relations with Beijing. Activists and politicians did express their anger but political analysts also warn that people might simply leave the movement out of frustration.
Seventy nine days of sit-in protests have already changed Hong Kong a lot. But today's verdict might serve more as a reminder that this city remains divided.


Focusing on the virtue of 'Unity through Diversity', our students have been finding about their own ancestry this month. A map at the front entry of the school has been used to pin the locations where the ancestors immigrated from. During the Multicultural Day on Mar 17th, we witnessed great performances, staff and students in cultural dress and we feasted on amazing variety of food. We hosted a special performance by Jocelyn Pettit, a local Celtic fiddler. Thank you to the parents, staff and students for a great day.
Last Friday, the Gr. 4 students participated in the Ministry of Education Satisfaction Survey. The Gr. 4 parents still have a chance to complete the survey until the end of April.
The report card distribution and the Parent Teacher interviews went well. We always appreciate conversations with the parents regarding student learning.
The after school activities mentored by HSS students continues to be a success. In April, we have basketball and cartooning on Tuesdays and volleyball and crafts on Wednesdays between 3:30 and 4:30 pm. These activities are open to Gr.3 to 6 students.
The Cake walk was a huge success! The students had so much fun. A huge thank you to all parents who donated the cakes. We would also like to thank Nester's Market and Save On Foods for their generous donations. On the Wacky Hair Day, we witness a variety of interesting hair styles.
On another note, we are noticing that a fair number of our students are arriving at school late. We would like to remind the parents that school starts at 8:50 sharp and we would appreciate the student drop off before this time. As well, it would be helpful if you could book any appointments or holidays outside of instructional time if possible. We are concerned whenever students lose instructional time that may result in learning gaps.
Finally, we would like to wish a happy, restful and fun Spring Break! School reopens on April 7th.


Culture has always been in London's DNA. It is part of the story of our city and gives our capital its character and authenticity. It also plays a vital role in our economic success. The creative sector generates £52bn for London every year and is responsible for one in six jobs. It is what makes the city a place where people want to live, work and do business.
But while we're all used to seeing big cities plan their future needs when it comes to trains, roads and hospitals, it's never been the same for culture – until now. Our cultural infrastructure plays a huge role in our city, but until now we've not had a proper picture of our venues, spaces and studios, nor been able to highlight gaps or risk areas.
We know there's been a worrying decline in our cultural spaces and it's no secret that we have seen artists and creative businesses struggle in the face of rising rents. But without knowing the full picture, it's hard to support our creative communities and ensure culture can thrive.
That's why we have launched an online map capturing the city's full range of cultural spaces. From local facilities like arts centres, libraries, community centres and pubs, to LGBT+ venues, theatres and music venues, to affordable artists' studios and creative workspaces, our Cultural Infrastructure Map gives us a detailed snapshot for the first time.
The map shows us that Hackney and Camden are vying for the highest number of grassroots music venues, and that Westminster is the borough with the most pubs. It shows us that London currently has 240 artists' workspace buildings, with Hackney hosting the highest number of creative workspaces. Outside central London, the map indicates that Ealing plays an important role in providing prop and costume hire, and we can see that Brent has a high concentration of music businesses.
We have released this map alongside our wider Cultural Infrastructure Plan, which includes online toolkits and resources to help local authorities, property developers, businesses and cultural institutions to build new studios and venues to the right specification, and ultimately grow the culture on offer in London.
This new intelligence about where London's cultural infrastructure is located will help local planners better understand the cultural ecosystems in their areas. It will support smarter regeneration and enable businesses, local authorities and cultural leaders to support and develop the cultural spaces London really needs. We need to protect these important spaces if we are to cement London's place as an international cultural capital.
We've established the first ever Culture at Risk Office, which has already supported 350 cultural spaces at risk of closure, and we've created the most pro-culture planning framework the capital has ever seen.
Crucially, the map is part of our commitment to open data, free for all to use. The data joins more than 700 publicly available datasets in the London Datastore. Now Londoners, cultural institutions and culture lovers can help us fill in any gaps to fully capture the city's cultural gems on the map.
The Mayor's draft London Plan includes a requirement for developers to ensure existing venues, clubs and pubs still have a home in new developments, and includes the Agent of Change principle that helps protect venues by putting the onus on developers to meet the cost of soundproofing and noise-reduction measures.
We are working hard to support these venues, and we're seeing the first green shoots of recovery. For example, following a decade of steep decline, the numbers of LGBT+ venues and grassroots music venues has stabilised in the last year.
We're also working hard to support our artists. Last year we launched the city's first-ever Creative Enterprise Zones which will create more than 3,500 jobs and 40,000 square meters of new affordable creative workspace. This year we joined forces with Bloomberg Philanthropies and Outset Contemporary Art Fund to launch the Creative Land Trust, an independent organisation which will secure a thousand affordable creative workspaces in five years for artists in the capital.
London's cultural spaces play a vital role in bringing our communities together and the creative influence of our artists is felt in every corner of the city. That's why it's so important that we protect our creative communities, and help Londoners access the wide range of culture on their own doorstep.
Justine Simons is Deputy Mayor, Culture and the Creative Industries in the Mayor of London's Office.


