OBJECTIVE To compare the incidence of type 1 diabetes (T1D) before and during the coronavirus disease 2019 (COVID-19) pandemic and determine whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with T1D development. RESEARCH DESIGN AND METHODS All Danish residents age <30 years free of diabetes from 2015 to 2021 were included. Individuals were followed from 1 January 2015 or birth until the development of T1D, the age of 30, the end of the study (31 December 2021), emigration, development of type 2 diabetes, onset of any cancer, initiation of immunomodulating therapy, or development of any autoimmune disease. We compared the incidence rate ratio (IRR) of T1D using Poisson regression models. We matched each person with a SARS-CoV-2 infection with three control persons and used a cause-specific Cox regression model to estimate the hazard ratio (HR). RESULTS Among 2,381,348 individuals, 3,579 cases of T1D occurred. The adjusted IRRs for T1D in each quarter of 2020 and 2021 compared with 2015-2019 were as follows: January-March 2020, 1.03 (95% CI 0.86; 1.23); January-March 2021, 1.01 (0.84; 1.22), April-June 2020, 0.98 (0.80; 1.20); April-June 2021, 1.34 (1.12; 1.61); July-September 2020, 1.13 (0.94; 1.35); July-September 2021, 1.21 (1.01; 1.45); October-December 2020, 1.09 (0.91; 1.31); and October-December 2021, 1.18 (0.99; 1.41). We identified 338,670 individuals with a positive SARS-CoV-2 test result and matched them with 1,004,688 control individuals. A SARS-2-CoV infection was not significantly associated with the risk of T1D development (HR 0.90 [95% CI 0.60; 1.35]). CONCLUSIONS There was an increase in T1D incidence during April-June 2021 compared with April-June 2015-2019, but this could not be attributed to SARS-CoV-2 infection.

Introduction Drugs that influence cardiac electrophysiological properties by impacting on cardiac ion channels have been associated with an increased risk of out-of-hospital cardiac arrest (OHCA) due to ventricular tachycardia/ventricular fibrillation (VT/VF). It is unknown whether dihydropyridines, which block L-type calcium channels, are associated with increased risk of OHCA. Purpose To determine whether the widely used dihydropyridines nifedipine and amlodipine are associated with increased OHCA risk. Methods We performed a multi-country case-control study using data from the Dutch Amsterdam Resuscitation Studies registry (ARREST, 2005-2011) and the Danish Cardiac Arrest Registry (DANCAR, 2001-2014). Both registries are community-based registries of all-cause OHCA and are part of the ESCAPE-NET consortium that studies OHCA across Europe. Cases were cardiac-caused OHCA patients with VT/VF, and controls (up to 5 per case) were non-OHCA individuals matched on age, sex and index (OHCA) date. Dutch controls were sampled from PHARMO Database Network and Danish controls from the general (Danish) population. We compared current use on the index date of the study drugs (prescription within 90 days before OHCA) to no use of any dihydropyridine, using conditional logistic regression analysis with adjustment for well-known risk factors of OHCA. Results We studied 2,503 cases and 10,543 controls in ARREST (median age 67.0 years, interquartile range [IQR] 57.0-77.0 years; 77.4% male), and 22,208 cases and 111,040 controls in DANCAR (median age 74 years, IQR 64-82 years; 62.9% male). In both registries, current use of high-dose nifedipine (≥60mg/day), but not low-dose nifedipine (

s e427 whom BP did not decrease. Pts in whom cIMT decreased had greater arterial injury and lower metabolic abnormalities at diagnosis. After 12 months these pts had greater decrease of leptin and greater increase of SAT. Pts in whom LVH decreased were younger and had greater decrease of WC,WHR and lesser decrease of adiponectin concentration compared to pts in whom LVH did not decrease. When pts were divided according to the changes in fat tissue distribution it occurred that pts in whom VAT/SAT ratio decreased had greater regression of metabolic abnormalities and regression of TOD. The step-wise regression analysis revealed that the main predictor of LVH and cIMT regression was the decrease of waist circumference (R = 0.205; β = 0.481; p = 0.005), the main predictor of WCSA was the decrease of iVAT/ SAT (R = 0.472; β = 0.476; p = 0.004). Conclusions: Visceral obesity is strictly related to metabolic abnormalities and TOD in children with PH. The main predictors of TOD regression are the decrease of iVAT/SAT. It suggest protective role of SAT. PP.LB2.450 AUTOMATED OFFICE BLOOD PRESSURE RECORDED AT ONE MINUTE INTERVALS M. Myers. Sunnybrook Health Sciences Centre, Toronto-Canada Background: Automated office blood pressure (AOBP) is replacing conventional manual office BP (MOBP) in routine clinical practice in Canada and elsewhere. AOBP provides more accurate readings and virtually eliminates the white coat effect seen with routine MOBP. Most studies on AOBP have used the BpTRU device which does not require any antecedent period of rest, takes a single ‘test’ reading and then automatically records 5 readings at 1 or 2-minute intervals (timed from the start of one reading to the start of the next reading) with the patient resting alone in the examining room. Objective: To examine the time-course of the decrease in BP when AOBP is recorded at 1-minute intervals and to compare AOBP with the awake ambulatory BP. Methods: Patients (n = 139) with a manual systolic BP ≥ 140 mmHg who were referred for 24-hour ambulatory BP monitoring (ABPM) were enrolled in the study. A series of 5 AOBP readings recorded over 5 minutes with the patient resting alone in an examining room was obtained using the BpTRU device prior to initiating ABPM. Results: The initial ‘test’ reading (mmHg) with the observer present averaged 153.6/86.6. The next 5 mean AOBP readings in sequence with the patient resting alone were 148.2/83.3, 142.2/82.1, 140.8/80.8, 138.1/80.8 and 136.2/79.9. The mean of all 5 AOBP readings was 142.1/80.9 compared to a mean awake ambulatory BP of 142.3/81.8. If only the first 3 or 4 readings taken with the patient being alone were used to calculate the AOBP, the mean values would be 143.7/82.1 and 142.3/81.8, respectively. Conclusion: In previous studies in which AOBP was recorded 5 times at 2-minute intervals, the entire decrease in BP occurred after the second of 5 readings. In contrast, readings taken at 1-minute intervals show a gradual decrease in BP from the first to last reading. AOBP taken at 1-minute intervals is similar to the awake ambulatory BP when either 4 or 5 readings are recorded under research conditions. Including the time taken for an initial ‘test’ reading, AOBP can be obtained over 5–6 minutes without any antecedent period of rest. PP.LB2.451 INSULIN PROMOTES VASCULAR SMOOTH MUSCLE CELL PROLIFERATION VIA MICRORNA-208 MEDIATED DOWN-REGULATION OF P21 Y. Zhang, Y. Wang, X. K. Wang, Y. Zhang, C. Zeng. Daping Hospital,