A several meters long mock-up ship for children to play, a canopy stage, an open-air playground - to name only a few attractions of the world-class recreation area in Warszów which is being constructed by Polskie LNG.
A mock-up ship for children, a professional stage and a playground are being constructed on the 3.4 thousand square meters area adjacent to the Municipal Culture Centre.
The recreation area in Warszów is located near the LNG Terminal and it is one of the biggest projects run by Polskie LNG for the benefit of the local residents. The cost of the investment will amount to about PLN 1 million and will combine leisure facilities and innovative educational pursuits.
The recreation area will meet the needs of the residents of the district and the city who need a well-organised and safe recreation area. A mock-up ship for children, a professional stage and a playground are being constructed on the 3.4 thousand square meters area adjacent to the Municipal Culture Centre in 18, Sosnowa Street.
The entire area will be fenced, there will be lightning and a sound system on the stage and auditorium. The place will serve the dual purpose of a recreational and educational facility. The display will also include showcards presenting the history of Świnoujście and the district of Warszów as well as information on LNG Terminal. The site's commissioning is planned in 2014.


Angèle Dubeau is a Canadian violinist born on March 24, 1962. She studied at Juilliard and at the Montreal Conservatory of Music. She is best known for her work with the group called La Pieta. This ensemble is an all-female string band. As far as I know, she still plays the Rosiers Stradivarius violin from 1733. There are many CDs of her playing solo and in ensemble.


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Why I'm Stumbling
Share Your Story / Contact me
More things we like
Stumbling on Sexuality
The sultry affair with romance novels
Kim from Canada
I have always been really into reading. When I was growing up, the most easily available books where those dime store romance novels, usually Harlequin brand. My mom had quite a collection of them and new ones were always coming. Between the ages of ten and thirteen, I easily read over a hundred of these books. My mom had no problem with me reading them either. She was like whatever, she's in her room reading, at least I know where she is.
It's funny where parents choose to draw their lines. I think she was more concerned about me going out and doing stuff in the world than reading about it. If it was outright porn she would be like fuck this and it would be done in two seconds but this was ok. If it's sold in a pharmacy, then it probably wasn't too bad. It was breaking her Judeo-Christian rules to some degree but at least she knew where I was. I was the baby out of five kids so she couldn't give too many fucks. She was just trying to survive.
I really loved reading but it was a lot of escapism too, it was so much easier to build worlds back then. I started reading these romance novels and recognizing in a very non-critical way that there were all of these kinds of tropes, dark princes, the stern guys who were hard to love and unyielding. Then there were some who were super flirty, which are the ones I liked. I didn't like the stern ones, I thought they were assholes. Women were supposed to love you because you have rough hands? Who cares if you have rough hands? Treat me nice.
I never wanted to tell anyone I was reading these books. It was my private world, like Dungeons and Dragons for girls. I didn't want to tell anyone else because if you hear their reaction to it and they don't like it, it's going to shatter your world. It's so fragile, why would you do that? You have to protect so much about yourself when you are young. North America is a bully culture; there is no debate about that. You have to be so proactive in being a different person just to get some form of acceptance. You are trying to build something nobody else can touch. Not telling someone doesn't mean you are shutting them out, it means you are maintaining it for yourself.
In these made up worlds in my books, I could imagine complete faces of people I had never seen before and really get into it. I was good at textures and how people looked, where they lived, houses they lived in. I was really into the details.
It's interesting to see that kind of dance the two characters go through because it has this rhythm about it. It's usually these people who meet and it's intriguing but there is always some kind of weird conflict that is going on. Something tears them apart and there is some kind of misunderstanding. Then afterwards she realizes or he tells her that there is this misunderstanding, it's like any rom-com. The misunderstanding is not what it seemed and then they can actually get together.
The getting together part was the most boring for me. It's satisfying only for that moment. It's like an orgasm. I was more interested in the whole thing leading up to it, the sexual exploration and figuring out what the boundaries were.
Since the characters weren't able to be in each other's company very often, the words were so sparse that they meant so much more. Usually the author is filling in a lot with things like, "he turned to her in this kind of a way," or "he turned as if to say." I found that interesting because it spoke to the way that we speak without speaking.
One thing I liked was most of the books didn't speak down to you. There were some of course where the boy enters and you are supposed to be excited that they are there. That was boring. I didn't want to faun over some guy who didn't deserve it. I knew the important part was the way he acted or the way he held himself or the way that he talked to me. He had to do something to make you interested. Not just because this is the story and he's the only person there is so make it work.
There was one that I loved a lot, it was called Unconquered, I think by Bertrice Small. What a name. If your name is Bertrice, what else can you do besides write romance novels? That book changed my life. It started off, spoiler alert, with a privileged woman in Maryland. They had this big estate and her father died and the rule was that the estate would go to the next male heir. So it was going to something like a half cousin and she was like fuck this, this is my house, I grew up here, it should go to me.
It had this feminist streak and I loved it off the bat. The guy, the partial cousin, was partial enough to be romantic, was her romantic aspiration in the end but there was so much fighting. At times I thought she would give in and other times she was so over him and couldn't stand him. I thought that was kind of cool because she didn't give in too soon. If they give in too soon it's boring. She was losing something important, she was losing her estate so she fought tooth and nail but eventually, in order to keep her family estate, she had to marry him.
At some point, she gets sold into slavery into this harem in Egypt or somewhere but she has a good experience, which of course never happens. She experiences all of these orgasms and sexual pleasures with the man that runs the harem. There is always the possibility to go off to the consulate and be rescued but she has a real deep relationship with this guy who was not her husband. She said to him, "I feel really conflicted because I am a wife and I know I was kidnapped but here I am with you and I have had pleasures with you outside of my husband."
He said "those are your pleasures, that's no ones business" and it blew my fucking mind.
As a kid it's just like what? Is this possible? I hope I get kidnapped! Ok for the record no, but for me it was so crazy. She had different relationships and then she went back to her husband. That was what was intriguing about it. She had all of these different lives. She was fiercely independent and fiercely herself. That was what made it interesting. Any time you get a whiff of different possibilities and different narratives you really feel alive and that is what I connect it to.