Scandinavian Journal of ImmunologyVolume 15, Issue s9 p. 223-240 Synaptic Membrane Proteins in Mammalian Brain E. BOCK, E. BOCK The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorI. DIVAC, I. DIVAC The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorB. NORRILD, B. NORRILD The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorN. A. THORN, N. A. THORN The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorC. TORP-PEDERSEN, C. TORP-PEDERSEN The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorM. TREIMAN, M. TREIMAN The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this author E. BOCK, E. BOCK The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorI. DIVAC, I. DIVAC The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorB. NORRILD, B. NORRILD The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorN. A. THORN, N. A. THORN The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorC. TORP-PEDERSEN, C. TORP-PEDERSEN The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this authorM. TREIMAN, M. TREIMAN The Protein Laboratory; Institute of Neurophysiology, Panum Institute; Institute of Medical Microbiology; and Department of Physiology C, Panum Institute; University of Copenhagen, Copenhagen, DenmarkSearch for more papers by this author First published: November 1982 https://doi.org/10.1111/j.1365-3083.1982.tb03766.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume15, Issues9November 1982Pages 223-240 RelatedInformation

In neurosecretosomes, isolated from ox neurohypophyses, both guanylate and adenylate cyclase activity was shown to be predominantly membrane-bound. Membrane-bound adenylate cyclase was inhibited by increasing the ionized calcium concentration from 10(-7) M to 10(-5) M, but was stimulated by calmodulin in the presence of 10(-7) M and 10(-5) M ionized calcium. In contrast, neither calcium ions nor calmodulin affected the activity of membrane-bound guanylate cyclase. Soluble cyclic AMP and cyclic GMP phosphodiesterase activities increased with increasing ionized calcium concentration (10(-7) M to 10(-3) M). At 10(-7) M ionized calcium concentration, both soluble phosphodiesterase activities were stimulated by calmodulin. Both the membrane-bound phosphodiesterase activities were inhibited by a high ionized calcium concentration (10(-3) M) and not affected by calmodulin.

Annals of the New York Academy of SciencesVolume 356, Issue 1 p. 369-370 EFFECTS OF Ca2+ AND CALMODULIN ON ENZYMES OF CYCLIC NUCLEOTIDE METABOLISM IN OX NEUROHYPOPHYSEAL SECRETOSOMES Darlene A. Dartt, Darlene A. Dartt Institute of Medical Physiology C University of Copenhagen DK 2200 Copenhagen N Denmark Present Address: Department of Physiology, Tufts University School of Medicine, Boston, Mass. 02111.Search for more papers by this authorChristian Torp-Pedersen, Christian Torp-Pedersen Institute of Medical Physiology C University of Copenhagen DK 2200 Copenhagen N DenmarkSearch for more papers by this authorNiels A. Thorn, Niels A. Thorn Institute of Medical Physiology C University of Copenhagen DK 2200 Copenhagen N DenmarkSearch for more papers by this author Darlene A. Dartt, Darlene A. Dartt Institute of Medical Physiology C University of Copenhagen DK 2200 Copenhagen N Denmark Present Address: Department of Physiology, Tufts University School of Medicine, Boston, Mass. 02111.Search for more papers by this authorChristian Torp-Pedersen, Christian Torp-Pedersen Institute of Medical Physiology C University of Copenhagen DK 2200 Copenhagen N DenmarkSearch for more papers by this authorNiels A. Thorn, Niels A. Thorn Institute of Medical Physiology C University of Copenhagen DK 2200 Copenhagen N DenmarkSearch for more papers by this author First published: December 1980 https://doi.org/10.1111/j.1749-6632.1980.tb29631.xCitations: 1 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume356, Issue1Calmodulin and Cell FunctionsDecember 1980Pages 369-370 RelatedInformation

ABSTRACT Secretory granules isolated from bovine neurohypophyses released vasopressin in the presence of a buffered medium containing ATP, Mg 2+ and KCl. Substitution of K + in the medium with Na + or choline did not affect the release. Substitution of Cl − with either sucrose, sulphate or acetate strongly reduced the release. Analogues of ATP, substituted at the β-γ anhydride bond with methylene or imido groups caused a smaller release which was not related to a very small breakdown of analogues that occurred. It is suggested that at least part of the ATP induced release is due to a physicochemical action.