She also had a baby and her baby wasn't the center of the story after. I resented that in a lot of novels. The ending in a lot of romance novels was oh they got married! I don't need to see that, I was here for the sex and the intrigue. I don't really care about you getting married, it's implied. I was really bored by that and I felt kind of abandoned when a story ended that way.
That book also had one of my favorite lines out of all of the books I was reading. "His phallus was l like an ivory tower, veined and blue."
You can't beat that.
One of the things that I really liked about the novels was that it was exactly at the level that I needed at the moment.
As a kid I would draw things that were sometimes overtly sexual. I thought it was funny, haha look it's a dick type of thing or people kissing. I would show them to my friends and I just thought it was funny. I never drew anything like penetration, that was so gross and foreign and violent to me. But people kissing, oh yeah, that was the level I was at. I was horrible at drawing people so they were distorted with these huge lips.
One time my teacher found some drawings and she called my mom. I was like oh no my life is over, she is going to murder me! You don't understand man, it's not a joke! It's not a joke! My mom asked me where I saw this kind of stuff and I told her, in these magazines that I found from my brother and she lost it. My brothers were in their early teens so they weren't exactly careful about hiding their porn.
He got in massive trouble, especially because she had some fucking teacher calling her. It's always bad news when your kid's teacher calls you. I'm sure you feel so much judgment as a parent, they are looking down on you. She's this black woman raising kids by herself, it's like I don't need to deal with this shit, I am trying to keep shit together. Don't bring me this crap.
Between the magazines I found from my brother and a soft-core porn that I saw once accidentally on late night television, I was able to understand the gist of what sex was. What surprised me about the difference between porn and the novels I was reading was that there didn't seem to be any joy attached to the porn. I couldn't attach those anguished sounds with pleasure.
There is the kind of porn where it feels like I am a potential victim and the kind of porn that is more drawn out with a story. Somebody has earned my interest, my care. I would have liked that kind of story where people didn't have to have this forced coquettishness or coyness of oh my god, what are you doing to me?
You know what the fuck is going on. It's either that or she is being attacked or violated and it's not romantic, it's not even cool. You never encounter sex as a good thing in porn. It's something from a male gaze. It's not about you, it just involves you because you have the parts.
I don't remember where I heard this from but it really stuck with me:
"When it comes to women and sex, women like everything around sex almost as much as the sex itself."
That is exactly what it was, sex itself wasn't the plan. I liked everything around sex, especially since I didn't fully understand sex. I knew how it worked mechanically but I didn't quite understand how it worked organically. You don't learn that kind of thing from porn and I didn't get much information from anywhere else.
My sex talk with my mom was about three sentences at most. She said, "you know what it is, don't do it." That was it basically.
I am sure these romance novels affected the way I thought about relationships when I started dating, probably in some ways that I can't even describe. I feel some of it gave me high standards and maybe some of it kind of entrenched me with a lot of bullshit. There are probably weird connotations going around in my subconscious that I don't know about. My subconscious and I are friends but we don't talk.
I had to get past a lot of things to get to the point of who I know myself to be. At least it gave me a place to start because what else is going to teach you? A lot of kids are starting with porn and that's so far from what sex actually is. I try not to have too much judgment about it but sex is a powerful thing. It's not a moralistic thing at all, sex is just reality, it's where we come from.
There is a lack of diversity in terms of thinking about sex and how organic it is. It's really to the point and to the detriment of the woman sometimes. You have to divorce yourself from it. Most of the time when you watch porn you're like oh my god do I hate women? Just even to enjoy it you have to fracture parts of your mind because your empathy can't stand a lot of it. Here the empathy wasn't lacking because it was given the dignity of the story, some kind of evolution or background to say context matters and things lead up to other things and they all matter in their own way. In the way that life actually does.
Eventually I stopped reading the books kind of all at once. My friends started to have boyfriends and the mysticism of the relationships and sensuality and sexuality kind of fell away. None of these interesting things that were happening in the stories would ever happen in real life. By learning more and more about the real world, these imaginary worlds stopped being so intriguing.
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June 11, 2018 64 MIN READ TAGS: bullying, Canada, childhood, Children, discovery, experimentation, exploration, exploring sexuality, kids, learning, learning about sex, learning about sexuality, pleasure, ponography, porn, porno, puberty, reading, romance, romance novels, sex, stories, youth BY: stumbling 0 COMMENT
The making of a pansexual polyamorist
Playing house, the rated R edition
Stories Learning to be a rebel
Stories I want you to want me
Stories A/S/L?
Stories The Russian super women
Stories Growing up with zero shame
Stories Education through media
COPYRIGHT © 2017 Stumbling o Sexuality


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Q: Regex for query entities I am looking for a regex able to differentiate substrings within a query. A practical example would be a query for a movie database, where the goal is to return the results:
# query 1
title:movie one year:2018 rating:10
# query 2
year:2019 rating:20

For the first example, I want a regex able to identify the title, year and rating, which is movie one, 2018 and 10, respectively.
I achieved a solution that is close but doesn't fully satisfy the requirements:
title:\w+
year:\w+
rating:\w+

This works for queries composed of single words (e.g. title:movie), but doesn't work for those with multiple entities (e.g. title:movie one). Is there a way I can accomplish this?

A: You could use non-capture groups to match the "labels" and then use capture groups to match all characters between the labels (instead of just word characters, so that you capture spaces, etc). For example:
import re

s = 'title:movie one year:2018 rating:10'

matches = re.match(r'(?:title:)(.*)?(?:year:)(.*)?(?:rating:)(.*)?', s).groups()
print(matches)
# ('movie one ', '2018 ', '10')

A: Something like this?
import re
string='Movie One'
pattern='[\w\s]*'
result=re.match(pattern,string)
print(result)

Result:
<_sre.SRE_Match object; span=(0, 9), match='Movie One'>

redpajama_set_name: RedPajamaStackExchange


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Being A Fan Week 7 Previews: Part Two
Week 7 Previews: Part One
By Isaac On May 18, 2017 · Add Comment
By BTSH Media Writers
Butchers (L/W/L/L/W) at Rehabs (W/L/W/W/W), Tompkins East, 1300
Burke's got his work cut our for him in this game.
Don't let the last five games for the Butchers fool you. Two of their three losses came from teams in the better conference (go ahead and roll your eyes), and no loss was a blowout. The Rehabs, conversely, have been cruising through six weeks without a serious hiccup, with their only loss to Bob "Olmec" Weyersberg's old team, Fresh Kills, who still haven't faced a regulation loss. Just goes to show how strong the top teams really fare out this season.
With the top female scorer (Cherie "Go Ducks!" Stewart) as well as the #4 top male scorer to date (Joey "Fodas-se Benfica" Batista), the Rehabs are likely to seize the day. Awaken the beast in David St. Jules—watch this guy in scrimmage, by the way—and the Butchers will give the rossonero a hard time.
Prediction: Rehabs grapple with the meat cleavers, but will find themselves victorious within 50. It will be a dogfight, but not to Mr. Vick's palate.
Gut Rot (W/W/L/L/W) at Corlears Hookers (L/W/W/L/W), Tompkins West, 1300
Don't peel your eyes off this beauty of a matchup; that is, if you weren't going on a bender the night before and miraculously show up just to watch a 1pm game. It's Ellery versus Cro—a duel for the ages. What's absolute: Ellery will have his shirt off long before regulation (because the O's are still 0.5 games behind the Yankees); Cro will have yet ordered his 958th cherished red hat during the halftime break (because New Yorkers are in love with Chinese fashion /s).
Hockey has been interesting for both sides this season. The royal purple a-la- Los-Angeles- Kings squad acquired much talent (namely, Dark Rainbows imports) and has been flourishing thus far. The other franchise in green/black/I don't know continues to make historical leaps and bounds in the last weeks, securing a crowd-infused win against Fuzz (in their throwback 2012 Elves regalia, sleeved and unsleeved) in Week 6.
Although it's my job to write a prediction, I'm crestfallen to realistically choose the Hookers to win. Bill L will probably notch a brace and Kamen will put the nail in the coffin. Longwell will contend to post a shutout, but the persistence of Jeff "Peaches" Hendricks, Tommy, and Becca could put them on the board. Let's hope so.
Prediction: As he's reading this, Peaches will surely flip me the bird for not choosing his side, but trust me… my heart—like the rest of the league—cheers for Gut Rot to continue pulling upsets this year.
What The Puck at Dark Rainbows
Emily and the Pucks have a lot to smile about this season.
Bright orange and dayglo pink. Stare too long at this game and the two colors are going to start swirling together as you enter a hypnotic trance. You won't know if you're watching WTP v. Rainbows or the "Groove Is In The Heart" music video.
I was going to talk about the addition of Claire to WTP this season, but then I'd have to bring up the Caps' heartbreaking loss and how the Pucks are still depressed about it. Well, I guess I already did. And, depressed they are. I recently saw Holden McNeil and he told me that Justin has been walking around like a morose motherfucker whose cereal has been shit in (please someone get this reference). Dudolevitch quit his band because he felt like their show jinxed the Caps.
I don't want to say that WTP are kind of a mess right now, but, again…..I guess I already did.
Will the Rainbows take advantage of WTP being down in the dumps? They themselves are coming off a rough loss to the mighty Fresh Kills, and additionally they are still looking for their first win. I can never remember if Tia is actually going to be there on a given week, but if she is, and she, Josh, and new Rainbow Paul go on the attack, it could spell trouble for the bright orange portion of the swirling vortex.
Prediction: Emily cheers her team up enough to win, and the Rainbows are left searching for that elusive first W. 4-2, Pucks. (Susie or Liz score in this game. I won't say which one of them.)
Filthier at Fresh Kills
Cupcakes are muffins that believed in miracles. This Sunday Ann, Tim, Kate and the rest of Filty could be that cupcake. Stick together, communicate, don't get caught out of position and get the ball to Suvin. That dude can cut through a defense like he's peeling the skin off of tangerine.
Well, perhaps not against Gabe when he's out on defense. Soko's surprise move this season to put his superstar player on D raised more than just a couple eyebrows. But the doubters have been quieted as everyone on Fresh Kills, even Natasha, has been rowing in the same direction.
Prediction: Filthy will have to wait for another Sunday to collect their first division win of the season. Ariel does work and the Kills moonwalk to 5-2.
Gremlins at Instant Karma
Fuck you Jamie.
Back in 2010, one of Adriano's first big moves was to integrate the teams for a week. So it would have been What the Elves vs. the Happy Little Puck. God thankfully intervened and Adzo scrapped the idea after every player in the league besides Walker hated it. (Think Seinfeld name tags.)
This game reminds me of that terrible idea. These two teams are the most friendliest of friends. Sure, Mark is going to complain to the refs about something, but for the most part there will be laughs, pats on the back and an amazing time had by all. It's the Spirit of BTSH. And just writing this paragraph makes me puke and want to send Diana Marko through a fence.
Prediction: The Gremlins are littered all over the scoring list. Erich is 2nd in the league, Cody just got his (I'm assuming) first career BTSH hat trick, Maire is in there for the women and Jamie is having an ok season with a 1.83 goals against average. Personally, I think you need to be 1.82 or better to be considered good, but whatever.
For Karma….Brianna is on the scoring list because she scored twice in one game.
Crickets.
OK, so maybe they aren't as prolific as the Gremlins but Pete, Al and Bill are so old and have been in the league so long, Gil calls them, "sir." So maybe they won't score that many goals, but they probably are good positionally or something?? But not good enough as Grems take this 4-2. The league takes solace in the fact that Jamie adds to his already horrendous GAA.
Part 1 of the Week 15 Previews
Playoffs Round of 16 Previews – Part 2
Week 2 Previews Part 2


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